Podcasts about mmhg

Today's Case A 44-year-old female presents to the emergency department with acute onset epigastric pain for the past 2 days, constant, with radiation to the back. Her eyes and skin “turned yellow” 1 day ago. She denies any fevers. The patient drinks one or two beers per week, does not smoke, denies nonsteroidal antiinflammatory drug (NSAID), use and is not on glucocorticoids. She denies any heartburn or acid reflux symptoms. She had right upper quadrant (RUQ ) abdominal pain that was colicky and worsened with food intake 1 week before, which resolved spontaneously after 1 day and she therefore did not seek medical attention. Her blood pressure is 118/55 mmHg, pulse rate is 105/min, respiration rate is 20/min, oxygen saturation is 97% on room air, and body mass index is 38. Her skin is noted to be jaundiced and scleral icterus is present. Murphy's sign is negative. Today's Reader Jared Fehlman is an Internal Medicine Resident at Huntington Health Hospital in Pasadena, California. About Dr. Raj Dr Raj is a quadruple board certified physician and associate professor at the University of Southern California. He was a co-host on the TNT series Chasing the Cure with Ann Curry, a regular on the TV Show The Doctors for the past 7 seasons and has a weekly medical segment on ABC news Los Angeles. More from Dr. Raj The Dr. Raj Podcast Dr. Raj on Twitter Dr. Raj on Instagram Want more board review content? USMLE Step 1 Ad-Free Bundle Crush Step 1 Step 2 Secrets Beyond the Pearls The Dr. Raj Podcast Beyond the Pearls Premium USMLE Step 3 Review MedPrepTGo Step 1 Questions MedPrepTGo Step 2 Questions Learn more about your ad choices. Visit megaphone.fm/adchoices

The Lancet Volume 353, Issue 9146 p9-13 January 02, 1999Background: Accumulating data at the time suggested functional benefits of antagonism of beta-adrenoreceptors in patients with heart failure. Multiple specific beta-blockers were being tested in trials. The CIBIS 1 trial found a trend towards 20% lower mortality in the bisoprolol (a highly cardio-selective beta-blocker) group and 30% fewer admissions to hospital for worsening heart failure. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II) trial was designed to test this evidence further.Patients Eligible patients had New York Heart Association Class III-IV symptoms with LVEF ≤ 35% and were stable on diuretics and ACE-inhibitors. Exclusion criteria included recent MI or coronary intervention, AV block or resting heart rate less 60 bpm and systolic BP < 100 mmHg. Patients already on beta-blockers or with planned therapy with beta-blockers were also not enrolled.Cardiology Trial's remains independent, free of industry ads, due to reader generosity. Please consider becoming a free or paid subscriber.Baseline Characteristics The mean age of patients was 61 years, 81% male, and 83% Class III. The mean LVEF was 28%. About half the patients had ischemic heart disease, 12% primary dilated cardiomyopathy and nearly 40% had a mixture of valvular heart disease, hypertensive heart disease or unproven ischemic disease.The mean SBP on enrollment was 130 mmHg and resting HR was 80 bpm. The mean duration of heart failure before enrollment was 3.5 years. About 20% had AF at baseline. Nearly all patients were on ACE-I and half were on digoxin.Trial Procedures There was no run-in period. CIBIS II was double blinded. Slightly more than 2,600 patients were randomized 1:1 to bisoprolol or placebo in 274 hospitals across 18 countries.Patients in the bisoprolol group were started at 1.25 mg daily and titrated up weekly to as high as 10 mg daily. The goal was to attempt the highest tolerated dose. Patients were seen every 3 months.Endpoints The primary endpoint was all-cause mortality. Secondary endpoints included all-cause hospital admissions, cardiovascular mortality, combined CV death and CV hospital admissions, and premature treatment withdrawals.The authors estimated a 11.2% mortality in the placebo group and powered the trial to find a 25% reduction in death in the bisoprolol arm over 2 years.Results The trial was sopped early (mean follow-up 1.3 years) after the planned second interim analysis for benefit. The primary outcome of all-cause death occurred in 11.8% in the bisoprolol group vs 17.3% in the placebo arm (HR 0.66 (95% CI 0.54-0.81, p < 0.0001)).Bisoprolol reduced sudden death (3.6% vs 6.3%), all-cause hospitalization (33% vs 39%), CV death (9% vs 12%). Permanent treatment withdrawal occurred in 15% of both arms.The subgroup analysis showed no substantial treatment heterogeneity. The most common dose was 10 mg daily reached in 43% of patients.Conclusion The 34% reduction in death was clinically meaningful and statistically robust. Our confidence in such a large effect size stems from a) previous data on beta-blockers, which found similar effects, b) the 42% reduction in sudden death in the bisoprolol arm and c) the large reductions in all-cause hospitalization. In addition, the trial conduct appeared strong with almost no lost-to-follow up. The lack of run-in period strengthens the external validity of CIBIS II.The same caveats seen in the US carvedilol trial also apply to CIBIS II, namely that patients were ambulatory, outpatients, mostly with Class III symptoms. Patients enrolled in the trial had a mean SBP of 130 mmHg and a resting heart rate of 80. Nearly all patients were tolerating ACE-I and half were taking digoxin. In addition, patients were started on low-dose and gradually titrated higher. The majority of patients were on higher than 5 mg daily.The authors warned against applying these results to non-ambulatory patients with Class IV symptoms, especially if there was recent instability. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

14th ACC 2025: SBP < 130 mmHg Linked to Reduced CV Mortality in Adults +80 Y

La hipertensión arterial es una enfermedad silenciosa que puede provocar infartos, accidentes cerebrovasculares y daño renal si no se trata a tiempo. Es importante acudir al cardiólogo si tus cifras superan 140/90 mmHg, tienes antecedentes familiares, diabetes, obesidad, o si presentas síntomas como mareos, palpitaciones o dolores de cabeza frecuentes. Un diagnóstico y tratamiento temprano son clave para proteger tu salud cardiovascular y evitar complicaciones graves. Cuidar tu corazón es invertir en tu salud a largo plazo.El Dr. David Arturo Castán Flores invita a escuchar el #podcast para conocer más del tema. ¡No te pierdas sus recomendaciones! ¡Disfruta del episodio 265 y continúa escuchando cada uno de nuestros #PodcastsMédicos  preparados especialmente para ti!➡️ ENLACES DE INTERÉSOtros episodios de Actitud Saludable | Hipertensión arterial

Lancet 1999;353:2001-07Background: Beta-blockers directly reduce cardiac contractility and myocardial oxygen demand. For decades, they were avoided in patients with acute and chronic heart failure over concerns they would facilitate decompensation of the condition. The therapeutic cornerstones of treatment, prior to the modern era of clinical trials, focused on managing symptoms and quality of life with diuretics and inotropic agents like digoxin; however, new paradigms were arising that focused on addressing neurohormonal mechanisms of chronic disease that were over-activated in the failing heart. The first major success came with inhibition of the renin angiotensin aldosterone system with angiotensin converting enzyme inhibitors whose effect on mortality for patients with mild and severe forms of chronic heart failure were demonstrated in the V-HEFT II, CONSENSUS, and SOLVD trials. Additional benefits were demonstrated with the mineralocorticoid receptor antagonist spironolactone in the RALES trial. These drug classes primarily work by reducing afterload and volume retention. Appreciating why they work for improving cardiac performance and managing symptoms in heart failure patients is straightforward when we consider the major factors that effect cardiac stroke volume - preload, afterload and contractility; however, it is also noteworthy the effects these agents have on sudden death. How beta-blockade benefits the failing heart is less obvious (outside prevention of sudden death). Mechanistic studies in patients with chronic heart failure have consistently shown that when beta blockers are used for more than 1 month, left ventricular function improves. Beta blocker therapy appears to restore the density of beta-adrenergic receptors after they have been downregulated by the chronic overactivity of the sympathetic nervous system. The first major placebo-controlled RCT to demonstrate a mortality benefit used the non-selective beta blocker carvedilol. The trial was small and not originally designed to test mortality and was stopped early without clearly predefined stopping rules. Furthermore, 8% of total patients selected for participation in the trial were excluded prior to randomization after a 2 week, open-label run-in phase with the study drug, which saw 2% of all patients experience worsening heart failure or death representing 24 patients (the difference in total deaths between groups was 9 when the trial was stopped). The Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) was the first large scale trial designed to test the hypothesis that beta-blockade with metoprolol controlled/extended release (CR/XL) added to optimum medical therapy reduces mortality in patients with chronic systolic heart failure.Patients: Patients were recruited from 313 sites in 13 European countries and the United States. Eligible patients were men and women between the age of 40 to 80 years with symptomatic heart failure (NYHA class II-IV) for >/= 3 months before randomization. They had to be on a diuretic and ACE inhibitor for at least 2 weeks. Other drugs, including digoxin, could also be used. Patients also had to have an EF of /=68 beats per minute.Patients were excluded if: they had an MI or unstable angina within 28 days; had an indication or contraindication for treatment with beta-blocker; beta blockade within 6 weeks; heart failure due to systemic disease (i.e., amyloidosis) or alcohol abuse; scheduled or performed cardiac transplant; an ICD; procedures such as CABG or PCI planned or performed in the past 4 months; 2nd or 3rd degree AV block unless a pacemaker was present; unstable or decompensated heart failure defined by pulmonary edema or hypoperfusion or supine systolic BP 25% deviation of the number of observed versus expected consumed placebo tablets during the run-in period.Baseline characteristics: The mean age of patients was 64 years and approximately 78% were male. Slightly more than 30% of patients were above the age of 70. The average EF was 28%. The average SBP was 130 mmHg and heart rate was 82 bpm. Most patients had mild to moderate heart failure, with 41% in NYHA Class II, 56% in Class III, and only 3% in Class IV. Ischemic cardiomyopathy accounted for 65% of cases and nonischemic causes accounted for 35%. Most patients were on an ACE inhibitor or ARB (95%) and diuretic (90%). Digoxin was used in 63%. Trial procedures: Prior to randomization, the study was preceded by a single-blind, 2-week placebo run-in period. Patients meeting eligibility were then randomized to placebo or metoprolol CR/XL. The starting dose of placebo or metoprolol CR/XL was 12.5 mg daily for patients in NYHA class III or IV and 25 mg daily for patients in NYHA class II. The dose was doubled every 2 weeks until the target dose of 200 mg daily was reached. Patients were followed every 3 months.Endpoints: The primary outcome was all-cause mortality. It was estimated that 3,200 patients would need to be followed for 2.4 years to detect a 30% relative reduction in mortality based on annual mortality rate of 9.4% in the placebo group. This would achieve at least 80% power with a 2-sided alpha of 0.04. Patients were recruited faster then planned and so the final sample size of 3,991 patients increased the power of the study.The study was monitored by an independent safety committee and predefined stopping rules for efficacy were based on all-cause mortality, done when 25%, 50%, and 75% of expected deaths had occurred. Results: The trial was stopped early after the 2nd preplanned interim analysis when 50% of expected deaths had occurred. The mean duration of follow-up at the time of stopping was 1 year. The mean daily dose of metoprolol CR/XL was 159 mg once daily, with 87% receiving 100 mg or more and 64% receiving the target dose of 200 mg daily. In the placebo group, the corresponding values were 179 mg daily, 91% and 82%. The study drug was discontinued permanently in 14% of patients in the metoprolol group and 15% in the placebo group. Six months after randomization, heart rate decreased by 14 bpm in the metoprolol group compared to only 3 bpm in the placebo group. Systolic blood pressure decreased less in the metoprolol group (-2.1 vs 3.5 mmHg).Compared to placebo, metoprolol significantly reduced all-cause mortality (7.3% vs 10.8%; RR 0.66; 95% CI 0.53—0.81). Cardiovascular mortality accounted for 91% of all deaths; with sudden death accounting for 58% and death from worsening heart failure accounting for 24% of all deaths. All 3 of these causes of death were significantly reduced by metoprolol. The relative and absolute effects on death were greatest for patients with NYHA class III heart failure.Conclusions: In this trial of stable patients with mild to moderate chronic systolic heart failure, who were optimized on an ACEi or ARB and diuretic, metoprolol CR/XL significantly reduced all-cause mortality. Approximately 30 patients would need to be treated with metoprolol compared to placebo for 1 year to prevent 1 death. This trial represents a significant win for beta blockade in patients with chronic systolic heart failure. While the NNT in this trial is slightly higher than in SOLVD, it is important to appreciate that follow-up time in SOLVD was more than 3x longer. Limitations to external validity in this trial include the run-in period and stringent inclusion and exclusion criteria. Our enthusiasm is also tempered by early stopping, which has been found to be associated with false positive or exaggerated results but this concern is mitigated to some extent in this trial because the rules for early stopping were clearly defined in the protocol.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

