Podcasts about Clopidogrel

In this podcast, Dr. David Kao discusses the AJHP Descriptive Report, “Implementation of clopidogrel pharmacogenetic clinical decision support for a preemptive return of results program,” with host and AJHP Editor in Chief Dr. Daniel Cobaugh. The information presented during the podcast reflects solely the opinions of the presenter. The information and materials are not, and are not intended as, a comprehensive source of drug information on this topic. The contents of the podcast have not been reviewed by ASHP, and should neither be interpreted as the official policies of ASHP, nor an endorsement of any product(s), nor should they be considered as a substitute for the professional judgment of the pharmacist or physician.

N Engl J Med 2010;363:930-942Background By 2010, dual antiplatelet therapy had been established as beneficial during and after percutaneous coronary intervention for acute coronary syndromes. Optimal dosing however remained unknown. This included the best loading dose of clopidogrel and optimal dose of aspirin.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 Clopidogrel and Aspirin Optimal Dose Usage to Reduce Recurrent Events−Seventh Organization to Assess Strategies in Ischemic Syndromes (CURRENT–OASIS 7) trial was designed to determine whether a doubling of the loading and initial maintenance doses of clopidogrel is superior to the standard-dose regimen and whether higher-dose aspirin (300 to 325 mg daily) is superior to lower-dose aspirin (75 to 100 mg daily) in patients with acute coronary syndromes referred for an early invasive strategy.Patients Adult patients who presented with a non-ST-segment elevation acute coronary syndrome (ACS) or an ST-segment elevation myocardial infarction. Patients had to have had coronary angiography with a plan to perform PCI within 72 hours. Major exclusion criteria were an increased risk of bleeding or active bleeding and a known allergy to clopidogrel or aspirin. Baseline Characteristics Nearly all patients had angiography. About 68% had PCI and 32% did not have PCI due to lack of significant (≤70%) stenosis. About a quarter of patients had coronary-artery bypass surgery. The average age of patients was 61 years; 27% female sex, and 70% had a diagnosis of unstable angina or NSTEMI. The median time to randomization in patients with unstable angina/NSTEMI was 3.4 days vs 0.6 days in patients with STEMI. About 60% of patients were white, and 22% were Asian. The co-existing cardiac risk factors, such as smoking, hypertension, diabetes and previous MI were similar in all the trial arms, and typical of most trials at the time.Procedures The CURRENT-OASIS 7 trial had 2x2 factorial design. First, comparing in a double-blind fashion, a double dose vs standard dose clopidogrel regimen. In the second component, patients were randomly assigned in an open-labeled fashion to higher- or lower-dose aspirin.Immediately after randomization and before coronary angiography, patients randomly assigned to double-dose clopidogrel received a loading dose of 600 mg on day 1, followed by 150 mg once daily on days 2 through 7. Patients assigned to standard-dose clopidogrel received a 300-mg loading dose on day 1 before angiography, followed by 75 mg once daily on days 2 through 7. On days 8 through 30, both the double-dose and standard-dose groups received 75 mg of clopidogrel once daily.Patients randomly assigned to lower-dose aspirin received 75 to 100 mg daily on days 2 through 30, and those randomly assigned to higher-dose aspirin received 300 to 325 mg daily on days 2 through 30. An initial loading dose of aspirin 300 mg was used in both arms on day 1. Other therapies, such as anti-thrombotics were left to the discretion of the treating doctors. Endpoints The primary endpoint was cardiovascular death, myocardial infarction, or stroke at 30 days. The sample-size calculation estimated an event rate of 11% at 30 days with standard-dose clopidogrel or lower-dose aspirin. That would have led to 14,000 patients to have 90% power to detect a 16% reduction in the primary endpoint. Lower-than expected event rates required an increase in sample size to 25,000 patients. This allowed for an 80% power to detect a 16% reduction in the primary endpoint.Results  A primary outcome event occurred in 4.2% of patients in the double-dose clopidogrel group at 30 days, as compared with 4.4% in the standard-dose group (hazard ratio, 0.94, 95% confidence interval [CI], 0.83 to 1.06; P=0.30). The rate of death from any cause did not differ significantly between the double-dose and standard-dose groups (2.3% and 2.4%, respectively; hazard ratio with the double dose, 0.96; 95% CI, 0.82 to 1.13; P=0.61). Major bleeding occurred more often in the double-dose arm (2.5 vs 2.0% HR 1.24; 95% CI 1.05-1.46).For the aspirin comparison, the rate of primary outcome events did not differ: 4.2% in the higher-dose arm vs 4.4% in the lower-dose arm. Death from any cause was not statistically different in either arm. Major bleeding rates were also similar in the two aspirin arms (2.3% in both arms).The authors described a “nominally significant” interaction between clopidogrel dose and aspirin dose for the primary outcome. Among patients assigned to higher-dose aspirin, the primary outcome occurred in 3.8% of patients in the double-dose clopidogrel group, as compared with 4.6% of patients in the standard-dose clopidogrel group (hazard ratio, 0.82; 95% CI, 0.69 to 0.98; P=0.03). But in the lower dose aspirin group, there were no significant differences in the primary outcome between double-dose and standard-dose clopidogrel (4.5% vs 4.2% HR 1.07 95% CI 0.90-1.26, respectively). The p-value for the interaction here was 0.04. Subgroup analyses showed generally consistent results. One possible heterogenous treatment effect in the double- vs standard-dose clopidogrel comparison turned on whether the patient had PCI or did not have PCI. In the 68% (≈17,000) of patients who had PCI, double dose clopidogrel reduced the primary outcome by 15% (3.9% vs 4.5%) vs increasing it by 14% in the no PCI group (4.9% vs 4.3%). The p-value for interaction was 0.03. There were no indications of heterogenous treatment effects depending on aspirin.Conclusions In patients with ACS, double dose clopidogrel or aspirin compared to standard dose did not significantly reduce the composite endpoint of cardiovascular death, MI or stroke. Double dose clopidogrel did increase major bleeding with a NNH of approximately 200 patients. Treatment effect heterogeneity, favoring the double dose clopidogrel strategy, was suggested for patients undergoing PCI.This trial serves as a good example of the limitations of surrogate endpoints in predicting hard outcomes. Previous studies had demonstrated that higher doses of clopidogrel led to faster and more substantial platelets inhibition. The observed increase in bleeding events with double-dose clopidogrel supported these findings. Nonetheless, it did not correspond to better ischemic outcomes.As for the dose of aspirin, there was no added benefit (or increase in bleeding) with higher dose aspirin beyond 75-100 mg. 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 2012;367:1297-1309Background: In patients with acute coronary syndrome, clinical guidelines recommend early angiography particularly in those deemed moderate to high risk. However, a proportion of patients do not undergo revascularization, and these patients have poorer outcomes compared to those who do undergo revascularization.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 TRITON-TIMI 38 trial demonstrated that prasugrel, when compared to clopidogrel, reduces ischemic events in patients with acute coronary syndrome undergoing percutaneous coronary intervention (PCI). Notably, in the TRITON-TIMI 38 trial, 99% of the patients underwent PCI at the time of randomization.Expanding upon the findings of TRITON-TIMI 38, the TRILOGY ACS trial sought to test the hypothesis that aspirin plus prasugrel is superior to aspirin plus clopidogrel in patients with acute coronary syndrome, without ST segment elevation, who are managed medically without revascularization.Patients: Patients were enrolled if they had unstable angina or non-ST elevation myocardial infarction and were treated medically without revascularization, within 10 days of the index event. Patients with non-ST elevation myocardial infarction had elevated cardiac biomarkers. Patients with unstable angina had ST-segment depression of more than 1 mm in two or more electrocardiographic leads and negative cardiac biomarkers. Patients had to have one of the following: age of 60 years or older, diabetes mellitus, prior myocardial infarction or prior revascularization with either PCI or coronary-artery bypass grafting (CABG). Main exclusion criteria were history of stroke or TIA (this group had net harm with prasugrel in TRITON-TIMI 38), renal failure requiring dialysis and patients taking oral anticoagulants.Baseline characteristics: The trial enrolled 9,326 patients at 966 sites in 52 countries. The average age of patients was 66 years, with 78% were below 75 years old, and 61% were men. About 70% of the patients had non-ST elevation myocardial infraction as their index event. The average GRACE score was 122. About 82% had hypertension, 59% had hyperlipidemia, 38% had diabetes, 43% had prior myocardial infarction and 20% were current or recent smokers. The majority of patients were stable, with 88% classified as Killip class I.Angiography before randomization was performed in 41% of the patients. Medications at randomization included beta-blockers in 78% of the patients, ACEi or ARB in 75%, statins in 83% and proton pump inhibitors in 25%.Procedures: The trial was conducted as double-blind double-dummy study. Patients who underwent randomization within 72 hours after the first medical contact received a loading dose of 30mg of prasugrel followed by 10mg daily. The maintenance dose of prasugrel was 5mg daily for patients aged 75 years or older or patients who weighed less than 60 kg. Patients who underwent randomization after 72 hours of the first medical contact received open label clopidogrel before randomization and the maintenance study drug after randomization. Clopidogrel was given as a loading dose of 300mg followed by a maintenance dose of 75mg daily. Aspirin was given in all patients and the recommended dose was 100mg per day or less. Study drugs were given for a minimum of 6 months and a maximum of 30 months.Endpoints: The primary efficacy endpoint was a composite of death from cardiovascular causes, nonfatal myocardial infarction or nonfatal stroke among patients < 75 years old. Safety endpoints were bleeding not related to CABG based on Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) criteria for severe or life-threatening bleeding and Thrombolysis in Myocardial Infarction (TIMI) criteria for major bleeding, and neoplasms.Analysis was performed based on the intention-to-treat principle. The trial was event-driven. To ensure 90% power to detect 22% relative risk reduction of prasugrel over clopidogrel with a two-sided alpha of 5%, a total of 688 patients,