N Engl J Med 1996;334:1349-1355Background Before 1990, the prevailing idea held that the negative inotropy of beta-blockers would harm patients with impaired systolic function. Yet part of the progression of systolic heart failure involved over stimulation of the sympathetic nervous system. Norepinephrine can exert adverse effects on the circulation, both directly and indirectly. Smaller trials of beta-blockers in systolic heart failure found trends for benefit with beta-blockers, however, a mortality benefit had not yet been proven. The U.S. Carvedilol Heart Failure Study aimed to study mortality in patients with heart failure with a reduced ejection fraction.Cardiology Trial's Substack remains free of industry ads because of your support. Thank you. Please consider becoming a free or paid subscriber.Patients The study enrolled 1094 patients with chronic heart failure symptoms for at least 3 months, LVEF ≤ 0.35%, at least 2 months of treatment with diuretics and an angiotensin-converting enzyme (ACE) inhibitor (if tolerated). Treatment with digoxin, hydralazine, or nitrates was permitted but not required.Exclusion criteria were extensive and important to understand. These included any recent major cardiac events or surgery within the previous 3 months, uncorrected valvular disease, active myocarditis, sustained VT or higher degrees of AV block not controlled by pacing, systolic blood pressure of more than 160 or less than 85 mm Hg or diastolic blood pressure of more than 100 mm Hg, clinically significant kidney or liver disease or use of calcium-channel blockers, adrenergic agonists/antagonists, or class IC/III antiarrhythmic agents. Patients receiving β-adrenergic agonists or antagonists (presumably for another indication) were not enrolled.Baseline Characteristics The results of this and other beta-blocker trials in heart failure will be clear. One of the most important points for translating this evidence to patients will be the baseline characteristics. It is vital to understand who these patients were.The mean age was 58 years and approximately 76% were male. Most patients had mild to moderate heart failure, with 53% in NYHA Class II, 44% in Class III, and only 3% in Class IV. The etiology of heart failure was nearly evenly split between coronary artery disease (47%) and nonischemic cardiomyopathy (53%). Patients had significantly impaired cardiac function with a mean LVEF of 0.23. The mean six-minute walk distance ranged from 386 to 390 meters. Hemodynamic parameters were relatively stable, with mean systolic blood pressure of 116 mmHg, and mean heart rate of 83-84 beats per minute. Most patients were receiving standard heart failure therapy at baseline, including digitalis (90-91%), loop diuretics (95%), and ACE inhibitors (95%), while approximately one-third (32%) were on direct-acting vasodilators.Trial Procedures Patients were assessed for eligibility during a 3-week screening period during which exercise capacity was assessed with a 6-minute walk test. Notable was that these were outpatients able to complete a 6-minute walk test. Enrollment was stratified to one of four treatment protocols on the basis of the patients' performance on the exercise test: patients able to walk between 426 and 550 m when tested were assigned to the mild-heart-failure protocol; those able to walk between 150 and 425 m were assigned either to the moderate-heart-failure protocol or to a dose-ranging protocol, depending on the location of the study center; and those able to walk only less than 150 m were assigned to the severe-heart-failure protocol.After this base-line testing, all patients received 6.25mg of carvedilol twice daily for two weeks in an open-label run-in period. Those who tolerated this initial dose were then randomized to receive either placebo (n=398) or carvedilol (n=696) on a double-blind basis, in addition to their usual medications.The allocation ratio (carvedilol:placebo) was 2:1 in the mild and severe heart failure protocols and 1:1 in the moderate heart failure protocol. The dose was gradually increased to target levels of 25-50mg twice daily over 2-10 weeks, followed by maintenance therapy for an additional 6 months (12 months for mild heart failure).Endpoints At the time of trial planning, the original intent was safety. That is, to show that carvedilol did not increase mortality. The original intent was to enroll 1100 patients. As smaller trials on beta-blockers were published, the statistical plan included the possibility of beta-blocker benefit. The trialists therefore planned two sided statistical analysis.Cumulative survival curves were constructed as time-to-first-event plots by Kaplan–Meier survivorship methods and differences between the curves were tested for significance by the log-rank statistic with use of a Cox proportional-hazards regression model (which included the protocol as a covariate).Results Median follow-up was only 6.5 months due to early termination for benefit. The patients mean total daily dose of carvedilol was 45±27 mg. Overall mortality was 7.8% in the placebo group vs. 3.2% in carvedilol group. The relative risk reduction from carvedilol vs placebo was 65% (95% CI, 39-80%; p

N Engl J Med 1987; 314:1429-35Background Prior to the publication of this study, digoxin and diuretics were the mainstay of chronic heart failure management. No therapy had yet been shown to reduce mortality or improve heart failure outcomes in patients with severe disease. The results of the V-HEFT trial had been published in the prior year, which demonstrated that the vasodilator combination of hydralazine and isosorbide reduced death in patients with chronic, stable heart failure. CONSENSUS was the first study to test whether vasodilator therapy in general, and angiotensin converting enzyme inhibitors in particular could modify heart failure disease trajectory for those with severe disease when used as part of chronic disease management. The CONSENSUS trial was designed to test the hypothesis that Enalapril compared to placebo reduced mortality in patients with severe (NYHA IV) congestive heart failure.Patients Men and women with severe (NYHA IV) congestive heart failure and cardiomegaly based on heart size >600 ml/m2 in men or >550 ml/m2 in women were recruited from 35 centers in Finland, Norway and Sweden. Measurement of LV function was not required. Patients were excluded if they had 1) acute pulmonary edema, 2) hemodynamically important aortic or mitral valve stenosis, 3) MI within the previous 2 months, 4) unstable angina, 5) planned cardiac surgery, 6) right heart failure due to pulmonary disease, or 7) serum creatinine >3.4 mg/dL.It is not specified whether patients could be recruited from the inpatient or outpatient setting or both but prior to randomization, a 14-day period was allowed to stabilize patients on digoxin and diuretics. If during this period, their condition improved to NYHA class III or less they were not randomized.Baseline characteristics The majority of participants were male (70%) and their average age was 70. The average heart rate and blood pressure were 80 bpm and 120/75 mmHg and the average serum creatinine was about 1.5 mg/dL. Coronary artery disease was present in over 70% of participants and nearly 50% had suffered a previous heart attack. Hypertension and diabetes were present in over 20% and atrial fibrillation in 50%. The use of medications at baseline was evenly distributed between groups with nearly all patients being on digoxin and furosemide. About 50% of participants were also taking spironolactone as well as other vasodilator drugs. About 50% of patients had heart failure for more than 4 years.Procedures Treatment with enalapril or an identical placebo was initially started in the hospital with a dose of 5 mg twice a day. After 1 week it was increased to 10 mg twice a day if the patient did not have symptoms of hypotension or other side effects. According to the clinical response, a further increase in dosage could occur up to a maximum dose of 20 mg twice a day.Patients were evaluated after 1, 2, 3, 6, and 16 weeks, 6, 9, and 12 months and at the end of the study. In patients with worsening symptoms, additional vasodilator therapy with isosorbide dinitrate, hydralazine, or prazosin, in that sequence was recommended.Early in the trial the occurrence of symptomatic hypotension led to revision of the protocol after 67 patients had been randomized. No patient's treatment was unblinded but in patients with 1) serum sodium

N Engl J Med 1986; 314:1547-52Background Into the mid-1980's, digoxin and diuretics were the mainstay of chronic disease management for congestive heart failure. Vasodilator agents were also commonly used based on limited data of their favorable hemodynamic effects. No sufficiently powered trials in this space had been performed to assess whether administration of vasodilators or any other agents improved long-term morbidity or mortality for heart failure patients. The V-HEFT trial was undertaken to test the hypotheses that 2 widely used vasodilator regimens (prazosin or a combination of hydralazine and isosorbide dinitrate) were superior for reducing death versus placebo. The trial was sponsored by the Veterans Administration and only enrolled men.Patients Men between the ages of 18 and 75 were recruited from 11 participating Veterans Administration hospitals and had to have chronic congestive heart failure based on either evidence of cardiac dilatation or left ventricular dysfunction (EF 0.7 ng/mL and euvolemic volume status. Clinical evaluations and exercise-tolerance tests on 2 consecutive visits, two weeks apart, had to reveal clinical and exercise stability before randomization could occur. Following randomization, patients continued to receive the optimal dose of digoxin and diuretic along with 1 of 3 study regimens. The placebo group was given placebo tablets and placebo capsules and instructed to take them 4 times a day. The prazosin group took 2.5 mg prazosin capsules and placebo tablets 4 times a day. The hydralazine-isosorbide dinitrate group took 37.5 mg hydralazine capsules and 20 mg isosorbide dinitrate tablets 4 times a day.In all groups, therapy began with 1 capsule and 1 tablet to be taken 4 times a day. In the absence of side effects, this was increased to 2 capsules and 2 tablets 4 times a day for a total of 20 mg of prazosin or 300-160 mg of hydralazine-isosorbide dinitrate. If drug-related side effects occurred, the dose could be reduced to half a tablet 4 times per day or to one capsule 2 times per day. If the dose was reduced, an attempt was made later to reinstitute the full dose.In order to limit dropouts, rigorous criteria were established for “treatment failures.” Physicians were advised to hospitalize patients with worsening symptoms, and, if appropriate, to use temporary intravenous vasodilator or inotropic interventions for stabilization. Physicians were encouraged to resume study medications upon discharge. At least 2 such hospitalizations were required, along with objective evidence of deterioration, before the study medications were discontinued and replaced with known therapy.Endpoints The primary endpoint was all-cause mortality.Results 642 patients were enrolled (273 in placebo group, 183 in prazosin group and 186 in the hydralazine-isosorbide dinitrate group). Excluding discontinuations that took place within 1 month before death, 47 patients (17%) discontinued one or both types of placebos, 43 patients (23%) discontinued prazosin, and 60 patients (32%) discontinued either one or both drugs in the hydralazine-isosorbide group. Six months after randomization, the average prescribed doses were 18.6 mg per day of prazosin, 270 mg per day of hydralazine, and 136 mg per day of isosorbide dinitrate. More than 85% of the prescribed drugs were taken in each treatment group.The mean follow-up was 2.3 years (range 6 months to 5.7 years). Only 4 patients were lost to follow up (2 in placebo group, 1 in prazosin group, and 1 in hydralazine-dinitrate group). There were 120 deaths in placebo group (44%; 19 per 100 patient years), 91 in the prazosin group (50%; 22 per 100 patient years), 72 in the hydralazine-dinitrate group (39%; 17 per 100 patient years). A reduction in mortality over the entire follow-up period was observed in the hydralazine-nitrate group compared with placebo (p = 0.093 on the log-rank test and p = 0.046 on the generalized Wilcoxon test, which gives more weight to treatment differences occurring in the earlier part of the mortality curves and less weight to the latter part, where the numbers are smaller). The absolute difference in mortality between these groups increased during three years and then began to diminish. The absolute difference in mortality between the placebo group and hydralazine-isosorbide groups at years 1 through 4 was 7%, 9%, 11% and 4%, respectively.Prespecified subgroup analysis in CAD vs no CAD stratification showed no significant treatment effect heterogeneity for hydralazine-nitrate among those with CAD although the absolute difference in mortality between groups was numerically higher for patients with CAD.At 8 weeks and 1 year, SBP (-4.1 and -4.6 mmHg) and DBP (-3.2 and -2.7 mmHg) decreased the most in the prazosin group compared to placebo. Hydralazine-nitrate was not associated with a statistically significant nor clinically significant difference in BP with exception of DBP at 8 weeks. The EF rose significantly at 8 weeks and 1 year in the hydralazine-nitrate group (+2.9 and +4.2) compared to placebo but not in the prazosin group.Side effects were reported in 4.0% of placebo patients, 11% of prazosin patients and 19% of hydralazine-nitrate patients, respectively. The most common side effects were headache and dizziness. Headache was reported in 12% of hydralazine-nitrate patients.Conclusions This study compared the combination of hydralazine-isosorbide dinitrate or prazosin to placebo in patients with chronic congestive heart failure who were optimized on digoxin and diuretic therapy. In what appears to be a young (58 years) and highly selected population of clinically stable, male veterans with dilated cardiomyopathies and low symptom burdens, the combination of hydralazine-isosorbide reduced death by 2 per 100 patient years, increased EF by 4% at 1 year and did not significantly alter BP compared to placebo. Side effects were reported in approximately 1 out of 5 patients with the most common being headache and approximately 1 out of 3 discontinued 1 or both study drugs. Prasozin did not reduce death or increase EF but did reduce BP compared to placebo. The internal validity of the study is high with only a few minor imbalances in baseline characteristics, which do not appear clinically relevant nor to consistently favor any one group. Less than 1% of patients were lost to follow up with no significant imbalances between groups. The external validity is limited by the fact that this is a population of male veterans and the etiologic distribution of cardiomyopathy and heart failure is likely different from a general heart failure population; etiologic causes of death are also likely to be different. Furthermore, the population is highly selected and its unclear how many patients from the general heart failure population would meet study criteria.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

A recent 12-week randomised controlled trial involving healthy adults aged 55-70 yielded significant positive findings regarding pomegranate extract's effect on blood pressure. While the study might not have shown significant differences compared to placebo across all initially measured markers, it revealed important reductions within the group taking pomegranate extract daily. Specifically, participants supplementing with pomegranate extract saw a statistically significant average decrease in Systolic Blood Pressure (SBP) by 5.22 mmHg and Diastolic Blood Pressure (DBP) by 3.6 mmHg. The researchers highlight the potential clinical relevance of the SBP reduction, noting that a 5 mmHg drop is associated with an estimated 10% decrease in the risk of major cardiovascular events. These findings align with previous research and meta-analyses confirming pomegranate's blood pressure-lowering effects, suggesting pomegranate extract could be a supportive strategy for hypertension prevention in older adults."This information is for educational purposes only and should not be interpreted as medical advice.""The study discussed was a randomised controlled trial in healthy adults aged 55-70.""The significant positive findings highlighted are the reductions in Systolic and Diastolic blood pressure observed within the group taking pomegranate extract. The authors note the SBP reduction is potentially clinically relevant.""These blood pressure findings are consistent with other studies and meta-analyses on pomegranate, strengthening the evidence for this specific effect.""Always consult with a qualified healthcare professional before making any changes to your diet, supplement regimen, or treatment plan, especially regarding blood pressure management or if you have existing health conditions or take medications.""This channel is not monetized and does not provide medical advice."#PomegranateExtract, #BloodPressure, #SystolicBloodPressure, #ClinicalRelevance, #HypertensionPreventionFarhat G, Malla J, Vadher J, Al-Dujaili EAS. Effects of Pomegranate Extract on Inflammatory Markers and Cardiometabolic Risk Factors in Adults Aged 55–70 Years: A Randomised Controlled Parallel Trial. Nutrients. 2025; 17(7):1235.