Commentary by Dr. Valentin Fuster

Note to readers: Since going live with Cardiology Trials Substack in January of 2024 we have been exclusively covering trials that we have categorized as belonging to the major subject heading “Acute Coronary Syndrome” belonging to the subsection “Medicines”. Our indexing scheme was described in one of our original posts and we encourage our audience to read it if you have not already. This is pertinent because the next several trials being presented may seem to come out of the blue but we assure you there is a method.N Engl J Med 2007;357:2011-15.Background Up to now we have presented trials involving major foundational medical therapies for acute coronary syndrome which include aspirin, thrombolytic agents and anticoagulation, but not those involving percutaneous coronary intervention (PCI) as they are reserved for another section. But, by the turn of the 21st century, PCI had become the dominant up-front strategy for revascularization in many countries around the world. Clinical trials demonstrated it improved outcomes, the main one being re-infarction, compared to thrombolysis in patients with STEMIs, and there was an evolving evidence for it in non-ST-segment elevation acute coronary syndrome (STEACS) as well, where thrombolysis had not demonstrated any significant benefits.As PCI became dominant, antithrombotic strategies for optimizing outcomes following PCI evolved along with it. These early trials generally involved a mixture of patient phenotypes (acute vs elective PCI) and were relatively small and of limited quality by comparison to many of the seminal trials presented thus far. Instead of presenting each of these smaller studies, we direct readers to a narrative review that nicely describes the evolution of dual-antiplatelet therapy for PCI and other indications.Briefly: dual-antiplatelet therapy with aspirin and ticlopidine, an antiplatelet agent belonging to the drug class of thienopyridines, which inhibits platelet aggregation induced by ADP, was found superior to aspirin alone or aspirin plus anticoagulation when PCI was performed; however, there were concerns about its safety. Clopidogrel was developed after ticlopidine; it had a similar mechanism of action but less safety concerns and could be given as a loading dose to produce more rapid effects. Despite limited evidence from clinical trials comparing it head-to-head with ticlopidine it became the dominant thienopyridine agent on the market and still has a prominent role in the management of cardiovascular diseases today.Following PCI and dual-antiplatelet therapy with aspirin and clopidogrel, patients continue to have an elevated risk of coronary events, in general, and in-stent related coronary events, in particular. Some of this risk has been attributed to limitations of clopidogrel itself. Clopidogrel has modest antiplatelet effects (compared to other thienopyridines) with substantial interpatient variability due to genetic polymorphisms that impact clopidogrel metabolism and antiplatelet efficacy. Clopidogrel also has a delayed onset of action, which is especially relevant regarding its ability to protect against the dreaded adverse event of early in-stent thrombosis.Prasugrel is a thienopyridine—developed after clopidogrel—that inhibits platelet aggregation more rapidly, consistently and to a greater extent. The Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel–Thrombolysis in Myocardial Infarction (TRITON–TIMI) 38 trial sought to test the hypothesis that prasugrel would reduce major cardiovascular events compared to clopidogrel in patients with acute coronary syndrome undergoing PCI.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 had either moderate-to-high risk unstable angina (UA) or NSTEMI or STEMI. UA and NSTEMI were defined by ischemic symptoms lasting 10 minutes or more and occurring within 72 hours before randomization, a TIMI risk score of 3 or more, and either ST-segment deviation of 1 mm or more or elevated levels of a cardiac biomarker of necrosis. STEMI was traditionally defined. Key exclusion criteria included an increased risk of bleeding, anemia, thrombocytopenia, a history of pathologic intracranial findings, or the use of any thienopyridine within 5 days before enrollment.Baseline characteristics The median age of patients was 61 years with 13% being ≥75 years and 74% were men; over 90% were white. The index event was UA or NSTEMI in 74% and STEMI in 26%.  PCI was performed in 99% of patients and split evenly between those receiving bare metal or drug eluting stent(s).  18% of patients had a prior MI, 23% had diabetes, 64% had hypertension and 38% were tobacco users. Only 11% of patients had CKD defined as a creatinine clearance ≤60 ml/min.Procedures A loading dose of prasugrel 60 mg or clopidogrel 300 mg was given in a double blind manner anytime between randomization up to 1 hour after leaving the catheterization laboratory. In order to be randomized, the plan for PCI had to be known. This could occur before going to the cath lab for planned PCI, if the anatomy was already known or occur in the cath lab during the case where anatomy was determined and PCI was performed. If PCI was planned, patients were eligible to undergo pretreatment with the study drug for up to 24 hours prior to PCI.Treating physicians determined the vessels treated, devices used, and adjunctive medication administered to support PCI. After PCI, patients received maintenance doses of either prasugrel 10 mg daily or clopidogrel 75 mg daily. Use of aspirin at a dose of 75 to 162 mg daily was recommended. Study visits were conducted at hospital discharge, 30 days, 90 days, and 3-month intervals thereafter, for a total of 6 to 15 months.Endpoints The primary efficacy endpoint was a composite of cardiovascular death, nonfatal MI or stroke during the follow up period. A prespecified “landmark” analysis was undertaken to compare the primary endpoint event rate up to 3 days following randomization and from day 3 to the end of the study. The sample size calculation was event-driven and it was determined that 875 primary endpoint events would provide 90% power to detect a relative risk reduction of 20%. A prespecified analysis performed after 650 events revealed a lower than anticipated event rate and the investigators increased the sample size accordingly.Results A total of 13,608 patients (10,074 with UA or NSTEMI and 3534 with STEMI), from 707 sites in 30 countries were enrolled. There were 6,813 patients assigned to the prasugrel group and 6,795 assigned to clopidogrel. The median duration of therapy was 14.5 months. Prasugrel significantly reduced the primary composite endpoint compared to clopidogrel (9.9% vs 12.1%; HR 0.81; 95% CI 0.73-0.90; P

N Engl J Med 2001;345:494-502.Background The established medical treatments for acute coronary syndrome reviewed so far include aspirin and thrombolytics along with a smaller role for short-term anticoagulation. Angiotensin converting enzymes inhibitors and, to a lesser extent, beta blockers were also found to reduce recurrent ischemic events and death as well as heart failure and ventricular remodeling. The EPHESUS trial, which studied Eplerenone in this patient population was not published until several years later.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Despite the benefits of the above therapies, patients who experienced an ACS event were still at a substantially higher risk for experiencing recurrent events compared to patients who never experienced an ACS event. Significant interest remained in finding additional agents to reduce “residual risk” (i.e., the risk of recurrent events that is left over after initiating effective therapies). Imagine a heart attack survivor has a 20% risk of experiencing death, non-fatal MI or heart failure over the next 5 years. Now imagine that all known effective therapies cumulatively reduce that risk by 30% (a 6% absolute reduction in risk); the residual risk for events over 5 years would still be 14%, which is still high, and significantly higher than patients who never experienced an ACS event (e.g., primary prevention patients).Thienopyridine derivatives, including clopidogrel, are antiplatelet agents with a different mechanism of action than aspirin. Up to this point in time they demonstrated efficacy in patients who had received a coronary stent for reducing myocardial infarction compared to either aspirin alone or warfarin. The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial sought to test the hypothesis that 3 to 12 months of clopidogrel plus aspirin versus aspirin alone would reduce the rate of cardiovascular events (a composite endpoint) compared to aspirin alone in patients with ACS and no ST-segment elevation.Patients Patients were eligible if they had been hospitalized within 24 hours after the onset of symptoms, who had either ECG changes or an elevation in cardiac enzymes at entry, and did not have ST-segment elevation. Exclusion criteria included a contraindication to antithrombotic or antiplatelet therapy, high bleeding risk or severe heart failure, those who were taking oral anticoagulants, and those who had undergone coronary revascularization in the previous 3 months or had received intravenous glycoprotein IIb/IIIa receptor inhibitors in the previous 3 days.Baseline characteristics No information in the main manuscript is provided on the ratio of patients eligible to those enrolled, which limits our ability to make inferences about external validity. The average age of participants was 64 years of age and nearly 40% were woman, which is historically higher than the trials reviewed up to this point. The average time from pain onset to randomization was 14 hours. The diagnoses at study entry were unstable angina in 75% and MI in 25%. Many patients in the trial has a history of MI (32%) or revascularization (18%) in the past and the majority were either current or former smokers (61%). Most patients (94%) had some ECG abnormality; the most common being ST depression (42%) and T-wave inversion (36%).Procedures Immediately following randomization patients were administered a 300 mg loading dose of clopidogrel or matching placebo followed by 75 mg per day of clopidogrel or matching placebo for 3 to 12 months (the mean duration of treatment was 9 months). Aspirin was started or continued simultaneously with the study drug or placebo. Follow-up assessments occurred at discharge, at 1 and 3 months, and then every 3 months until the end of the study (12 months).Endpoints The first primary endpoint was the composite of death from cardiovascular causes (death for which there was no clearly documented nonvascular cause), nonfatal MI (which required at least 2 of 3 findings: ischemic chest pain, elevation of cardiac markers or ECG changes consistent with MI) or stroke (new focal neurological deficit of vascular origin lasting >24 hr and was subdivided into intracranial hemorrhage, ischemia, or uncertain cause) at 12 months. The second primary endpoint was the composite of the first primary endpoint or refractory ischemia. Secondary outcomes included severe ischemia, heart failure, and the need for revascularization. Safety related outcomes included life-threatening, major bleeding (requiring transfusion of ≥2 units of blood) or all other bleeding.The study was initially designed to include 9000 patients, with an anticipated primary event rate of 12-14% in the placebo group; however, because the event rate was lower than anticipated, the size of the study was increased as the trial was ongoing, with an adjusted rate of 10% in the placebo group. A final sample size of 12,500 patients was based on an anticipated 17% risk reduction for the primary composite endpoint with 90% power and a two-sided alpha level of 0.045.Results 12,562 patients were included in the final analysis; 6,303 in the placebo group and 6,259 in the clopidogrel group. During the initial hospital stay, 21% of patients in the clopidogrel group and 23% of patients in the placebo group underwent revascularization. At 1-year clopidogrel significantly reduced the occurrence of the first primary composite endpoint (RR 0.80; 9.3% vs 11.4%; 95% CI 0.72-0.90) and second primary composite endpoint (RR 0.86; 16.5% vs 18.8%; 95% CI 0.79-0.94). These differences were driven primarily by reducing nonfatal MI (RR 0.77; 5.2% vs 6.7%; 95% CI 0.0.67-0.89). There were no significant differences in death from cardiovascular or non-cardiovascular causes, stroke or refractory ischemia.Compared to placebo, clopidogrel significantly increased major bleeding (RR 1.38; 3.7% vs 2.7%; 95% CI 1.13-1.67). However, there was no significant excess of major bleeding in patients undergoing CABG surgery (RR 1.48; 1.3% vs 1.1%; 95% CI 0.93-1.71). The median time for clopidogrel discontinuation before CABG surgery was 5 days.Results from various subgroups are presented for the first primary composite endpoint and suggest the possibility of important treatment effect heterogeneity. Patients with a history of revascularization represented a minority of patients in the study (18%) and experienced higher rates of events but derived a significantly greater benefit from clopidogrel compared to those not previously revascularized (RR 0.58 vs 0.89).Patients >65 years of age made up about half of study participants, and experienced event rates >2x higher than those ≤65 years of age, but derived less benefit from clopidogrel (RR 0.87 vs 0.71). The same was true based on risk tertiles. Patients at low and intermediate risk of experiencing events based on risk scores, experienced similar risk reductions from clopidogrel of 76% and 69% respectively; however, those at the highest risk received less benefit (RR 91%). Finally, women appeared to benefit less than men (RR 89% vs 76%).Notably, there was no evidence of treatment effect heterogeneity based on whether patients underwent revascularization or not following randomization.During the trial, clopidogrel was discontinued temporarily (≥5 days) in 46% of patients mainly due to the need for a surgical procedure. A total of 21% of patients discontinued clopidogrel permanently compared to 18% in the placebo group.Conclusions In patients admitted to the hospital for unstable angina or NSTEMI, clopidogrel for 3-12 months plus aspirin, reduced the rate of a composite primary endpoint compared to aspirin alone and was associated with a number needed to treat of approximately 50 patients. This benefit was driven almost entirely by reducing nonfatal MI. Clopidogrel increased major bleeding with an NNH of approximately 100 patients.In our opinion, the benefit conferred by clopidogrel in this patient population is modest and the external validity is uncertain as no information is provided on patients enrolled compared to those who were eligible/screened. Patients with prior histories of revascularization derived the greatest benefit; however, several higher risk subgroups including older patients (>65 years of age) and the third of patients who were at the highest risk of experiencing events derived significantly less benefit. Women, also derived less benefit. In the groups less likely to benefit, we would expect them to experience higher rates of adverse events as well and thus, it is possible they derive no net benefit from clopidogrel or could even experience net harm.While thienopyridines have come to be considered a foundational treatment for ACS, evidence of their benefit from the CURE trial is modest at best; based mainly on reduction of a nonfatal endpoint.The CURE trial results should be translated cautiously, especially for patients who are older, frail and more susceptible to adverse events.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