Story at-a-glance Breastfeeding for at least six months increases gut microbiome diversity in infants, reducing inflammation and supporting immune function, which contributes to lower blood pressure in early childhood A one-unit increase in gut microbiome diversity at one month of age correlates with a 1.86 mmHg decrease in systolic blood pressure by age 6, lowering long-term cardiovascular risk Formula-fed infants have a less diverse gut microbiome with more inflammatory bacteria, increasing the likelihood of gut imbalance, immune dysfunction, and higher blood pressure later in life Human milk oligosaccharides (HMOs) in breastmilk selectively feed beneficial bacteria, enhancing digestion, immune support, and disease protection, advantages formula cannot replicate Secretory immunoglobulin A (SIgA) in breastmilk strengthens gut lining integrity, prevents infections, and trains the immune system to differentiate between harmful and harmless substances

N Engl J Med 2017;377:2419-2432Background: A small fraction of patients with acute myocardial infarction (5-10%) have cardiogenic shock. These patients have a high baseline mortality. Early revascularization had been established as better than initial stabilization with medical therapy. Many patients with cardiogenic shock due to acute myocardial infarction (AMI) have multivessel disease. The question arises about whether to do culprit-only percutaneous coronary intervention (PCI) or more complete PCI at the time of the initial intervention.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock (CULPRIT-SHOCK) trial was designed to test the hypothesis that PCI of the culprit lesion only, with the option of staged revascularization of nonculprit lesions, would result in better clinical outcomes than immediate multivessel PCI among patients who have multivessel coronary artery disease and acute myocardial infarction with cardiogenic shock.Patients: The trial enrolled 706 patients with acute myocardial infarction (ST-segment elevation or non-ST-segment elevation) complicated by cardiogenic shock who had multivessel coronary artery disease. Cardiogenic shock was defined as SBP < 90 mmHg for more than 30 minutes or requiring pressors, clinical signs of pulmonary congestion, and signs of organ hypoperfusion (altered mental status, cold/clammy skin, oliguria, or lactate > 2 mmol/L).Exclusion criteria were extensive and designed to exclude patients with extremely poor prognosis: prolonged resuscitation, no intrinsic heart action, fixed dilated pupils, an indication for urgent CABG, a mechanical cause of shock, age > 90 years, massive pulmonary embolism, or severe renal insufficiency at baseline.Baseline Characteristics: The median age was 70 years, and approximately 75% were male. About 63% of patients had three-vessel disease. More than half the patients had ST-segment elevation myocardial infarction (about 62%), and anterior ST-segment elevation MI accounted for approximately 54% of these cases. About 53% of patients required resuscitation before randomization. The median left ventricular ejection fraction was between 30-33%.Procedures: In the culprit-lesion-only PCI group, only the culprit lesion was treated during the initial procedure, with staged revascularization encouraged based on residual ischemic lesions. In the multivessel PCI group, PCI of all major coronary arteries with >70% stenosis was performed, including attempts to recanalize chronic total occlusions. Crossover from the culprit-lesion-only PCI group to the multivessel PCI group occurred in 12.5% of patients, while crossover in the opposite direction happened in 9.4% of patients. The overall dose of contrast material was significantly higher and the duration of fluoroscopy significantly longer in the multivessel PCI group. Other interventional therapeutic measures were allowed, independent of the assigned treatment strategy.Endpoints: The primary endpoint was a composite of death from any cause or severe renal failure leading to renal-replacement therapy within 30 days after randomization. Secondary endpoints included the individual components of the primary endpoint, recurrent myocardial infarction, rehospitalization for heart failure, repeat revascularization, time to hemodynamic stabilization, catecholamine therapy duration, ICU stay duration, and measurements of renal and myocardial injury. Safety end points included bleeding, which was defined as type 2, 3, or 5 on the Bleeding Academic Research Consortium (BARC) scale.Trialists estimated an event rate of the composite primary endpoint of 38% in the culprit-only group vs 50% in the complete group. Using a global type I error level of 0.05, the authors calculated that a sample of 684 patients would give the trial 80% power to rule out the null hypothesis of no difference between the two treatment groups in the event rate for the primary end point.Results: At 30 days, the composite primary endpoint occurred in 45.9% of patients in the culprit-lesion-only PCI group versus 55.4% in the multivessel PCI group (relative risk, 0.83; 95% CI, 0.71 to 0.96; P=0.01). Death occurred in 43.3% of the culprit-lesion-only PCI group versus 51.6% of the multivessel PCI group (relative risk, 0.84; 95% CI, 0.72 to 0.98; P=0.03). The rate of renal-replacement therapy was 11.6% in the culprit-lesion-only PCI group and 16.4% in the multivessel PCI group (relative risk, 0.71; 95% CI, 0.49 to 1.03; P=0.07).Rates of recurrent myocardial infarction, rehospitalization for heart failure, bleeding, and stroke did not differ significantly between groups. Subgroup analyses showed consistent results across all prespecified subgroups. The time to hemodynamic stabilization, the use of catecholamine therapy and the duration of such therapy, the duration of the ICU stay, and the use of mechanical ventilation and the duration of such therapy also did not differ significantly between the two groups.Conclusion: In patients with myocardial infarction and cardiogenic shock, culprit-only PCI was superior to multivessel PCI. Both components of the primary endpoint, death and severe renal failure were lower in the culprit-only arm. The authors and editorialists speculate why these findings contrast with trials in hemodynamically stable myocardial infarction patients, where early multivessel PCI showed benefit over culprit-only PCI.If you accept the thesis that multi-vessel PCI was superior to culprit-only PCI in stable AMI patients, the likely reason for the disparate results are that patients with cardiogenic shock differ substantially from stable patients. The sicker patients with cardiogenic shock benefit from a less-is-more approach where culprit-only PCI reduces treatment harm relative to multivessel PCI.We at CardiologyTrials, however, find the evidence for complete revascularization in stable AMI patients less than clear. The COMPLETE trial found benefit from multivessel PCI over culprit-only, but both composite endpoints were driven largely by non-fatal MI. CV death was not substantially different. The difference in MI could have been related to excluding procedure-related MI.What's more, the FULL-REVASC trial, which also compared culprit-only and multivessel PCI, failed to replicate the COMPLETE trial results. In FULL-REVASC the rates of the composite primary outcome of death, MI or unplanned revascularization were not significantly different. Sadly, FULL-REVASC was stopped early when COMPLETE results were published, which led to a possible loss of power.It's possible, likely even, that the null results of CULPRIT-SHOCK are not really that disparate from prior trials in patients with more stable AMI.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Jamie is a 62-year-old female who is referred to outpatient cardiac rehabilitation 3 weeks after a myocardial infarction. She reports feeling fatigued with moderate exertion but denies chest pain. Her resting vitals are HR 80 bpm, BP 128/82 mmHg, and SpO₂ 98%. She completed Phase I rehabilitation without complications and is eager to begin exercising to improve her endurance. Which activity is MOST appropriate to initiate during Phase II of cardiac rehabilitation?A) Jogging on a treadmill at 70% maximum heart ratB) Cycling on a stationary bike at 3-5 METsC) Strength training at 50% of 1-rep maxD) Stretching and light walking onlyDOWNLOAD THIS EPISODES CHEATSHEET:www.nptecheatsheet.com/cardiac-rehab1

In this video on research published in JACC and presented at ACC.25, Yuan Lu, ScD, JACC: Executive Associate Editor, discusses her study on optimal blood pressure management for adults aged 80 and above. Her study found that systolic blood pressure below 130 mmHg is associated with lower cardiovascular risk, while levels above 145 mmHg increase heart-related mortality. The study supports intensive blood pressure management but emphasizes the need for personalized treatment and further research on long-term effects and potential risks.#jacc #jaccjournals #acc25

Ich und hoher Blutdruck? Kann gar nicht sein! Doch, kann es. Selbst wenn die Werte immer ganz niedrig oder sogar unangenehm niedrig waren. Denn sie steigen in der Lebensmitte an. Noch dazu ist es total von gestern, den Blutdruck erst ab 140 zu 90 mmHg so richtig zu beachten. Denn für die Gesundheit ist 120 zu 70 am besten. Diana im Gespräch mit der Kardiologin Dr. Christa Bongarth über den Einfluss der Menopause auf den Blutdruck, den enormen Nutzen von Blutdrucksenkern und warum sie sie trotzdem auch bei erhöhten Werten nicht immer verordnet.INFOS ZUR FOLGE:Dr. Christa Bongarth im Internet: https://hoehenried.de/home/abteilungen/kardiologie/... und in einem Text der Deutschen Herzstiftung über Frauen und Blutdruck: https://herzstiftung.de/ihre-herzgesundheit/gesund-bleiben/bluthochdruck/frauen-bluthochdruck (Darin steht auch ein bisschen was zur Hormonersatztherapie, das Thema machen wir in einer weiteren Folge zum weiblichen Blutdruck auf.)Hier kommt Ihr zu einem Text der Deutschen Hochdruckliga über die neuen Leitlinien vom August 2024: https://www.hochdruckliga.de/pressemitteilung/deutsche-hochdruckliga-begruesst-esc-empfehlung-zur-fruehzeitigen-medikamentoesen-intervention-bei-erhoehten-blutdruckwerten Hier geht es zum Positionspapier der Deutschen Gesellschaft für Kardiologie: https://leitlinien.dgk.org/2024/geschlechterspezifische-aspekte-kardiovaskulaerer-erkrankungenHier geht es zum Newsletter "Saisonwechsel" von der BRIGITTE: https://brigitte.guj-medien.de/newsletter-anmeldung-saisonwechselHier zum neuen meno_brigitte-Insta-Account: https://www.instagram.com/meno_brigitte/Diana auf Instagram: https://www.instagram.com/apothekerin_ihres_vertrauens/Julia auf Instagram: https://www.instagram.com/julia_jortzig/In unserer Eigenwerbung geht es um die BRIGITTE Masterclass Finanzen Premium: https://academy.brigitte.de/masterclass?utm_source=menoanmich&utm_medium=podcast&utm_campaign=mcf-premium-kh10Es gibt auch einen MENO AN MICH-Rabattcode, MENO15 (gilt für viele BRIGITTE-Angebote).WEITERE ANGEBOTE aus der BRIGITTE Redaktion:Masterclass Finanzen Basic: https://academy.brigitte.de/course/masterclass-finanzen-basic?utm_source=menoanmich&utm_medium=podcast&utm_campaign=mcf-basicKostenloses Webinar Rentenlücke berechnen: https://academy.brigitte.de/webinar-aufzeichnung-rentenluecke-berechnenETF Kurs: https://academy.brigitte.de/course/etf-kurs?utm_source=menoanmich&utm_medium=podcast&utm_campaign=etf-kurs-mOn Demand Video-Kurs "Wechseljahre: Wissen, was hiilft": https://academy.brigitte.de/course/wechseljahre?utm_source=podcast&utm_medium=meno&utm_campaign=wechseljahreDossier "Wechseljahre": https://produkte.brigitte.de/products/brigitte-dossier-wechseljahre?utm_campaign=briwebsite&utm_medium=link&utm_source=podcastmenoanmichDossier "Stoffwechsel anregen": https://produkte.brigitte.de/products/stoffwechsel-anregen?utm_source=podcast&utm_medium=menoanmich&utm_campaign=stoffwechselDossier "Gehen oder blieben?": https://produkte.brigitte.de/products/gehen-oder-bleiben?utm_source=podcast&utm_medium=menoanmich&utm_campaign=gobIhr habt Anregungen, wollt uns Eure Geschichte erzählen oder selbst bei uns zu Gast im Podcast sein? Dann schreibt uns beiden persönlich, worüber Ihr gern mehr wissen würdet, was Euch bewegt, rührt, entsetzt und Freude macht an podcast@brigitte.de. Wir freuen uns auf Euch! Und bewertet und abonniert unseren Podcast gerne auch auf Spotify, iTunes, Amazon Music oder Audio Now. Noch mehr spannende Beiträge findet Ihr zudem auf Brigitte.de sowie dem Instagram- oder Facebook-Account von BRIGITTE –schaut vorbei! +++ Weitere Infos zu unseren Werbepartnern finden Sie hier: https://linktr.ee/menoanmich ++++++Unsere allgemeinen Datenschutzrichtlinien finden Sie unter https://datenschutz.ad-alliance.de/podcast.html +++Wir verarbeiten im Zusammenhang mit dem Angebot unserer Podcasts Daten. Wenn Sie der automatischen Übermittlung der Daten widersprechen wollen, klicken Sie hier: https://datenschutz.ad-alliance.de/podcast.htmlUnsere allgemeinen Datenschutzrichtlinien finden Sie unter https://art19.com/privacy. Die Datenschutzrichtlinien für Kalifornien sind unter https://art19.com/privacy#do-not-sell-my-info abrufbar.

Teniah was admitted to the acute care hospital with community-acquired pneumonia. She reports shortness of breath and fatigue. Auscultation reveals decreased breath sounds in the right lower lobe, and SpO₂ drops from 95% to 88% with exertion. Resting vital signs: HR 92 bpm, BP 142/86 mmHg, RR 22 breaths per minute. Which finding requires the MOST immediate communication with the medical team?A) Decreased breath sounds in the right lower lobeB) Blood pressure of 142/86 mmHgC) Resting respiratory rate of 22 breaths per minuteD) Oxygen desaturation to 88% with exertionJoin the FREE Facebook Group: www.nptegroup.com

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the ARREST-AF Trial with expert faculty Dr. Prashanthan Sanders and Dr. Mehak Dhande. The ARREST-AF trial enrolled 122 patients with a BMI of 27 kg/m2 or greater and at least one cardiovascular risk factor with either paroxysmal or persistent AF and were scheduled to undergo de novo AF ablation. They were randomized to an intensive risk factor management (RFM) program versus usual care. The RFM program addressed obesity, sleep apnea, HTN, HLD, tobacco, and alcohol abuse, whereas the usual care arm had a discussion of risk factors but without an extensive risk factor modification or follow-up program. The study population had a mean age of 60 years, a mean BMI of 33 kg/m2, and 56-60% of patients with persistent AF. A third of the study population was female. The trial showed a significant improvement in the primary endpoint of the percentage of patients free from atrial fibrillation after ablation in those receiving the intensive lifestyle RFM program. At the end of the 12.3-month follow-up period, 66% percent of patients in the RFM group were free from AF compared to 42% in the usual care group (HR 0.53, p = 0.03). The RFM group also showed significant improvement in AF symptom severity, decline in body weight, systolic blood pressure, glycemic control, and exercise capacity. On average, patients in the RFM arm lost 9 kg of weight compared to 1 kg in the control group. Similarly, systolic blood pressure decreased by 13.1 mmHg in the RFM group but increased by four mmHg in the control group. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Pathak, Rajeev K., et al. "Aggressive Risk Factor Reduction Study for Atrial Fibrillation and Implications for the Outcome of Ablation: The ARREST-AF Cohort Study." Journal of the American College of Cardiology, vol. 64, no. 21, 2014, pp. 2222–2231.