Welcome to the Transatlantic series, a co-production of Audible Bleeding (a publication of the SVS) and the ESVS podcast. In today's episode, we explore the intersocietal guidelines on peripheral arterial disease in patients with diabetes and foot ulcers authored by the International Working Group on the Diabetic Foot (IWGDF), the European Society for Vascular Surgery (ESVS), and the Society for Vascular Surgery (SVS).   Dr. Robert Fitridge is a Professor of Vascular Surgery at University of Adelaide in Australia. He is a member of the IWGDF and is also a member of the steering committee for the Global Vascular Guideline on the management of Chronic Limb-threatening Ischaemia.    Dr. Vivienne Chuter is a Professor in the Department of Podiatry at Western Sydney University and Honorary Professor in the School of Health Science at The University of NewCastle. She is a member of the IWGDF. She has published extensively on diabetic foot disease and leads a clinically based research program focusing on the prevention and management of diabetes-related foot disease for Aboriginal and Torres Strait Islander people and for non-Indigenous Australians.   Dr. Nicolaas Schaper is an emeritus professor of Endocrinology at Maastricht University Hospital in the Netherlands. Dr. Schaper was the coordinator of the European diabetic foot research consortium, Eurodiale. He is Chair of the 2023 Diabetic Foot Symposium (ISDF 2023) and is Chair of the IWGDF.   Dr. Joseph L. Mills is a Professor of Vascular Surgery at Baylor in Houston, Texas. He is a member of the IWGDF. Dr. Mills is a leader in the vascular surgery global community, has served as president of the Peripheral Vascular Surgery Society, and is currently a member of the Surgery Residency Review Committee of the ACGME.   Further reading and links:   The intersocietal IWGDF, ESVS, SVS guidelines on peripheral artery disease in people with diabetes mellitus and a foot ulcer. Global vascular guidelines for CLTI Best-CLI Engaging patients and caregivers to establish priorities for the management of diabetic foot ulcers A systematic review of multidisciplinary teams to reduce major amputations for patients with diabetic foot ulcers A vein bypass first versus a best endovascular treatment first revascularisation strategy for patients with chronic limb threatening ischaemia who required an infra-popliteal, with or without an additional more proximal infra-inguinal revascularisation procedure to restore limb perfusion (BASIL-2): an open-label, randomised, multicentre, phase 3 trial Release of the National Scheme's Aboriginal and Torres Strait Islander Health and Cultural Safety Strategy 2020-2025; the impacts for podiatry in Australia: a commentary Editor's Choice - European Society for Vascular Surgery (ESVS) 2023 Clinical Practice Guidelines on Antithrombotic Therapy for Vascular Diseases Results of the CAPRIE trial: efficacy and safety of clopidogrel. Clopidogrel versus aspirin in patients at risk of ischaemic events Low-Dose Aspirin for the Primary Prevention of Cardiovascular Disease in Diabetic Individuals: A Meta-Analysis of Randomized Control Trials and Trial Sequential Analysis Diabetes, Lower-Extremity Amputation, and Death Outcomes in patients with chronic leg wounds in Denmark: A nationwide register‐based cohort study Pedal arch patency and not direct-angiosome revascularization predicts outcomes of endovascular interventions in diabetic patients with critical limb ischemia Effectiveness of bedside investigations to diagnose peripheral artery disease among people with diabetes mellitus: A systematic review.  Performance of non-invasive bedside vascular testing in the prediction of wound healing or amputation among people with foot ulcers in diabetes: A systematic review. Effectiveness of revascularisation for the ulcerated foot in patients with diabetes and peripheral artery disease: A systematic review. The Society for Vascular Surgery Lower Extremity Threatened Limb Classification System: Risk stratification based on Wound, Ischemia, and foot Infection (WIfI). Surgery or Endovascular Therapy for Chronic Limb-Threatening Ischemia. A vein bypass first versus a best endovascular treatment first revascularisation strategy for patients with chronic limb threatening ischaemia who required an infra-popliteal, with or without an additional more proximal infra-inguinal revascularisation procedure to restore limb perfusion (BASIL-2): an open-label, randomised, multicentre, phase 3 trial.   Mobile Applications:   Society for Vascular Surgery Mobile App for Staging of Chronic Limb-Threatening Ischemia.  European Society for Vascular Surgery Clinical Practice Guidelines Mobile Edition.   Hosts:    Dr. Naveed A. Rahman is a chief surgery resident at SUNY Upstate in Syracuse, NY. He will pursue a vascular surgery fellowship at the University of Maryland starting in 2024. His Doximity profile is https://www.doximity.com/pub/naveed-rahman-md. Twitter: @naveedrahmanmd Dr. Suzanne Stokmans is a fifth-year vascular surgery resident at the Isala Hospital in Zwolle, the Netherlands. Dr. Ezra Schwartz is a medical graduate from McGill University currently completing a Master of Medical Science in Medical Education at Harvard Medical School. He is an aspiring vascular surgeon and surgical education researcher. Twitter: @ezraschwartz10   Follow us @audiblebleeding Learn more about us at https://www.audiblebleeding.com/about-1/ and provide us with your feedback with our listener survey.

Welcome to the Transatlantic Series, a co-production of Audible Bleeding (a publication of the SVS) and the ESVS podcast. In today's episode, we explore the intersocietal guidelines on peripheral arterial disease in patients with diabetes and foot ulcers authored by the International Working Group on the Diabetic Foot, the European Society for Vascular Surgery, and the Society for Vascular Surgery.Dr. Robert Fitridge is a Professor of Vascular Surgery at University of Adelaide in Australia. He is a member of the IWGDF and a member of the steering committee for the Global Vascular Guideline on the management of Chronic Limb-threatening Ischaemia. Dr. Vivienne Chuter is a Professor in the Department of Podiatry at Western Sydney University and Honarary Professor in the School of Health SCiences at The University of NewCastle. She is a member of the IWGDF. She has published extensively on diabetic foot disease and leads a clinically based research program focusing on prevention and management of diabetes-related foot disease for Aboriginal and Torres Strait Islander people and for non-Indigenous Australians.Dr. Nicolaas Schaper is emeritus professor of Endocrinology at Maastricht University Hospital in the Netherlands. Dr. Schaper was coordinator of the European diabetic foot research consortium, Eurodiale. He is Chair of the 2023 Diabetic Foot Symposium and is Chair of the IWGDF.Dr. Joseph L. Mills is a Professor of Vascular Surgery at Baylor in Houston, Texas. He is a member of the IWGDF. Dr. Mills is a leader in the vascular surgery global community, has served as president of the Peripheral Vascular Surgery Society and is currently a member of the Surgery Residency Review Committee of the ACGME.Further reading:The intersocietal IWGDF, ESVS, SVS guidelines on peripheral artery disease in people with diabetes mellitus and a foot ulcer.Global vascular guidelines for CLTIBest-CLIEngaging patients and caregivers to establish priorities for the management of diabetic foot ulcersA systematic review of multidisciplinary teams to reduce major amputations for patients with diabetic foot ulcersA vein bypass first versus a best endovascular treatment first revascularisation strategy for patients with chronic limb threatening ischaemia who required an infra-popliteal, with or without an additional more proximal infra-inguinal revascularisation procedure to restore limb perfusion (BASIL-2): an open-label, randomised, multicentre, phase 3 trialRelease of the National Scheme's Aboriginal and Torres Strait Islander Health and Cultural Safety Strategy 2020-2025; the impacts for podiatry in Australia: a commentaryESVS 2023 Clinical Practice Guidelines on Antithrombotic Therapy for Vascular DiseasesResults of the CAPRIE trial: efficacy and safety of clopidogrel. Clopidogrel versus aspirin in patients at risk of ischaemic eventsLow-Dose Aspirin for the Primary Prevention of Cardiovascular Disease in Diabetic Individuals: A Meta-Analysis of Randomized Control Trials and Trial Sequential Analysis*Diabetes, Lower-Extremity Amputation, and DeathHosts: Dr. Naveed A. Rahman is chief surgery resident at SUNY Upstate in Syracuse, NY. He will be pursuing vascular surgery fellowship at University of Maryland starting in 2024. His Doximity profile is www.doximity.com/pub/naveed-rahman-md. X: @naveedrahmanmdDr. Suzanne Stokmans is a 5th year vascular surgery resident in the Isala hospital in Zwolle, the Netherlands.Dr. Ezra Schwartz is a medical graduate from McGill University currently completing a Masters of Medical Science in Medical Eduation at Harvard Medical School. He is an aspiring vascular surgeon and surgical education researcher. X: @ezraschwartz10