Caso real Controlar el colesterol alto sin recurrir a medicamentosHoy os traigo un caso real que creo que puede resonar con muchos de vosotros, porque se trata de una condición muy común: el colesterol alto.Anamnesis del pacienteSe trata de un paciente de 45 años, con un diagnóstico reciente de hipercolesterolemia y riesgo cardiovascular alto debido a un síndrome metabólico.Este diagnóstico incluía obesidad abdominal, hipertensión arterial y triglicéridos elevados.Cuando llegó a consulta, el paciente mostró preocupación por su colesterol alto y su riesgo cardiovascular. Quería evitar el tratamiento farmacológico, ya que prefería controlar su salud mediante cambios en su estilo de vida.Valores iniciales de colesterol y perfil lipídico:Colesterol total: 260 mg/dLLDL (colesterol malo): 180 mg/dLHDL (colesterol bueno): 35 mg/dLTriglicéridos: 220 mg/dLAdemás, tenía obesidad abdominal con un perímetro de cintura de 110 cm y presión arterial elevada (140/90 mmHg).Cambios iniciales mal enfocadosAntes de venir a consulta, el paciente ya había intentado hacer algunos cambios en su alimentación. Sin embargo, aunque bienintencionados, estos no eran efectivos. Por ejemplo:Había sustituido la leche de vaca por bebidas vegetales, pero las que estaba tomando eran azucaradas.Cambió los yogures naturales por yogures edulcorados pensando que eran más sanos.Redujo el consumo de carnes grasas, pero lo sustituyó por embutidos magros como pavo o jamón cocido.Consumía galletas "digestive" pensando que eran una buena fuente de fibra.Optaba por aceite de girasol en lugar de aceite de oliva por el precio.A pesar de estos esfuerzos, sus análisis seguían mostrando niveles altos de colesterol y triglicéridos, y no entendía por qué.Intervención en consultaTras analizar su dieta y su estilo de vida, diseñamos un plan personalizado enfocado en:Ajustes en la dieta:Reemplazar las bebidas vegetales azucaradas por opciones sin azúcar añadido o volver a la leche desnatada.Cambiar los yogures edulcorados por yogures naturales sin azúcar, añadiendo fruta fresca para endulzarlos.Sustituir los embutidos magros por fuentes de proteínas saludables, como pescado azul, huevo o legumbres.Eliminar las galletas "digestive" y optar por avena, pan integral 100% o frutas enteras como fuente de fibra.Incorporar grasas saludables, como aceite de oliva virgen extra, frutos secos y aguacate.Educación alimentaria:Le enseñamos a leer etiquetas nutricionales para identificar azúcares ocultos, grasas saturadas y elegir productos más saludables.Incorporación de actividad física:Empezó con caminatas de 30 minutos 4 días a la semana. A medida que se sintiera más cómodo, añadiría sesiones de fuerza moderada.Gestión del estrés:Introdujimos técnicas de relajación como respiración profunda y pausas activas durante su jornada laboral.Resultados tras cuatro mesesAl cabo de tres meses, el paciente mostró una mejora significativa en su perfil lipídico:Colesterol total: Reducido a 200 mg/dLLDL (colesterol malo): Reducido a 130 mg/dLHDL (colesterol bueno): Aumentado a 45 mg/dLTriglicéridos: Reducidos a 150 mg/dLAdemás, su perímetro de cintura disminuyó a 102 cm, su presión arterial bajó a 125/80 mmHg, y comenzó a sentirse con más energía y motivado para seguir cuidándose.ConclusiónEste caso nos demuestra que, aunque los cambios iniciales no siempre sean efectivos, con la guía adecuada y un plan bien estructurado, se pueden lograr grandes avances. Lo más importante es no desanimarse y buscar apoyo profesional.Recordad, pequeños pasos bien dirigidos pueden transformar vuestra salud.Conviértete en un seguidor de este podcast: https://www.spreaker.com/podcast/comiendo-con-maria-nutricion--2497272/support.

A cardiologist reveals his natural method for lowering blood pressure and treating hypertension.   Dr. Steve Lome joins Chuck Carroll on The Exam Room Podcast.   Key points discussed include:   Hypertension epidemic: The rising rates of hypertension are highlighted, with an emphasis on the fact that individuals have more control over their blood pressure than they may realize.   Blood pressure guidelines: Dr. Lome explains the American Heart Association's guidelines for normal blood pressure, which is defined as less than 120/80 mmHg, and discusses the implications of readings above this threshold.   Lifestyle vs. genetics: The conversation emphasizes that while genetics can play a role in hypertension, lifestyle choices, particularly diet, have a far more significant impact. Dr. Lome shares his personal journey of weight loss and how dietary changes can reverse hypertension.   Dietary recommendations: The discussion includes the importance of a whole food plant-based diet, the dangers of ultra-processed foods, and the high sodium content in common foods like chicken. Dr. Lome stresses the need to eliminate animal-based foods and processed foods to improve blood pressure.   Individual variability: The interview touches on the concept of individual variability in health outcomes, noting that while some may tolerate unhealthy foods, this does not mean they are beneficial for overall health.   — — SHOW LINKS — — Dr. Steve Lome YouTube: https://www.youtube.com/@DrStevenLome IG: https://www.instagram.com/stevenlome Web: https://www.PBNM.org — — EVENTS — — Dr. Bulsiewicz and Chuck in Miami Where: Dr. Barnard's Bon Voyage Bash Date: March 7, 2025 https://www.pcrm.org/events/bon-voyage-party-2025 — — — Free Athlete Nutrition E-Book https://www.pcrm.org/athlete — — BECOME AN EXAM ROOM VIP — — https://www.pcrm.org/examroomvip — — THIS IS US — — The Exam Room Podcast Instagram: https://www.instagram.com/theexamroompodcast — — — Chuck Carroll Instagram: https://www.instagram.com/ChuckCarrollWLC Facebook: http://wghtloss.cc/ChuckFacebook X: https://www.twitter.com/ChuckCarrollWLC — — — Physicians Committee Instagram: https://www.instagram.com/physicianscommittee Facebook: https://www.facebook.com/PCRM.org X: https://www.twitter.com/pcrm YouTube: https://www.youtube.com/user/PCRM Jobs: https://www.pcrm.org/careers — — SUBSCRIBE & SHARE — — 5-Star Success: Share Your Story Apple: https://apple.co/2JXBkpy​​ Spotify: https://spoti.fi/2pMLoY3 Please subscribe and give the show a 5-star rating on Apple Podcasts, Spotify, or many other podcast providers. Don't forget to share it with a friend for inspiration!

Hypertension is a silent killer; check it before it's too late. Synopsis: Every first Wednesday of the month, The Straits Times helps you make sense of health matters that affect you. Do you know if you have high blood pressure or what's also known as hypertension? According to the National Population Health Survey 2022, about one in three Singaporeans aged 18 to 74 has hypertension. This condition puts them at risk of heart disease and stroke. However, a significant proportion remains unaware because the symptoms become obvious only when the condition is severe.  Hypertension is present when a person's blood pressure is at 140/90 mmHg or higher. But a slightly lower reading doesn't reduce the risk. In August 2024, the European Society of Cardiology, an influential society among cardiologists, introduced a new high blood pressure or BP category of 120-139. This implies that even readings in this range are not 'normal' as doctors once thought. In this episode, ST senior health correspondent Joyce Teo talks to Assoc Prof Chin Chee Tang, a cardiologist from the National Heart Centre Singapore, about the new category and what to make of it. They also discuss renal denervation, a procedure that the same society said may be considered for some patients with uncontrolled, drug-resistant high blood pressure. Highlights (click/tap above): 2:19 Should I be worried about a new category of hypertension?  5:30 How do I manage my blood pressure? 11:39 Monitoring the impact of salt reduction on your blood pressure 13:32 Can high blood pressure be lowered to normal levels?  19:39 Is renal denervation the right procedure for resistant hypertension? Check out ST's new series, No health without mental health: https://str.sg/mentalhealthmatters Read Joyce Teo's stories: https://str.sg/JbxN Host: Joyce Teo (joyceteo@sph.com.sg) Produced and edited by: Amirul Karim Executive producers: Ernest Luis and Lynda Hong Follow Health Check Podcast here and get notified for new episode drops: Channel: https://str.sg/JWaN Apple Podcasts: https://str.sg/JWRX Spotify: https://str.sg/JWaQ Feedback to: podcast@sph.com.sg --- Follow more ST podcast channels: All-in-one ST Podcasts channel: https://str.sg/wvz7 ST Podcast website: http://str.sg/stpodcasts ST Podcasts YouTube: https://str.sg/4Vwsa --- Get The Straits Times' app, which has a dedicated podcast player section: The App Store: https://str.sg/icyB Google Play: https://str.sg/icyX --- #healthcheckSee omnystudio.com/listener for privacy information.

Hypertension is a silent killer; check it before it's too late. Synopsis: Every first Wednesday of the month, The Straits Times helps you make sense of health matters that affect you. Do you know if you have high blood pressure or what's also known as hypertension? According to the National Population Health Survey 2022, about one in three Singaporeans aged 18 to 74 has hypertension. This condition puts them at risk of heart disease and stroke. However, a significant proportion remains unaware because the symptoms become obvious only when the condition is severe.  Hypertension is present when a person's blood pressure is at 140/90 mmHg or higher. But a slightly lower reading doesn't reduce the risk. In August 2024, the European Society of Cardiology, an influential society among cardiologists, introduced a new high blood pressure or BP category of 120-139. This implies that even readings in this range are not 'normal' as doctors once thought. In this episode, ST senior health correspondent Joyce Teo talks to Assoc Prof Chin Chee Tang, a cardiologist from the National Heart Centre Singapore, about the new category and what to make of it. They also discuss renal denervation, a procedure that the same society said may be considered for some patients with uncontrolled, drug-resistant high blood pressure. Highlights (click/tap above): 2:19 Should I be worried about a new category of hypertension?  5:30 How do I manage my blood pressure? 11:39 Monitoring the impact of salt reduction on your blood pressure 13:32 Can high blood pressure be lowered to normal levels?  19:39 Is renal denervation the right procedure for resistant hypertension? Check out ST's new series, No health without mental health: https://str.sg/mentalhealthmatters Read Joyce Teo's stories: https://str.sg/JbxN Host: Joyce Teo (joyceteo@sph.com.sg) Produced and edited by: Amirul Karim Executive producers: Ernest Luis and Lynda Hong Follow Health Check Podcast here and get notified for new episode drops: Channel: https://str.sg/JWaN Apple Podcasts: https://str.sg/JWRX Spotify: https://str.sg/JWaQ Feedback to: podcast@sph.com.sg --- Follow more ST podcast channels: All-in-one ST Podcasts channel: https://str.sg/wvz7 ST Podcast website: http://str.sg/stpodcasts ST Podcasts YouTube: https://str.sg/4Vwsa --- Get The Straits Times' app, which has a dedicated podcast player section: The App Store: https://str.sg/icyB Google Play: https://str.sg/icyX --- #healthcheckSee omnystudio.com/listener for privacy information.

JACC Associate Editor Theresa McDonagh, MBBCH  speaks with author Akshay S. Desai, MD, FACC about this paper on pulse pressure published in JACC and presented at AHA. In a pooled analysis of 16,950 patients with chronic HFmrEF or HFpEF enrolled from 4 global randomized clinical trials, a J-shaped relationship was observed between SBP and the risk of adverse CV events, with the lowest risk occurring at SBP values between 120 and 130 mmHg. A similar pattern was seen with PP, with the lowest risk found between 50 and 60 mmHg. Both higher SBP and higher PP independently predicted adverse CV events. Notably, PP remained a strong predictor of CV risk, independent of baseline SBP.

The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling's sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #38 Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention Answer #38 ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF

The following question refers to Sections 2.1 and 4.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by CardioNerds Academy Intern Dr. Adriana Mares, answered first by CardioNerds FIT Trialist Dr. Christabel Nyange, and then by expert faculty Dr. Shelley Zieroth. Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She has been a PI Mentor for the CardioNerds Clinical Trials Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #36 A 50-year-old woman presents to establish care. Her medical history includes COPD, prediabetes, and hypertension. She is being treated with chlorthalidone, amlodipine, lisinopril, and a tiotropium inhaler. She denies chest pain, dyspnea on exertion, or lower extremity edema. On physical exam, blood pressure is 154/88 mmHg, heart rate is 90 beats/min, and respiration rate is 22 breaths/min with an oxygen saturation of 94% breathing ambient room air. BMI is 36 kg/m2. Jugular venous pulsations are difficult to assess due to her body habitus. Breath sounds are distant, with occasional end-expiratory wheezing. Heart sounds are distant, and extra sounds or murmurs are not detected. Extremities are warm and without peripheral edema. B-type natriuretic peptide level is 28 pg/mL (28 ng/L). A chest radiograph shows increased radiolucency of the lungs, flattened diaphragms, and a narrow heart shadow consistent with COPD. An electrocardiogram shows evidence of left ventricular hypertrophy. The echocardiogram showed normal LV and RV function with no significant valvular abnormalities. In which stage of HF would this patient be classified?AStage A: At Risk for HFBStage B: Pre-HFCStage C: Symptomatic HFDStage D: Advanced HF  Answer #36 Explanation The correct answer is A – Stage A or at risk for HF. This asymptomatic patient with no evidence of structural heart disease or positive cardiac biomarkers for stretch or injury would be classified as Stage A or “at risk” for HF. The ACC/AHA stages of HF emphasize the development and progression of disease with specific therapeutic interventions at each stage. Advanced stages and disease progression are associated with reduced survival. The stages were revised in this edition of guidelines to emphasize new terminologies of “at risk” for Stage A and “pre...

Hola !!En el podcast de hoy os explico todo lo relacionado con el síndrome metabólicoOs dejo un breve resumen:Para diagnosticarlo hay que cumplir 3 o mas de los siguientes puntos: - Exceso de grasa abdominal: perímetro de la cintura > 80 cm en las mujeres y 94 cm en los hombres  - Glucosa en ayunas mayor o igual a 100 mg/dL ( o en tratamiento especifico para ella)Triglicéridos mayor de 150mg/dL ( o en tratamiento especifico) Colesterol HDL < 50 mg/dL en mujeres o < 40 mg/dL en hombres - Tension arterial mayor igual a 130 mmHg de “maxima” o mayor o igual de 85 mmHg de “minima” ( o en tratamiento para la tension) Sobre uno de los componentes del síndrome metabólico: la resistencia a la insulina, se calcula con la formula siguiente:Indice HOMA DE RESISTENCIA A LA INSULINA= [Glucosa en ayunas (mg/dL) x insulina en ayunas ] / 405 Si ese valor HOMA es > 2-2,5 nos indica que tus células son resistentes a la insulina Los tips para mejorar y prevenir el síndrome metabólico: Crear masa muscular con ejercicioAumentar el consumo de fibraSuplementos que mejoren todos los componentes del síndrome metabólico.Mi suple  MetabolicMax que esta en mi web https://ivbwellness.com  contiene los compuestos claves para optimizar los componentes del sindrome metabólico. Pero si por X motivo no lo queréis, en el podcast os digo cuales buscar ☝