Lancet 2005;366:1622-32Background Beta blockers were routinely used for the early management of patients with AMI; however, their efficacy and safety remained uncertain in this clinical scenario. Recall that in the BHAT trial, propranolol reduced death 2 years following an AMI with an NNT of approximately 33 but the cohort was highly selected, the drug was started, on average, 14 days following admission and those over the age of 70 were excluded. ISIS-1 found that atenolol reduced death with an NNT of approximately 100 when started immediately in lower risk AMI patients but treatment effect heterogeneity was observed in patient subgroups with higher risk features. The ClOpidogrel and Metoprolol Infarction Trial (COMMIT) sought to test the hypothesis that early beta-blockade with metoprolol would reduce cardiac events and death in a broad population of patients with 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.Patients Patients with suspected myocardial infarction, who presented with ST elevation, left-bundle branch block, or ST depression within 24 hours of symptom onset were eligible. Patient eligibility was ultimately determined by the responsible physician but protocol guidance suggested the following relative contraindications: persistently low blood pressure (SBP

Impact: SAPT 1 year after PCI

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021.Originally released: Jan 18, 2018When it comes to stroke, treatment is dependent on the stroke mechanism. But most patients wind up on aspirin anyway. Or Plavix (clopidogrel). And sometimes both. The question this week is, Why? I hope you're hungry for some fruit because we're comparing a bunch of apples to oranges in this episode of the BrainWaves podcast.Produced by James E Siegler. Music by William Ross Chernoff's Nomads, Steve Combs, Rui, Little Glass Men, and Peter Rudenko. Voiceover by Erika Mejia. BrainWaves' podcasts and online content are intended for medical education only and should not be used for routine clinical decision-making. Even if this episode is all about choosing aspirin or clopidogrel when you're treating stroke patients. Always talk with your doctor, and if you are a doctor, you should rely on institutional policies and your own clinical judgment when treating patients.REFERENCESAntithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324(7329):71-86. Erratum in: BMJ 2002;324(7330):141. PMID 11786451Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med 2006;354(16):1706-17. PMID 16531616CAST: randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke. CAST (Chinese Acute Stroke Trial) Collaborative Group. Lancet 1997;349(9066):1641-9. PMID 9186381Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration. BMJ 1994;308(6921):81-106. Erratum in: BMJ 1994;308(6943):1540. PMID 8298418CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet 1996;348(9038):1329-39. PMID 8918275Diener HC, Bogousslavsky J, Brass LM, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet 2004;364(9431):331-7. PMID 15276392Hong KS, Lee SH, Kim EG, et al. Recurrent ischemic lesions after acute atherothrombotic stroke: clopidogrel plus aspirin versus aspirin alone. Stroke 2016;47(9):2323-30. PMID 27418597Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44(3):870-947. PMID 23370205Kennedy J, Hill MD, Ryckborst KJ, et al. Fast assessment of stroke and transient ischaemic attack to prevent early recurrence (FASTER): a randomised controlled pilot trial. Lancet Neurol 2007;6(11):961-9.

GLP-1s and BaroStim Neo revisited, a new drug for transthyretin amyloid CM, clopidogrel vs ASA years after PCI and stent, and statins are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. GLP-1s and Obesity, BaroStim Neo Revisited FDA Expands Label for CVRx Barostim System in HF https://www.medscape.com/viewarticle/fda-expands-label-cvrx-barostim-system-hf-2023a1000wsx JAMA Cardiology Special Communication – BDP https://jamanetwork.com/journals/jamacardiology/fullarticle/2810726 II. ATTR Cardiomyopathy ATTRibute-CM NEJM paper https://www.nejm.org/doi/full/10.1056/NEJMoa2305434 Circulation Review of TTR https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.111.078915 ATTR-ACT (Tafadimis) https://www.nejm.org/doi/10.1056/NEJMoa1805689 III. Clopidogrel vs ASA Years After PCI Long-term Clopidogrel Has Advantages After Coronary Stenting https://www.medscape.com/viewarticle/long-term-clopidogrel-has-advantages-after-coronary-stenting-2024a10000c8 Stop DAPT Original Trial STOP DAPT at 5 Years https://doi.org/10.1016/j.jacc.2023.10.013 Network Meta-analysis of P2Y12-I vs ASA https://doi.org/10.1016/j.jcin.2022.08.009 IV. Statin Use Statin Use Remains Low for At-Risk Patients https://www.medscape.com/viewarticle/999043 Annals of Internal Medicine Observational Study https://doi.org/10.7326/M23-1915 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

Commentary by Dr. Valentin Fuster

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. The episode discusses common cardiac drugs and some potential drug interactions. It covers aspirin, warfarin, clopidogrel, proton pump inhibitors, beta blockers, ACE inhibitors, digoxin, nitrates, and amiodarone. Notably, grapefruit can increase serum levels of beta blockers, calcium channel blockers, and some statins, potentially leading to toxicity. Warfarin's effects can be altered by foods high in vitamin K like leafy greens. Clopidogrel's effectiveness may be reduced when taken with proton pump inhibitors like omeprazole. Combining nitrates with phosphodiesterase inhibitors like sildenafil can cause profound blood pressure drops. The host recommends being aware of possible drug interactions and maintaining regular communication with doctors.

Join us as we review recent articles and news featured in The DIGEST #45 and #46, including semaglutide in HFpEF and obesity (STEP HFpEF), TCAs for irritable bowel syndrome (ATLANTIS), clopidogrel versus aspirin as long-term secondary prevention after PCI (HOST-EXAM), statins in HIV (REPRIEVE), weight changes and diet, and heavy metal exposure in cannabis users. Fill your brain hole with a delicious stack of hotcakes! Featuring Drs. Paul Williams (@PaulNWilliamz), Nora Taranto (@norataranto), and Matt Watto (@doctorwatto). Claim free CME for this episode at curbsiders.vcuhealth.org! Episodes | Subscribe | Spotify | Swag! |Mailing List | Contact | CME! Credits Written and Hosted by: Nora Taranto MD; Paul Williams, MD, FACP, Matthew Watto MD, FACP Cover Art: Matthew Watto MD, FACP Reviewers: Nora Taranto MD; Paul Williams, MD, FACP; Matthew Watto MD, FACP; Sai Achi, MD MBA Technical Production: Pod Paste Showrunners: Matthew Watto MD, FACP; Paul Williams MD, FACP Show Segments Intro, disclaimer STEP HFpEF: semaglutide for HFpEF in obesity  TCAs for IBS  HOST-EXAM and post-PCI  clopidogrel versus aspirin after DAPT  REPRIEVE and pitavastatin in HIV Starchy vegetables and weight changes  Cannabis and heavy metal content  Outro Sponsor: Uncommon Goods To get 15% off your next gift, go to uncommongoods.com/CURB Sponsor: Locumstory  Get a comprehensive view of locums and decide if it's right for you at locumstory.com.