Contributor: Aaron Lessen, MD Educational Pearls: How does an automated blood pressure cuff work? Automated blood pressure cuffs work differently than taking a manual blood pressure. While taking a manual blood pressure, one typically listens for Korotkoff sounds (turbulent flow) while slowly deflating the cuff. An automatic blood pressure cuff only senses the pressure in the cuff itself and specifically pays attention to oscillations in the pressure caused by when the pressure of the cuff is between the systolic (heart squeezing) and diastolic (heart relaxed) pressures. These oscillations are at a maximum when the pressure in the cuff matches the mean arterial pressure (MAP) and therefore the machines are most accurate at reporting the MAP. The machines then use the MAP and other information about the oscillations to estimate the systolic and diastolic pressures, which are less accurate. What should you do if you need more accurate systolic and diastolic blood pressures? Take a manual blood pressure. Get an arterial-line (a-line), which provides continuous data for the blood pressure at the end of a catheter. What happens if the cuff is too big or too small for the patient? If the cuff is too small it will overestimate the pressure. If the cuff is too large it will underestimate the pressure. What should you do if the cuff cycles a bunch of times before reporting a blood pressure? It probably isn't very accurate so consider another method. Bonus fact! The MAP is not directly in the middle of the systolic and diastolic pressures but is weighted towards the diastolic pressure. The MAP can be calculated by adding two-thirds of the diastolic pressure to one third of the systolic pressure. For example if the BP is 120/90 the MAP is 100 mmHg. References Benmira, A., Perez-Martin, A., Schuster, I., Aichoun, I., Coudray, S., Bereksi-Reguig, F., & Dauzat, M. (2016). From Korotkoff and Marey to automatic non-invasive oscillometric blood pressure measurement: does easiness come with reliability?. Expert review of medical devices, 13(2), 179–189. https://doi.org/10.1586/17434440.2016.1128821 Liu, J., Li, Y., Li, J., Zheng, D., & Liu, C. (2022). Sources of automatic office blood pressure measurement error: a systematic review. Physiological measurement, 43(9), 10.1088/1361-6579/ac890e. https://doi.org/10.1088/1361-6579/ac890e Vilaplana J. M. (2006). Blood pressure measurement. Journal of renal care, 32(4), 210–213. https://doi.org/10.1111/j.1755-6686.2006.tb00025.x Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3  

N Engl J Med 2019;381:1524-1534Background Dual antiplatelet therapy after percutaneous coronary intervention had become a standard of care. Both prasugrel and ticagrelor had been shown to provide more rapid and consistent platelet inhibition than clopidogrel. Randomized controlled trials had shown both drugs were superior to clopidogrel in patients with acute coronary syndromes. Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.The two drugs have different loading strategies in patients who have acute coronary syndromes without ST-segment elevation. In these patients, ticagrelor is usually administered as pretreatment before diagnostic angiography, but prasugrel is administered only after the coronary anatomy has been assessed by means of diagnostic angiography since no advantage has been observed when prasugrel is used as pretreatment.Before ISAR-REACT 5, there had been no direct comparisons of the two antiplatelet drugs. ISAR-REACT 5 was an investigator-initiated multicenter, non-industry funded RCT to compare the efficacy and safety of the two treatments in patients with acute coronary syndrome. Patients The trial enrolled 4013 patients from 23 centers. Patients were eligible with either STEMI, NSTEMI or unstable angina for which intervention was planned. Exclusion criteria included intolerance of either drugs, history of stroke or intracranial bleeding or any condition that increased the risk of bleeding. Patients could not be on concomitant oral or i.v. therapy with drugs affecting CYP3A4 system. Baseline Characteristics There were 2012 patients assigned to ticagrelor and 2006 patients assigned to prasugrel. The suspected diagnosis at admission was STEMI in 41%, NSTEMI in 46%, and unstable angina in 13% of the patients. The average age was 64 years. Female sex was 24%. Average systolic blood pressure and heart rate was 144 mmHg and 77 bpm. All factors were well balanced. Trial Procedures Therapy with ticagrelor was started at a loading dose of 180 mg and continued at a maintenance dose of 90 mg twice daily. Patients who were assigned to ticagrelor received the loading dose as soon as possible after randomization. Therapy with prasugrel was started at a loading dose of 60 mg and continued at a maintenance dose of 10 mg once per day. A reduced maintenance dose of 5 mg daily was recommended in patients who were 75 years of age or older and in those who had a body weight of less than 60 kg. Prasugrel therapy turned on presentation. STEMI patients were given prasugrel as soon as possible after randomization. In those without STEMI, the loading dose was delayed until knowledge of the coronary anatomy. Prasugrel loading was given before crossing the lesion. In patients with a coronary angiography–confirmed acute coronary syndrome who were not considered to be candidates for PCI but who were considered to be candidates for conservative therapy, dual antiplatelet therapy (aspirin and the randomly assigned trial medication) was recommended. About 83% of patients received PCI, 2% CABG and 13-14% were managed conservatively. Clinical follow-up was scheduled at 30 days, 6 and 12 months.Endpoints The primary end point was a composite of death, MI, or stroke at 1 year after randomization. Secondary end points included the safety end point, which was the incidence of bleeding at 1 year (type 3, 4, or 5 on the Bleeding Academic Research Consortium [BARC] scale, which ranges from 0 to 5, with higher values indicating more severe bleeding), the incidence of the individual components of the primary end point at 1 year, and the incidence of definite or probable stent thrombosis at 1 year.The sample-size calculation assumed a primary endpoint would occur in 10% in the ticagrelor group vs 12.9% in the prasugrel group. This led to an estimate of 1900 patients in each group and 80% power to detect a relative risk reduction of 22% in the ticagrelor group. All analyses, including the analysis of the primary end point, were performed according to the intention-to-treat principle Only the safety end point was analyzed in a modified intention-to-treat population, which included all patients who received at least one dose of the randomly assigned trial drug and were assessed for bleeding events up to 7 days after discontinuation of the trial drug.Results At discharge, 81% of patients in both groups received the randomly assigned trial drug. Slightly more patients in the ticagrelor group stopped taking the study drug by one year (15.2 vs 12.5%). One-year follow-up was complete in all but 90 patients (41 patients in the ticagrelor group and 49 patients in the prasugrel group).A primary end-point event (death, MI, stroke) occurred in 184 of 2012 patients (9.1%) in the ticagrelor group and 137 of 2006 patients (6.8%) in the prasugrel group (hazard ratio, 1.36; 95% confidence interval [CI], 1.09 to 1.70; P=0.006). The composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 161 of 2012 patients (8.1%) in the ticagrelor group and 124 of 2006 patients (6.3%) in the prasugrel group (hazard ratio, 1.32; 95% CI, 1.04 to 1.66).The rates of death, stroke and stent thrombosis did not statistically differ in the two groups. But the risk of MI was 63% higher in the ticagrelor group (4.8% vs 3.0%; HR 1.63; 95% CI, 1.18 to 2.25).Major bleeding was observed in 5.4% of patients in the ticagrelor group and in 4.8% of patients in the prasugrel group (hazard ratio, 1.12; 95% CI, 0.83 to 1.51; P=0.46).No heterogenous treatment effects were obvious from the subgroup analyses. Discussion For patients with acute coronary syndrome who were considered for intervention, prasugrel was superior to ticagrelor for the reduction of the primary endpoint. The effect size was large (ticagrelor 36% worse compared to prasugrel), and this was statistically robust. The reduction was obtained without an increase in bleeding. The trialists noted that this was not simply a comparison of drugs, but a comparison of treatment strategies. Authors had assumed that pre-treatment of ticagrelor would be superior. But this trial showed that a prasugrel-based strategy with deferred loading (after knowing the coronary anatomy) was superior. The primary endpoint finding was bolstered by the composite of cardiovascular death, MI and stroke also being 32% higher in the ticagrelor arm. This was an investigator-initiated non-industry funded study with an event rate in the ticagrelor arm similar to expected findings. We find this compelling evidence for the superiority of prasugrel in this patient population. Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

The McCullough Report with Dr. Peter McCullough – Hypertension is diagnosed if, when it is measured on two different days, the systolic blood pressure readings on both days is ≥140 mmHg and/or the diastolic blood pressure readings on both days is ≥90 mmHg. Modifiable risk factors include unhealthy diets, physical inactivity, consumption of tobacco and alcohol, and being overweight or obese...

The McCullough Report with Dr. Peter McCullough – Hypertension is diagnosed if, when it is measured on two different days, the systolic blood pressure readings on both days is ≥140 mmHg and/or the diastolic blood pressure readings on both days is ≥90 mmHg. Modifiable risk factors include unhealthy diets, physical inactivity, consumption of tobacco and alcohol, and being overweight or obese...

We review Acute Respiratory Distress Syndrome Hosts: Sadakat Chowdhury, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ARDS.mp3 Download Leave a Comment Tags: Critical Care, Pulmonary Show Notes Definition of ARDS: Non-cardiogenic pulmonary edema characterized by acute respiratory failure. Berlin criteria for diagnosis include acute onset within 7 days, bilateral pulmonary infiltrates on imaging, not fully explained by cardiac failure or fluid overload, and impaired oxygenation with PaO2/FiO2 ratio 5 cm H2O. Severity based on oxygenation (Berlin criteria): Mild: PaO2/FiO2 200-300 mmHg Moderate: PaO2/FiO2 100-200 mmHg Severe: PaO2/FiO2

NEJM 2003;348:1309-21.Background In patients with chronic systolic heart failure, aldosterone blockade reduced death and cardiovascular hospitalizations when added to an ACE inhibitor (RALES trial), which will be reviewed in the section involving trials in patients with chronic heart failure. Efficacy of aldosterone blockade in patients with acute myocardial infarction, complicated by LV dysfunction, had not yet been tested. Aldosterone blockade was believed to prevent ventricular remodeling and collagen formation after AMI as well as a number of other important pathophysiological mechanisms. The Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) was designed to test the hypothesis that the selective aldosterone blocker, eplerenone, would reduce mortality and cardiovascular hospitalizations in patients with AMI complicated by LV dysfunction and heart failure.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Patients were eligible for randomization 3 to 14 days after AMI with LV dysfunction based on an EF of ≤40% and clinical heart failure based on the presence of pulmonary rales, chest X-ray showing pulmonary venous congestion or the presence of a third heart sound. In patients with diabetes, the presence of clinical heart failure was not a requirement. Exclusion criteria included the use of potassium-sparing diuretics, serum creatinine >2.5 mg/dl, or serum potassium >5 mmol/l.Baseline characteristics The average age of patients was 65 years and over 70% were men; 90% were white. Approximately one quarter of patients had a prior MI, more than 30% had diabetes and 60% had hypertension. The average ejection fraction was 34%. Patients were hemodynamically stable with an average blood pressure of 119/72 mmHg. The average time to randomization from AMI was 7 days. Nearly 50% of patients underwent thrombolysis or angioplasty for the primary MI and at the time of randomization 86% of patients were on an ACE inhibitor, 88% on aspirin, 47% on statins, 75% on beta-blockers, and 60% on diuretics.Procedures Patients received either eplerenone 25 mg daily or a matching placebo for 4 weeks and then the dose was increased to 50 mg daily. If at any time during the study the serum potassium was >5.5 mmol/l, the dose of the study drug was reduced or temporarily discontinued until the serum potassium was

NEJM 1995;333:1670-6.Background Up to this point in history, a series of trials had been conducted using ACEi's in post-MI patients. A small to moderate short-term benefit had been shown when the drugs were started immediately (GISSI-3 and ISIS-4) and much greater long-term benefits were demonstrated when the drugs were started 5-11 days, on average, following AMI in patients with LV dysfunction and congestive heart failure (SAVE and AIRE).The SAVE and AIRE trials, however, were more selective and it was not clear how representative they were among all potentially eligible patients. Thus, TRACE authors sought to re-test the hypotheses tested in SAVE and AIRE with a focus on generalizability of trial procedures and results. Specifically, the Trandolapril Cardiac Evaluation Study (TRACE) sought to test the hypothesis that trandolapril would reduce all-cause mortality in post-MI patients with LV dysfunction when used in the majority of consecutively screened, potentially eligible patients.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Consecutive patients ≥18 years of age who were hospitalized with a confirmed AMI were screened between day 2 and 6 after the onset of symptoms. All screen eligible patients underwent echocardiography and those with a wall motion index of ≤1.2, which corresponds to an EF ≤35%, were considered for enrollment. The key exclusion criteria included an absolute or relative contraindication to an ACEi or a definite need for an ACEi, severe uncontrolled diabetes, a serum sodium 2.3 mg/dl.Baseline characteristics The average age of patients was 68 years and 72% were men. Approximately one third of patients had a prior MI, 13% had diabetes, 23% had hypertension and smoking status was not listed. The average wall motion index was 1.0. Two thirds of patients had a Q wave MI (anterior 47% and inferior 19%). The mean time to randomization was 4.5 days. Forty-five percent of patients received thrombolysis. The average blood pressure and heart rate were 120/70 mmHg and 76 beats per minute, respectively. At the time of randomization 16% of patients were receiving a beta blocker and 28% digoxin. Before randomization, 60% of patients had been classified as Killip class ≥2 and at the time of randomization it was 21%.A total of 6,676 consecutive patients experienced an AMI of whom 2,606 had a wall motion index of ≤1.2. There was an inverse relationship between wall motion index and mortality. In patients with scores ≥1.3, 40% had signs of CHF and the 1-year mortality rate was 12%. Among patients with scores ≤1.2, 74% had signs of CHF and the 1-year mortality was 34%.Of the 2,606 eligible patients, 859 (33%) were excluded. The most common reasons for exclusion included need for mandatory ACE inhibition [6%], cardiogenic shock [4%], death during screening [3%], renal failure or a single kidney [2%], intolerance of the test dose of trandolapril [1%], lack of consent [8%], or other reasons [8%].Altogether, 1,749 (67%) of patients with a wall motion index score ≤1.2 were enrolled.Procedures Eligible patients were given a test dose of 0.5 mg of trandolapril, which led to the exclusion of 1% of patients. These patients were not included in the ITT analysis. Double-blind medication was started between day 3 and day 7 after AMI. Patients were randomly assigned to receive 1 mg of trandolapril once daily or matching placebo. After two days, the dose was increased to 2 mg once daily. After four weeks, the dose was again increased, to 4 mg once daily. If the highest dose was not tolerated, patients could continue with a dose of 2 mg or 1 mg once daily, but the drug was withdrawn if a dose of 1 mg once daily was not tolerated.Outpatient visits were scheduled one and three months after the infarction, with subsequent visits every three months. Echocardiography was repeated after 3, 6, and 12 months.The original protocol specified that treatment would continue for at least 12 months. When the results of the SAVE study were published in 1992, showing no survival benefit until after almost one year of treatment with ACE inhibitors, the steering committee decided (without any knowledge of the results of the study) to extend the closing date to 24 months after the last random assignment.Endpoints The primary study endpoint was all-cause mortality. Secondary endpoints were death from a cardiovascular cause, sudden death, progression to severe heart failure, recurrent MI, and change in wall motion index.The investigators estimated they would need a sample size of 1,500 patients to detect a 25% relative reduction in the risk of death with 80% power and 1-sided alpha of 2.5%. This was based on an estimated death rate of 30% at 12 months in the placebo group; however, the steering committee increased the sample size to 1,860 patients to allow for the possibility of a lower-than-expected placebo mortality rate.In the spring of 1992 the overall mortality of randomized patients followed for 1 year was 24%. Inclusion of patients was therefore terminated at the end of June 1992 at the point where 1,749 patients had been randomized.Results The final analysis included 1,749 patients; 876 in the trandolapril group and 873 in the placebo group.Information on the percentage of patients discharged on various doses of the study drug are not provided.Compared to placebo, trandolapril significantly reduced all cause death by 22% [(35% vs 42%; 95 percent confidence interval, 0.67 to 0.91 p = 0.001)}. The mortality curves diverged early (Kaplan–Meier estimate of mortality at one month 9% vs 11%) and continued to diverge throughout the follow-up period. Trandolapril also significantly reduced secondary endpoints, including death from CV causes, sudden death, and progression to severe heart failure but it did not significantly reduce reinfarction.Examination of subgroups showed no evidence of treatment effect heterogeneity for all cause mortality, but again, similar to the SAVE and AIRE trials, the size of TRACE limits subgroup testing.Premature withdrawals from study drug, not including death, occurred in 37% of patients in the trandolapril group compared to 36% in the placebo group. The most common reason for withdrawal was need for treatment with an open-label ACEi and this occurred more in the placebo group. Withdrawal due to cough, hypotension and reduction in kidney function were rare in both groups but slightly more common in patients on trandolapril compared to placebo.Conclusions In the majority (67%) of consecutively screened patients with AMI complicated by left ventricular dysfunction, trandolapril significantly reduced death over at least 2 years of follow-up with a number needed to treat of approximately 14 patients. Results from TRACE strengthen support for ACEi in post-MI patients, and the trial has high external validity. It not only tested the intervention in two-thirds of potentially eligible patients but was highly transparent about why patients were excluded. A clinician looking to apply the procedures used in TRACE to the management of patients in clinical practice would not have to guess whether or not their patient would have been included. This is rare in clinical research and the investigators should be applauded for their efforts.Investigators studying ACEi in post-MI patients have triangulated the population of patients who benefit from this therapy. In our opinion, TRACE provides the final piece to the puzzle. There is no doubt about the clinical efficacy of these drugs in the overwhelming majority of post-MI patients and higher risk patients stand to benefit the most.Thank you for reading Cardiology Trial's Substack. This post is public so feel free to share it. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Lancet 2001;357:1385-90.Background While beta blockers were frequently used in patients with acute myocardial infarction complicated by heart failure, at the time the CAPRICORN trial was undertaken, supportive evidence from contemporary, large scale randomized trials was lacking. The BHAT and ISIS-1 trials, reviewed in this section, were published in 1982 and 1986, respectively; before contemporary therapies like thrombolysis/revascularization and ACE-inhibition had been established. These early trials also excluded patients with overt heart failure or those who had concerning signals, such as soft hemodynamics. The CAPRICORN trial sought to test the hypothesis that early initiation of carvedilol in patients with AMI complicated by heart failure and LV dysfunction would reduce morbidity and mortality compared to placebo.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Eligible patients were 18 years or older with a stable, definite myocardial infarction occurring 3-21 days prior to randomization with either a left ventricular ejection fraction of ≤40% or a wall motion index score of ≤1.3 and who were receiving an ACE inhibitor for at least 48 hr and were on a stable dose for at least 24 hr. Patients could have received IV diuretics during the acute phase but were excluded if they continued to require IV diuretics or inotropes or had uncontrolled heart failure. Other reasons for exclusion included unstable angina, SBP 80 mmHg, the dose was increased to the next level. The patient remained in the outpatient department for 2hr to ensure that no side effects ensued.During the maintenance period patients were reviewed every 3 months during the first year and every 4 months thereafter. Investigators were encouraged to review the dose of study medication at every visit and to ensure that doses of other drugs, especially ACE inhibitors, were adjusted accordingly to achieve optimum dose levels.Endpoints The original primary endpoint was all-cause mortality and the trial was intended to run until a total of 633 primary endpoint events occurred. However, during a masked analysis the data and safety monitoring committee noted that overall mortality was lower than predicted and that the study could not be completed with the original sample size and power as planned. The steering committee, therefore, designated co-primary endpoints. The first was a new composite primary endpoint of all-cause mortality or cardiovascular hospital admission and the second was all-cause mortality. The trial was still intended to run until 633 primary endpoint events occurred with the original sample size. The alpha (false-positive) was divided between the 2 primary endpoints so that the composite endpoint of all-cause mortality and cardiovascular hospitalization was tested at 0.045 and all-cause mortality was tested at 0.005. Secondary endpoints included sudden death, hospitalization for heart failure, recurrent nonfatal MI, and all-cause mortality or nonfatal MI.Results 1,959 patients were included in the final analysis; 984 in the placebo group and 975 in the carvedilol group. The mean follow-up was 1.3 years. Compared to placebo, carvedilol did not significantly reduce the composite primary endpoint of all-cause death or cardiovascular hospitalization (HR 0.92; 35% vs 37%; 95% CI 0.80-1.07) or all-cause death alone (HR 0.77; 12% vs 15%; 95% CI 0.6-0.98). The authors present the all-cause mortality result as positive; however, it is NOT. In table 1, the p for all-cause mortality is 0.031, which is >0.005. Thus, there is a good chance that the mortality result represents a false positive finding.For the secondary endpoints, there were reductions in nonfatal MI and the combined endpoint of all-cause death or nonfatal MI for patients in the carvedilol group but these results are based on a relatively small number of events.Of the 940 patients who entered the maintenance phase in the carvedilol group, 74% reached the maximum dose of 25 mg bid while 11% and 7% reached 12.5 mg bid and 6.25 mg bid.There is no subgroup data or safety data presented in the main paper.   Conclusions In patients with AMI complicated by heart failure and significant LV dysfunction, carvedilol did not significantly reduce all-cause death or cardiovascular hospitalizations compared to placebo. This trial is often presented and discussed as a positive trial but it is not. The appropriately powered endpoint in this case was the composite primary endpoint, which was clearly negative. The difference in all-cause mortality is based on a small number of events with a post-hoc power of 19.3% at the prespecified alpha of 0.005. The reported p-value for all-cause mortality was 0.031, which was much higher than the prespecified p value of ≤ 0.005 to declare a positive result. Due to the underpowered nature of all-cause death, the investigators chose to make the alpha as low as it was to avoid making false positive claims but then they did so anyway!While power is generally taught to infer a trial's strength to avoid false negative results, low power also increases a trial's susceptibility to false positive results. We have discussed this with small trials involving magnesium and nitrates, which were highlighted by the meta-analyses presented in the ISIS 4 publication.In conclusion, CAPRICORN was a negative trial. Its primary results were negative and differences in secondary endpoints, including the reduction in death, should be viewed as “hypothesis generating” only. It does not clearly establish a beneficial role for beta blockers in post-MI patients with significant LV dysfunction and heart failure.Thank you for reading Cardiology Trial's Substack. This post is public so feel free to share it. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

NEJM 1992;327:669-77 Background After a large heart attack, cardiac hemodynamics are altered, which leads to a series of changes in the heart muscle itself. The immediate consequence of a large heart attack is decreased myocardial contractility. This leads to a reduction in stroke volume and cardiac output. Compensatory mechanisms governed by the renin-angiotensin-aldosterone system and sympathetic nervous system become activated and may lead to ventricular dilation or “remodeling”, which has negative short and long-term consequence for the heart muscle.By the mid-1980's, angiotensin converting enzyme inhibitors (ACEi) were commonly used for patients with chronic systolic heart failure and laboratory work had shown they could improve ventricular remodeling, reduce heart failure and prolong survival in animal models of AMI. Several studies had also shown promise in humans but they were too small to test hypotheses involving hard clinical endpoints. The Survival and Ventricular Enlargement (SAVE) trial sought to test the hypothesis that administration of captopril to patients with AMI complicated by left ventricular dysfunction but who did not have overt heart failure requiring vasodilatory therapy would reduce morbidity and mortality over long-term follow-up.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Eligible patients were between 21 to 80 years of age with a definite myocardial infarction occurring 3 to 16 days prior to randomization with a left ventricular ejection fraction (EF) ≤40%, measured by radionuclide ventriculography. Patients were excluded with relative contraindications to ACEi or if an ACEi was indicated for treatment of symptomatic congestive heart failure or systemic hypertension. Other exclusion criteria included serum creatinine >2.5 mg/dl, other conditions limiting survival (unspecified) or who had an unstable course following AMI (also unspecified).Baseline characteristics The average age of patients was 59 years and 82% were men. Approximately one third of patients had a prior MI, more than 20% had diabetes, 40% had hypertension and over 50% were current smokers. The average ejection fraction was 31% and over half of patients had an anterolateral Q wave MI. The mean time to randomization was 11 days. Prior to randomization approximately a third received thrombolysis, over 50% underwent coronary angiography, and approximately 25% underwent either percutaneous coronary angioplasty or coronary artery bypass surgery. At the time of randomization, the average blood pressure was 113/70 mmHg and heart rate was 78 beats per minute. Within 24 hours of randomization approximately one third of patients received a beta blocker and a quarter received digoxin.Procedures There was a mini run-in period where all 2,250 eligible patients were given a test dose of 6.25 mg of captopril. This led to exclusion of 19 patients (3 for ischemic discomfort and 16 for symptomatic hypotension).Patients received either captopril or placebo. The initial dose of the blinded study drug was 12.5 mg but could be administered at 6.25 mg to patients who had marked, yet asymptomatic, reduction in BP with the run-in dose. The target dose was 25 mg three times a day by the end of the in-hospital phase and was gradually increased to 50 mg three times a day unless side effects occurred. There was no prespecified level of blood pressure in the titration regimen.Outpatient visits were scheduled 2 weeks following randomization and then every 3 months during year 1 and every 4 months thereafter. Compliance with the study drug was assessed by pill count.Endpoints There were no prespecified hypothesis tests used to determine sample size. Prospectively defined measures of outcomes included all cause death, cardiovascular death, incidence of clinical congestive heart failure and first hospitalization for heart failure. Once the clinical endpoint committee was notified of a diagnosis of clinical heart failure the study medication was discontinued so open-label therapy with an ACEi could be started.Results 2,231 patients were included in the final analysis; 1116 in the placebo group and 1115 in the captopril group. The mean follow-up was 3.5 years. Blood pressure increased from baseline in both groups but to differing extents. At 3 months, BP was 125/77 in the placebo group compared to 119/74 in the captopril group. The average heart rate was 74 in both groups.Compared to placebo, captopril significantly reduced all cause death by 19% (20% vs 25%; p = 0.019) and cardiovascular death by 21% (17% vs 21%; p = 0.014). It also reduced clinical heart failure by 37% (11% vs 16%; p

La Sociedad de Medicina de Cuidado Crítico (Society for Critical Care Medicine, o SCCM) publicó en la revista JAMA la actualización a la definición de sepsis pediátrica en pacientes menores de 18 años. La revisión del 2016 que dio paso a la 3era definición por consenso solo aplicó a pacientes adultos. En este otro episodio del ECCpodcast discuto la definición de sepsis en pacientes adultos. Como especie, nuestra fisiología no ha evolucionado. Lo que ha evolucionado es nuestro entendimiento de la condición y por ende la forma en que definimos qué es sepsis. Definición Sepsis 3.0 del 2016 Sepsis no es solamente una infección severa. Sepsis es fallo orgánico asociado a una infección, debido a una respuesta anormal del cuerpo a la infección. Para definir el fallo orgánico, se utilizó la puntuación SOFA (Sequential Organ Failure Assessment) (también llamado Sepsis-Related Organ Failure Assessment y Systemic Organ Failure Assessment). Shock séptico fue definido como un paciente con que requiere vasopresores para mantener una presión arterial media de 65 mmHg y lactato mayor de 2 mmol/L. Debido a que la definición incluye números que aplican solamente a adultos, es necesario definirlos en el contexto de pacientes pediátricos. Debido a que la definición de Sepsis 3.0 aplica solamente a los pacientes adultos, la definición operante de sepsis pedíátrica incluía (hasta ahora) los criterios del síndrome de respuesta inflamatoria sistémica (SIRS por sus siglas en inglés). Ya sabemos, de la definición de Sepsis 3.0, que los criterios de SIRS tienen serias limitaciones a la hora de definir sepsis. No significa que no sea útiles como signos de alerta de que un paciente pudiera requerir atención médica de emergencia, pero no necesariamente están asociados a resultados adversos en pacientes pediátricos. Por lo tanto, desde que se publicó la definición de Sepsis 3.0 en el 2016 estamos esperando la definición de sepsis pediátrica. Poder hacer esto requiere el mismo rigor científico que para la contraparte adulta, pero al fin se completó y aquí lo tenemos. Conceptualmente hablando, sepsis en adultos y pediátricos es muy parecido. De hecho, desde el 2016, muchos estamos usando el fallo orgánico en el marco de referirnos a alguien con sepsis indistintamente de la edad. La razón es simple: el concepto de sepsis es que sepsis no es solamente la respuesta normal a una infección, sino una respuesta anormal que está causando una amenaza a la vida. El hecho de que el paciente tenga un fallo orgánico distal al punto de la infección original refleja la naturaleza sistémica del proceso que lleva a la sepsis. ¿Los niños son adultos pequeños? Obviamente hay diferencias entre los adultos y pediátricos: Signos vitales normales varían según la edad. Sistema inmune varía según la edad Comorbilidades son diferentes Así es que cuando se define la condición en pacientes pediátricos hay que utilizar números diferentes. Los números de la puntuación SOFA no aplican a los pediátricos. By Dr. Julio Javier Gamazo del RioServicio de Urgencias. Hospital Universitario de GaldakaoDr. Jesús Álvarez ManzanaresServicio de Urgencias. Hospital Universitario Río HortegaDr. Juan González del CastilloServicio de Urgencias. Hospital Universitario Clínico San Carlos - http://semes.org/sites/default/files/archivos/Los-Nuevos-Criterios-De-Sepsis.pdf, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=54877568 Puntuación de Sepsis Pediátrica de Phoenix En pacientes con infección, se define sepsis pediátrica cuando el paciente pediátrico tiene al menos 2 puntos en la Escala de Sepsis Pediátrica de Phoenix, que consiste en un agregado de fallo cardiovascular, respiratorio, neurológico y de coagulación. Es importante señalar que esta escala sirve en pacientes con una infección sospechada o confirmada. No es una escala que se puede utilizar en otro contexto que no sea la evaluación de un paciente pediátrico con infección. JAMA. Published online  January 21, 2024. doi:10.1001/jama.2024.0179 Aplica a pacientes de 18 años o menos, pero no aplica a recién nacidos, o neonatos que hayan nacido menores de 37 semanas de gestación. Toda recomendación hecha en base a evidencia obtenida de pacientes adultos tiene que ser investigada en una población pediátrica antes de concluir que es aplicable. Shock séptico = sepsis + disfunción cardiovascular La disfunción cardiovascular se puede medir funcionalmente como un paciente con al menos 1 punto en los criterios cardiovasculares. Es decir, un paciente pediátrico que tenga criterios de sepsis (2 puntos o más en la Escala de Sepsis Pediátrica) de los cuales al menos 1 punto provenga de los criterios cardiovasculares: Hipotensión severa para la edad Lactato > 5 mmol/L Uso de medicamentos vasoactivos Poniéndolo todo junto JAMA. Published online  January 21, 2024. doi:10.1001/jama.2024.0179 Generalizabilidad El artículo de la nueva definición detalla la sensibilidad de la nueva definición en contextos de altos recursos versus bajos recursos. Es decir, la nueva definición de sepsis pediátrica es más fácil de medir en lugares de bajos recursos en comparación a la puntuación SOFA para adultos. La Puntuación de Sepsis de Phoenix incluye criterios como la disfunción de la coagulación que pudieran no estar disponibles fácilmente en escenarios de bajos recursos, pero los autores concluyen que existe suficiente redundancia con los demás criterios para mantener una sensibilidad adecuada. La Escala de Sepsis Pediátrica de Phoenix utiliza evalúa solamente 4 órganos. Sin embargo, existe otra variante que es la Escala Phoenix-8 que evalúa otros órganos. Estas evaluaciones adicionales pudieran no estar disponibles en lugares de bajos recursos, pero no deja de ser criterios adicionales a considerar al evaluar pacientes que requieran algún apoyo multisistémico. Para más información sobre la validación de los Criterios de Sepsis Pediátrica de Phoenix, vea este otro artículo publicado simultáneamente a la nueva definición. Limitación La Puntuación de Sepsis Pediátrica de Phoenix es una forma de definir que el paciente ya tiene sepsis. No es una herramienta para identificar el paciente en riesgo de desarrollar sepsis. Entonces, es importante recordar que solamente porque un paciente NO cumpla con los criterios de la Puntuación de Sepsis de Phoenix no significa que no requiere atención agresiva a la infección. Referencias Sanchez-Pinto LN, Bennett TD, DeWitt PE, et al. Development and Validation of the Phoenix Criteria for Pediatric Sepsis and Septic Shock. JAMA. Published online January 21, 2024. doi:10.1001/jama.2024.0196 Schlapbach LJ, Watson RS, Sorce LR, et al. International Consensus Criteria for Pediatric Sepsis and Septic Shock. JAMA. Published online January 21, 2024. doi:10.1001/jama.2024.0179