Commentary by Dr. Candice Silversides

In the first of our special guest episodes, Professor Virginia Luis Fuentes from the Royal Veterinary College, London, joins Kieran and Jose to talk about treating cardiomyopathy in cats - beyond furosemide and clopidogrel. Listen in as Prof Luis Fuentes, a world-renowned expert and thought leader in feline heart disease, describes how she approaches a variety of treatment situations in cats, and the current thinking in human and feline medicine.

The Power of PharmacogenomicsJeff explains how pharmacogenomics, the study of how genes affect a person's response to medications, can revolutionize healthcare. By understanding a patient's genetic makeup, healthcare providers can prescribe the right medication and dosage, reducing trial and error, improving treatment effectiveness, and minimizing side effects. This approach acknowledges that each person is unique and recognizes the complex interplay of genetics and non-genetic factors to determine health outcomes. Real-World Impact of PharmacogenomicsJeff provides real-world examples of how pharmacogenomics can impact medication management. He discusses the role of the medication Clopidogrel, used with patients who are recieving a stent. He explains how genetic variations can affect the response to this medication, highlighting the importance of pharmacogenomics in ensuring effective treatment. The Future of HealthcareJeff discusses the future of healthcare, including the potential of wearable and implantable devices. He emphasizes the importance of giving healthcare professionals more tools to react in real-time and make informed decisions about patient care. He also discusses how companies like Coriell Life Sciences offer comprehensive medication management programs, highlighting the importance of scalability and accessibility in the adoption of pharmacogenomics.

"...we will take a look at how Strokes are diagnosed and then how Strokes the treated and managed the diagnosis of a stroke is and with imaging techniques being used to Aid in that diagnosis a big part of stroke diagnosis and management is the early recognition and tools such as and Razia a used Fast involves facial drooping arm weakness and speech disturbances while T is for the time indicating the need for timely action the Razia score which stands for recognition of stroke in the emergency room is similar and involves looking for any loss of consciousness or seizure activity which counts against a stroke diagnosis as well as facial arm or leg weakness speech disturbances or visual disturbances it physical exam should also be done which will cover the NIH SS school including levels of consciousness motor function sensory function language and attention generally suspected stroke patients will undergo a CT of the head without contrast as coagulated blood will appear hyper-dense on these scans however ischemia may not be seen in the early stages there for a CT scan is done more commonly to rule out further investigations may involve an MRI of the head which is more sensitive for chronic hemorrhages and areas of ischemia usually appear hyper-intense on diffusion-weighted a Doppler ultrasound of the Carotid may be done and if the stroke was suspected to be caused by an aneurysm and angiogram may also be done as well as lab investigations including lipids and coagulation screens you may have heard the expression time is brain in the early stages ischemic stroke the aim is to restore cerebral blood flow as fast as possible as this results in fewer brain cells dying according to the nice guidelines patients with non disabling stroke or t.i. a should have early carotid Imaging and Urgent in data Rekha me as well as stenting if they have carotid stenosis in patients who have an acute ischemic stroke 150 to 300 milligrams of aspirin should be given orally or rectally if the patient is dysphasic this 150 to 300 milligram should be continued for two weeks following the stroke until long-term antithrombotic treatment has been prescribed in patients with an allergy to aspirin Clopidogrel may be used and a proton pump inhibitor should be added in patients with a history of dyspepsia in cases of venous sinus thrombosis anticoagulation..." Learn more about your ad choices. Visit megaphone.fm/adchoices

"...we will take a look at how Strokes are diagnosed and then how Strokes the treated and managed the diagnosis of a stroke is and with imaging techniques being used to Aid in that diagnosis a big part of stroke diagnosis and management is the early recognition and tools such as and Razia a used Fast involves facial drooping arm weakness and speech disturbances while T is for the time indicating the need for timely action the Razia score which stands for recognition of stroke in the emergency room is similar and involves looking for any loss of consciousness or seizure activity which counts against a stroke diagnosis as well as facial arm or leg weakness speech disturbances or visual disturbances it physical exam should also be done which will cover the NIH SS school including levels of consciousness motor function sensory function language and attention generally suspected stroke patients will undergo a CT of the head without contrast as coagulated blood will appear hyper-dense on these scans however ischemia may not be seen in the early stages there for a CT scan is done more commonly to rule out further investigations may involve an MRI of the head which is more sensitive for chronic hemorrhages and areas of ischemia usually appear hyper-intense on diffusion-weighted a Doppler ultrasound of the Carotid may be done and if the stroke was suspected to be caused by an aneurysm and angiogram may also be done as well as lab investigations including lipids and coagulation screens you may have heard the expression time is brain in the early stages ischemic stroke the aim is to restore cerebral blood flow as fast as possible as this results in fewer brain cells dying according to the nice guidelines patients with non disabling stroke or t.i. a should have early carotid Imaging and Urgent in data Rekha me as well as stenting if they have carotid stenosis in patients who have an acute ischemic stroke 150 to 300 milligrams of aspirin should be given orally or rectally if the patient is dysphasic this 150 to 300 milligram should be continued for two weeks following the stroke until long-term antithrombotic treatment has been prescribed in patients with an allergy to aspirin Clopidogrel may be used and a proton pump inhibitor should be added in patients with a history of dyspepsia in cases of venous sinus thrombosis anticoagulation..." Learn more about your ad choices. Visit megaphone.fm/adchoices