Lancet 1990;336:65-71.Background Large trials up to this point had established the role of thrombolytic therapy and aspirin in patients with acute MI. The next question centered on the different types of thrombolytic agents as well as the merits of adding high dose heparin to aspirin following revascularization. Data from smaller studies showed that alteplase (tPA) had a higher recanalization rate at 90 minutes compared to streptokinase (SK). “Recanalization” is a surrogate endpoint – a person doesn't necessarily care whether their artery is open or not at 90 minutes, but instead, whether they live or die, and how they live in the aftermath of a heart attack. The GISSI-2 trial sought to test the hypothesis that tPA would reduce the composite hard endpoint of mortality and extensive LV dysfunction compared to streptokinase (SK) and that heparin plus aspirin compared to aspirin alone would do the same.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Patients were eligible who presented with chest pain and ST segment elevations of ≥1 mm in any limb lead of the ECG and/or ≥2 mm in any precordial leads and were admitted to the CCU within 6 hr from the onset of symptoms. Absolute contraindications included: recent or current bleeding, stroke within the previous 6 months, a surgical or invasive procedure or trauma within the previous 2 weeks, uncontrolled hypertension defined as SBP ≥200 mmHg or DBP ≥110 mmHg, or previous treatment with SK within 6 months.Baseline characteristics The number of patients who were admitted to CCUs with acute myocardial infarctions (MI) over the study period was 38,086 and 12,490 (33%) were ultimately enrolled. Reasons for exclusion included: more than 6 hr from onset of symptoms (61%), contraindications to fibrinolysis (15%), unlikely to have acute MI (13%), administrative reasons (5%), ST depressions (4%) and 1% were not reported. Similar to GISSI-1, which also provided information on patients enrolled versus those who were not, women were more likely to be excluded (30% of excluded vs 20% of enrolled) as were patients >70 years of age (41% of excluded vs 22% of enrolled). The death rate of those excluded was higher (11% of excluded vs 9% of enrolled).Approximately 80% of patients enrolled were men under the age of 70. Patients with inferior (34%) and anterior STEMI's (31%) composed more than half of the cohort. 72% of patients presented within 3 hours of symptom onset and over 95% had Killip scores of II or below with the vast majority being Killip I (78%).Procedures Immediately following randomization half of all patients received either 1.5 MU of SK infused over 1 hour or 100 mg of tPA infused over 3 hours. Since this was a 2x2 factorial design, half of all patients also received 12,500 U of subcutaneous heparin twice daily starting 12 hours after the beginning of the tPA or SK infusion and to be continued until hospital discharge.All patients without specific contraindications were recommended to receive oral aspirin 325 mg/day and 5-10 mg of IV atenolol, even before randomization, as soon as evolving MI was diagnosed.Endpoints The combined primary endpoint consisted of all-cause mortality plus the number of patients who had late (day 4 or later) clinical congestive heart failure, or extensive LV damage (LVEF

Lancet 1986;397-401Background This study by the Italian Group for the Study of Streptokinase in Myocardial Infarction (GISSI) is the first large trial to test the hypothesis that opening blocked heart arteries, in this case via use of the intravenous thrombolytic agent Streptokinase, reduces death in patients presenting with acute myocardial infarction (MI). Opening blocked arteries or revascularization is now a foundational element of cardiovascular medicine that arguably spurred much of the growth in the field over the 1990's and early 2000's. Therefore, it is critical to revisit this historic trial and appreciate the lessons it taught us.Patients Patients were eligible who presented with chest pain and ST segment elevations of ≥1 mm in any limb lead of the electrocardiogram and/or ≥2 mm in any precordial leads and were admitted to the cardiac intensive care unit (CCU) within 12 hours from the onset of symptoms. Absolute contraindications included recent or current bleeding, stroke within the previous 2 months, a surgical procedure or trauma within the previous 10 days, invasive procedures within the previous 10 days, SBP ≥200 mmHg, DBP ≥110 mmHg, previous treatment with streptokinase, or any other life-threatening condition.Baseline characteristics The number of patients who were admitted to CCUs with acute MIs over the study period was 31,826 and 11,806 (37%) were ultimately enrolled. Reasons for exclusion included being more than 12 hr from onset of symptoms (51%), contraindications to Streptokinase (21%), unlikely to have acute MI (19%), administrative reasons (8%) and 2% were not reported. Notably, women were more likely to be excluded (27% of excluded vs 20% of enrolled) as were patients >75 years of age (21% of excluded vs 11% of enrolled).Not a lot of demographic information is provided on the cohort in the main manuscript but it was composed primarily of men (80%) who were ≤65 years of age (65%). Only a small percentage of patients were unstable, as evidenced by SBP ≤90 mmHg (

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CardioNerds (Drs. Amit Goyal, Jason Feinman, and Tiffany Dong) discuss Beyond the Boards: Diseases of the Peripheral Arteries with Dr. Amy Pollak. We review common presentations of peripheral vascular disease, ranging from aortic disease to the more distal vessels in an engaging case-based discussion. Dr. Pollack talks us through these cases, including the diagnosis and management of peripheral vascular diseases. Show notes were drafted by Dr. Matt Delfiner and episode audio was edited by student doctor Tina Reddy. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Disease of the Peripheral Arteries Risk factors for abdominal aortic aneurysm include traditional atherosclerotic risk factors such as age, hypertension, hyperlipidemia, and tobacco use. Screening for AAA should be for men over the age of 65 years with a history of tobacco use. If present, medical management includes blood pressure and lipid lowering therapies to decrease the risk of expansion. Decision for surgical intervention relies on size and rate of growth of AAA, with clear indications if it grows> 10 mm in a year or diameter of 5.5 cm in men and 5.0 cm in women. When diagnosis of PAD is not straightforward (presence of symptoms but ABI is normal), an exercise ankle-brachial index (ABI) test can be useful. An exercise-induced decrease in ABI by 20% or in ankle pressure by 30 mmHg is consistent with PAD. For PAD, treatment with low dose rivaroxaban and aspirin yields lower event rates than with antiplatelet therapy alone. This in combination with lifestyle therapies (diet + exercise) and risk factor management (hypertension and hyperlipidemia) are the cornerstones of therapy. Revascularization is indicated for continued PAD symptoms despite conservative therapy. Acute limb ischemia is an “acute leg attack” and is a life-threatening emergency. Common symptoms include pain, pallor, pulselesess, parasthesias, cold temperature (poikilothermia), and paralysis. Restoration of blood flow is paramount, and emergent or urgent revascularization is the first line therapy for those with symptoms < 2 weeks. Notes - Disease of the Peripheral Arteries Learning Objectives: Describe screening and therapeutic strategy for AAA management. Understand the risk factors and diagnosis of peripheral arterial disease. Compare different management approaches for PAD. Be able to recognize acute limb ischemia. Describe the overall treatment strategy for acute limb ischemia. Abdominal Aortic Aneurysms Abdominal aortic aneurysms are a source of high morbidity and mortality. The US Preventative Services Task Force recommends one time screening ultrasound for AAA in men older than 65 years of age with a tobacco use history. Risk factors include age, hypertension, hyperlipidemia, and tobacco use. Patients with AAA between 3-3.9 mm should be monitored every 2-3 years. Sizes 4-5 cm should be re-imaged every 6-12 months.  Additional screening can be done for individuals < 65 years who have a first degree relative with AAA. Women are more likely to have aortic dissection at smaller diameters than men, which is why intervention (open vs endovascular repair) is recommended at 5 cm diameter for women versus at 5.5 cm for men. Additionally, repair is also warranted if a AAA grows more than 5 mm in 6 months or 10 mm in one year. Risk factor management is key with AAA, including blood pressure, glucose, and lipid targeting.  The presence of an AAA should be treated as secondary ASCVD prevention like coronary a...

Did you know high blood pressure usually has no symptoms? According to the Centers for Disease Control and Prevention, about half of adults have high blood pressure, defined as a systolic (top) blood pressure greater than 130 mmHg or a diastolic (bottom) blood pressure greater than 80 mmHg, or are taking medication for high blood pressure. What's more concerning, is only about 1 in 4 adults with high blood pressure have it under control. Having high blood pressure increases your risk of heart attack and stroke. And it's estimated that in the United States alone, $131 billion is spent on the condition each year.On today's episode, you'll hear from Jay Shah, MD. He is an expert cardiologist, having practiced at Massachusetts General Hospital and the Mayo Clinic, and now is Chief Medical Officer for Aktiia. He believes the time has come in medicine for individuals to understand and optimize their own health. This includes a better understanding of your blood pressure, and not relying on a sole reading at the doctor's office to say “You have high blood pressure, take this medication.”In this interview, he talks about a better way to measure high blood pressure - continuously and automatically. Similar to a continuous glucose monitor but for blood pressure. For the right person, this technology can be life-saving. Highlights From This Episode: Prevalence of high blood pressure.Importance of proper medication dosing.What is Aktiia and how to use it properly.Why a continuous blood pressure device increases the Hawthorne effect and behavior change. Lifestyle changes to lower blood pressure.  Subscribe & ReviewSubscribing and leaving a rating and review are important factors in helping the Reshape Your Health Podcast and the YouTube Channel reach more people. If you haven't already subscribed, please do that today.We would also be grateful if you left a rating and review, too. In your listening app, scroll to the “Ratings and Reviews” section, then click “Write a Review” and let us know what you enjoy about our show. We appreciate you taking the time to show your support. Thank you!Resources From This Episode>> Join Zivli>> Book a Free Zivli Discovery Call>> Freebie: The Ultimate Food Guide>> Aktiia's Website>> Register for the FREE Healthy Holidays Workshop

Welcome to my podcast. I am Doctor Warrick Bishop, and I want to help you to live as well as possible for as long as possible. I'm a practising cardiologist, best-selling author, keynote speaker, and the creator of The Healthy Heart Network. I have over 20 years as a specialist cardiologist and a private practice of over 10,000 patients. Doctor Warrick Bishop discusses various topics related to heart health and inflammation in this podcast. He talks about a study that found intensive periodontal treatment reduced blood pressure by 5-10 mmHg by reducing inflammation. Another interesting finding was that rats who experienced a stroke showed changes in their gut microbiome and increased gut permeability, leading to systemic infection. Doctor Bishop also discusses how a high-salt diet can directly damage the gut microbiome and allow inflammatory proteins to enter the bloodstream, triggering inflammation in blood vessels even before high blood pressure occurs. He recommends keeping salt intake low, staying hydrated, and consuming fiber to help protect the gut from these salt-related harms.

The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #29 A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient? A Start metoprolol succinate B Start sacubitril/valsartan C Perform genetic sequencing of the TTR gene D Perform endomyocardial biopsy Answer #29 Explanation The correct answer is C – perform genetic sequencing of the TTR gene.   This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt).   Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis.

The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Faculty Dr. Ty Sweeny, and then by expert faculty Dr. Gregg Fonarow. Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA's Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA's Preventative Cardiology Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #28 Mr. Gene D'aMeTi, a 53-year-old African American man with ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 30-35%), is recently admitted with acutely decompensated heart failure and acute kidney injury on chronic kidney disease stage III. His outpatient regiment includes sacubitril-valsartan 97-103mg BID, carvedilol 25mg BID, and hydralazine 50mg TID. Sacubitril-valsartan was held because of worsening renal function. Despite symptomatic improvement with diuresis, his renal function continues to decline. He is otherwise well perfused & with preservation of other end organ function.   Throughout this hospitalization, he has steadily become more hypertensive with blood pressures persisting in the 170s/90s mmHg. What would be an appropriate adjustment to his medication regimen at this time? A Resume Losartan only B Start Amlodipine C Increase current Hydralazine dose D Start Isosorbide dinitrate therapy E Both C & D Answer #28 ExplanationThe correct answer is E – both increasing the current hydralazine dose (C) and starting isosorbide dinitrate therapy (D). Although ACEI/ARB therapy (choice A) has shown a mortality and morbidity benefit in HFrEF, caution should be used in patients with renal insufficiency. In this patient with ongoing decline in renal function, RAAS-inhibiting therapies (ACEi, ARB, ARNI, MRA) should be avoided. In this case, as his RAAS-I has been stopped, it would be reasonable to increase current therapies to target doses (or nearest dose tolerated), as these demonstrated both safety and efficacy in trials (Class 1, LOE A). Considering that his high dose ARNI was stopped, it is unlikely that either hydralazine or isosorbide dinitrate alone, even at maximal doses, would be sufficient to control his blood pressure (Options C and D, respectively). Interestingly, in the original study by Massie et. Al (1977), the decision was made to combine these therapies as the result was thought to be superior to either medication alone. ISDN would provide preload reduction, while Hydralazine would decrease afterload. Consequently, we do not have data looking at the individual benefit of either medication in isolation. In self-identified African Americans with NYHA class III or IV HFrEF already on optimal GDMT, the addition of hydralazine & isosorbide dinitrate is recommended to improve symptoms and reduce mortality and morbidity (Class 1, LOE A). In this case, as the patient has evidence of progressive renal disfunction, we are limited in using traditional RAAS-I, such as ACEI, ARB, or ARNI.

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Michael Wesley Milks.Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center, where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology's Cardiovascular Disease Prevention Leadership Council.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #32 Mr. Daniel Collins is a 58-year-old man with hypertension, chronic kidney disease (CKD), and obesity who presents to your clinic for a routine physical examination. Vitals are as follows: BP 143/79 mmHg, HR 89 bpm, O2 99% on room air, weight 106 kg, BMI 34.5 kg/m2. Recent laboratory testing revealed: creatinine 1.24 mg/dL, total cholesterol 203 mg/dL, HDL 39 mg/dL, LDL 112 mg/dL, TG 262 mg/dL. His current medications include lisinopril and rosuvastatin. You recommend increasing the dose of lisinopril to treat uncontrolled hypertension. What additional step(s) are indicated at this visit? A Order urine albumin-to-creatinine ratio B Ask the patient how often they have been bothered by trouble falling or staying asleep, or sleeping too much C Perform depression screening D All of the above Answer #32 Explanation The correct answer is D – all of the above.Answer A is correct. The ESC gives a Class I (LOE C) indication that all CKD patients, with or without diabetes, should undergo appropriate screening for ASCVD and kidney disease progression, including monitoring for changes in albuminuria. Cardiovascular disease is the leading cause of morbidity and death among patients with CKD. Even after adjusting for risk factors, including diabetes and hypertension, there is a linear increase in CV mortality with decreasing GFR below ~60-75 mm/min/1.73m2. Specific CKD-related risk factors include uremia-mediated inflammation, oxidative stress, and vascular calcification.Answer choice B is also correct. In patients with ASCVD, obesity, and hypertension, the ESC gives a Class I (LOE C) indication to regularly screen for non-restorative sleep by asking the question related to sleep quality as follows: “‘How often have you been bothered by trouble falling or staying asleep or sleeping too much?”. Additionally, if there are significant sleep problems that are not responding within four weeks to improving sleep hygiene, referral to a specialist is recommended (Class I, LOE C). However, despite the strong association of OSA with CVD, including hypertension, stroke, heart failure, CAD, and atrial fibrillation, treatment of OSA with CPAP has failed to improve hard CVD outcomes in patients with established CVD. Interventions that focus on risk factor modification, including reduction of obesity, alcohol intake, stress, and improvement of sleep hygiene, are important.Answer choice C is also correct. The ESC gives a Class I (LOE C) recommendation that mental health disorders with either significant functional impairment or decreased use of healthcare systems be considered as influencing total CVD risk. All mental disorders are associated with the development of CVD and reduced life expectancy. Additionally, the onset of CVD is associated with an approximately 2-3x increased risk of mental health disorders compared to a ...

The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Eldrin Lewis.Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #26 A 45-year-old man presents to cardiology clinic to establish care. He has had several months of progressive dyspnea on exertion while playing basketball. He also reports intermittent palpitations for the last month. Two weeks ago, he passed out while playing and attributed this to exertion and dehydration. He denies smoking and alcohol intake.   Family history is significant for sudden cardiac death in his father at the age of 50 years. Autopsy has shown a thick heart, but he is unaware of the exact diagnosis. He has two children, ages 12 and 15 years old, who are healthy.   Vitals signs are blood pressure of 124/84 mmHg, heart rate of 70 bpm, and normal respiratory rate. On auscultation, a systolic murmur is present at the left lower sternal border. A 12-lead ECG showed normal sinus rhythm with signs of LVH and associated repolarization abnormalities. Echocardiography reveals normal LV chamber volume, preserved LVEF, asymmetric septal hypertrophy with wall thickness up to 16mm, systolic anterior motion of the anterior mitral valve leaflet with 2+ eccentric posteriorly directed MR, and resting LVOT gradient of 30mmHg which increases to 60mmHg on Valsalva.   You discuss your concern for an inherited cardiomyopathy, namely hypertrophic cardiomyopathy. In addition to medical management of his symptoms and referral to electrophysiology for ICD evaluation, which of the following is appropriate at this time? A  Order blood work for genetic testing B  Referral for genetic counseling C  Cardiac MRI D  Coronary angiogram E  All of the above Answer #26 Explanation   The correct answer is B – referral for genetic counseling.  Several factors on clinical evaluation may indicate a possible underlying genetic cardiomyopathy. Clues may be found in: ·       Cardiac morphology – marked LV hypertrophy, LV noncompaction, RV thinning or fatty replacement on imaging or biopsy ·       12-lead ECG – abnormal high or low voltage or conduction, and repolarization, altered RV forces ·       Presence of arrhythmias – frequent NSVT or very frequent PVCs, sustained VT or VF, early onset AF, early onset conduction disease ·       Extracardiac features – skeletal myopathy, neuropathy, cutaneous stigmata, and other possible manifestations of specific syndromes In select patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). In first-degree relatives of selected patients with genetic or inherited cardiomyopathies, genetic screening and counseling are recommended to ...

The following question refers to Sections 6.1 and 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident and CardioNerds Academy Fellow Dr. Alaa Diab, and then by expert faculty Dr. Mark Drazner. Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the past President of the Heart Failure Society of America.  The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #25 A 50-year-old man with a history of type 2 diabetes mellitus, persistent atrial fibrillation, coronary artery disease with prior remote percutaneous coronary intervention, and ischemic cardiomyopathy with HFrEF (LVEF 38%) presents to your outpatient clinic. He denies dyspnea on exertion, orthopnea, bendopnea, paroxysmal nocturnal dyspnea, or peripheral edema. His heart rate is irregularly irregular at 112 beats per minute and blood pressure is 112/67 mmHg. Routine laboratory studies reveal a hemoglobin A1c of 7.7%. Which of the following medications should not be used to control this patient's comorbidities? A Metoprolol succinate B Verapamil C Dapagliflozin D Pioglitizone E Both B and D Answer #25 Explanation The correct answer is E – both verapamil and pioglitazone should be avoided here. Both verapamil and pioglitizone are associated with harm in patients with LVEF < 50% (Class 3: Harm). Verapamil and diltiazem are non-dihydropyridine calcium channel blockers. These medications can cause negative inotropic effects through inhibition of calcium influx and may be harmful in this patient population. Pioglitizone belongs to a class of diabetic medications known as the thiazolidinediones. This class of medications may increase the risk of fluid retention, heart failure, and hospitalization in patients with LVEF of less than 50%. Metoprolol succinate, and other evidence-based beta blockers, have a Class 1 recommendation for patients with reduced ejection fraction ≤ 40% to prevent symptomatic heart failure and reduce mortality. It may additionally help with rate control in this patient with atrial fibrillation and rapid ventricular response. SGLT2 inhibitors including dapagliflozin have a Class I recommendation for patients with symptomatic chronic HFrEF to reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes (Class 1, LOE A). They also have a Class I recommendation in patients with type 2 diabetes and either established CVD or at high cardiovascular risk to prevent hospitalization for HF (Class 1, LOE A). Our patient has asymptomatic, or pre-HF (Stage B) heart failure with poorly controlled diabetes, and so use of an SGLT2 inhibitor would be appropriate. Main Takeaway Non-dihydropyridine calcium channel blockers and thiozolidinediones both have Class 3 recommendations for harm in patients with reduced LV systolic dysfunction. Guideline Loc. Section 6.1 and 7.3   Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds Academ...

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH internal medicine resident Dr. Christian Faaborg-Andersen, answered first by UCSD early career preventive cardiologist Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos. Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women's heart disease; she is the Director of Women's Heart Health at Lenox Hill Hospital and Director of Cardiovascular Prevention for Northwell Health. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #30 A 65-year-old woman with a history of hypertension, type 2 diabetes mellitus, and coronary artery disease with remote PCI to the RCA presents for follow-up. She has stable angina symptoms that are well controlled with metoprolol tartrate 25 mg BID and are not lifestyle limiting. She takes aspirin 81 mg daily and atorvastatin 40 mg daily. Her LDL-C is 70 mg/dL, hemoglobin A1c is 7.0%, and eGFR is >60. In clinic, her BP is 118/80 mmHg. What is the next step in management?AIncrease atorvastatin for goal LDL-C < 55 mg/dLBNo change in managementCAdd isosorbide mononitrate 30 mg dailyDStop aspirinEStart a sulfonylurea Answer #30 Explanation The correct answer is A – increase atorvastatin for goal LDL-C < 55 mg/dL.In patients with established ASCVD, the ESC guidelines advocate for an LDL goal of < 55 mg/dL with at least a 50% reduction from baseline levels (Class I, LOE A). This patient has stable angina which is not lifestyle limiting; as such, further anti-anginal therapy is not necessary. She has known CAD with prior PCI, so aspirin therapy is appropriate for secondary prevention (Class I, LOE A). There is no indication for a sulfonylurea as her diabetes is well controlled. Notably, in persons with type 2 DM and ASCVD, the use of a GLP-1RA or SGLT2 inhibitor with proven outcome benefits is recommended to reduce CV and/or cardiorenal outcomes (Class I, LOE A).Main TakeawayFor people with established ASCVD, the ESC-recommended LDL-C goal is < 55 mg/dL with a goal reduction of at least 50%.Guideline Loc.Section 6.1 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Orthostatic hypotension (OH) occurs when the body has an inadequate response to postural changes and, as a result, is unable to maintain a steady blood pressure when moving from a lying to standing position. It is defined as a decrease in systolic or diastolic blood pressure that occurs within three minutes of moving from a sitting or supine position to a standing position. The parameter for OH is a decrease of 20 mmHg systolic or a decrease of 10 mmHg diastolic. In this episode you'll learn: * The physiology of orthostatic hypotension * The key difference between acute and chronic OH * How neurogenic OH differs from non-neurogenic OH * Conditions that exacerbate OH * Why drug-induced OH occurs * Medical conditions that can cause an individual to have acute or chronic OH * The complications of orthostatic hypotension * How orthostatic hypotension is diagnosed * How orthostatic hypotension is treated * Pharmacology for OH Read the article and view references here. Are you looking for an easier way to learn Med Surg? Enroll in Med Surg Solution and get lessons on 57 key topics as well as out-of-this-world study guides! If this episode helped you, please take a moment to rate and review the show! This helps others find the podcast, which helps me help even more people _____________________________________ The information, including but not limited to, audio, video, text, and graphics contained on this podcast are for educational purposes only. No content on this podcast is intended to guide nursing practice and does not supersede any individual healthcare provider's scope of practice or any nursing school curriculum. Additionally, no content on this podcast is intended to be a substitute for professional medical advice, diagnosis or treatment. Straight a Nursing is a proud member of the Airwave Media Network. Learn more about your ad choices. Visit megaphone.fm/adchoices

The following question refers to Section 9.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Cedars Sinai medicine resident, soon to be Vanderbilt Cardiology Fellow, and CardioNerds Academy Faculty Dr. Breanna Hansen, and then by expert faculty Dr. Anu Lala.Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is Deputy Editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program's leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #23 Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea.   At home, she takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily.   On admission, her exam revealed a blood pressure of 111/79 mmHg, HR 80 bpm, and SpO2 94%. Her cardiovascular exam was significant for a regular rate and rhythm with an audible S3, JVD to 13 cm H2O, bilateral lower extremity pitting edema with warm extremities and 2+ pulses throughout.  What initial dose of diuretics would you give her? A Continue home Furosemide 40 mg PO B Start Metolazone 5 mg PO C Start Lasix 100 mg IV D Start Spironolactone Answer #23 Explanation The correct answer is C – start Furosemide 100 mg IV. This is the most appropriate choice because patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to improve symptoms and reduce morbidity (Class 1, LOE B-NR). Intravenous loop diuretic therapy provides the most rapid and effective treatment for signs and symptoms of congestion. Titration of diuretics has been described in multiple recent trials of patients hospitalized with HF, often initiated with at least 2 times the daily home diuretic dose (mg to mg) administered intravenously. Titration to achieve effective diuresis may require doubling of initial doses, adding a thiazide diuretic, or adding an MRA that has diuretic effects in addition to its cardiovascular benefits. Choice A is incorrect as continuing oral loop diuretics is not recommended for acute decongestion. Moreover, Ms. Hart has become congested despite her home, oral diuretic regimen. Choice B and D are incorrect as starting a thiazide diuretic or a mineralocorticoid receptor antagonist are not first-line therapy for acute HF. Rather, in patients hospitalized with HF when diuresis is inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: a.

The following question refers to Section 4.7 and Table 18 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Student Dr. Shivani Reddy, answered first by Fellow at Johns Hopkins Dr. Rick Ferraro, and then by expert faculty Dr. Roger Blumenthal.Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. Dr. Blumenthal has also been an incredible mentor to CardioNerds from our earliest days.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #28 Mr. A. C. is a 78-year-old gentleman with a long-standing history of HTN receiving antihypertensive medications & dietary management for blood pressure control. What is the target diastolic blood pressure recommendation for all treated patients such as Mr. A.C.?A< 80 mmHgB< 90 mmHgC< 70 mmHgD< 95 mmHgE< 100 mmHg Answer #28 Explanation The correct answer is A: DBP < 80 mmHg Blood pressure treatment targets: when drug treatment is used, the aim is to control BP to target within 3 months. Blood pressure treatment targets in the 2021 ESC Prevention guidelines are more aggressive than previously recommended, as evidence now suggests the previously recommended targets were too conservative, especially for older patients. The magnitude of BP lowering is the most important driver of benefit. ·       It is recommended that the first objective of treatment is to lower BP to