"...we will take a look at how Strokes are diagnosed and then how Strokes the treated and managed the diagnosis of a stroke is and with imaging techniques being used to Aid in that diagnosis a big part of stroke diagnosis and management is the early recognition and tools such as and Razia a used Fast involves facial drooping arm weakness and speech disturbances while T is for the time indicating the need for timely action the Razia score which stands for recognition of stroke in the emergency room is similar and involves looking for any loss of consciousness or seizure activity which counts against a stroke diagnosis as well as facial arm or leg weakness speech disturbances or visual disturbances it physical exam should also be done which will cover the NIH SS school including levels of consciousness motor function sensory function language and attention generally suspected stroke patients will undergo a CT of the head without contrast as coagulated blood will appear hyper-dense on these scans however ischemia may not be seen in the early stages there for a CT scan is done more commonly to rule out further investigations may involve an MRI of the head which is more sensitive for chronic hemorrhages and areas of ischemia usually appear hyper-intense on diffusion-weighted a Doppler ultrasound of the Carotid may be done and if the stroke was suspected to be caused by an aneurysm and angiogram may also be done as well as lab investigations including lipids and coagulation screens you may have heard the expression time is brain in the early stages ischemic stroke the aim is to restore cerebral blood flow as fast as possible as this results in fewer brain cells dying according to the nice guidelines patients with non disabling stroke or t.i. a should have early carotid Imaging and Urgent in data Rekha me as well as stenting if they have carotid stenosis in patients who have an acute ischemic stroke 150 to 300 milligrams of aspirin should be given orally or rectally if the patient is dysphasic this 150 to 300 milligram should be continued for two weeks following the stroke until long-term antithrombotic treatment has been prescribed in patients with an allergy to aspirin Clopidogrel may be used and a proton pump inhibitor should be added in patients with a history of dyspepsia in cases of venous sinus thrombosis anticoagulation..." Learn more about your ad choices. Visit megaphone.fm/adchoices

EpicMedia-EP.32 Ticagrelor o prasugrel frente a clopidogrel en la ICP del síndrome coronario crónico. Dr Pablo Baglioni

Visit: https://nursing.com/140meds to request your free copy of "140 Must Know Meds" Generic Name Clopidogrel Trade Name Plavix Indication Atherosclerotic events, MI, CVA, PVD, acute coronary syndrome Action Inhibits platelet aggregation Therapeutic Class Antiplatelet agent Pharmacologic Class Platelet aggregation inhibitors Nursing Considerations • May cause GI bleeding, neutropenia, hypercholesterolemia • May increase risk for bleeding in warfarin, aspirin, heparin • Can increase risk for bleeding with garlic, ginkgo, ginger • Monitor for signs of bleeding • Monitor bleeding times • Monitor CBC and platelet count • Discontinue use 5-7 days before surgery

 In this week's View, Dr. Eagle discusses the value of the balloon pulmonary angioplasty procedure for patients with chronic thromboembolic pulmonary hypertension. He then reviews the sub analysis of the HOST EXAM trial assessing the benefit of aspirin versus clopidogrel as a maintenance strategy after coronary stenting.    Finally, Dr. Eagle explores the BIOVASC trial weighing in on immediate versus staged complete revascularization in patients presenting with acute coronary syndrome and multivessel coronary disease.    Subscribe to Eagle's Eye View  

Commentary by Dr Michael Spartalis

Title: ASA and Clopidogrel - When is it Too Much of a Good Thing? Host: Sabine von Preyss-Friedman, MD, FACP, CMD Guests: Nicole Orr, MD Recorded (in front of a live audience): March 11, 2023 Resources: Aspirin Use to Prevent Cardiovascular Disease (JAMA) ACC/AHA CV Risk Calculator  (for ages 40-79) Learn More About AMDA's Drive to Deprescribe Initiative Available Credit: The American Board of Post-Acute and Long-Term Care Medicine (ABPLM) issues CMD credits for AMDA On-The-Go and affiliate podcast episodes as follows: Claim CMD Credit

⁠DozeNews PRIME⁠: as melhores e mais didáticas revisões de cardiologia direto na sua caixa de entrada! Assine agora e tenha acesso à todo material já produzido! - ⁠https://dozeporoito.substack.com/

Commentary by Dr Davide Capodanno

A quick review on PANTHER study

Trade – PlavixClass – Antiplatelet MOA – Blocks platelet aggregation by antagonizing the IIb/IIIa receptors Indications – ACS, chronic coronary and vascular disease, ischemic stroke.Contraindications – Hx of intracranial hemorrhage, GI bleed or trauma.Side effects – Nausea, Abdominal pain, hemorrhage. Dosing : Unstable angina pectoris or non Q wave AMI.Adult – Loading dose 300-600mg POPedi – Not recommended for pedi patients

Commentary by Dr Jack Tan

ALS treatment news; Evusheld fact sheet update; an at-home epilepsy diagnostic aid gets cleared; drug recalls; and a laser therapy for fibromyalgia.

Top 5 Most Read RNS's on Vox Markets for Monday 22nd August 2022 5. Dev Clever Holdings - Funding Facility Dev Clever have obtained A Three-Year Unsecured Convertible Funding Facility With Riverfort Global Opportunities For Up To $30 Million (Click here to read the RNS) 4. Dev Clever Holdings - Annual Financial Report. Total revenue up 486% to £7.36 million (2020: £1.25 million), reflecting revenue arising from the Aldebaron agreement. Adjusted EBITDA profit was £1.30 million (2020: loss £0.79m). The loss before tax was £2.54 million (2020: £1.06 million). (Click here to read the RNS) 3. Genedrive PLC - NICE includes CYP2C19-ID Kit in new programme. Genedrive plc announces that the UK's National Institute for Health and Clinical Excellence ('NICE') has commenced an evaluation of CYP2C19 genotype testing for Clopidogrel treatment, via a new NICE Diagnostics Assessment Programme ('DAP'). Genedrive's CYP2C19 ID Kit, currently in development, has been included in the assessment. Both of genedrive's new emergency Point of Care genetic screening tests are now included in new NICE reviews, following the MT-RNR1 DAP announcement on 16 June 2022. (Click here to read the RNS) 2. Open Orphan PLC - £10.4m contract with existing Big Pharma client. Open Orphan plc (AIM: ORPH), a rapidly growing specialist contract research organisation (CRO) and world leader in testing infectious and respiratory disease products using human challenge clinical trials, announces that hVIVO, a subsidiary of Open Orphan, has signed a £10.4m contract with an existing top 5 global pharmaceutical client to manufacture a new batch of H1N1 influenza challenge virus, leveraging off an existing in-house generated challenge model, and to conduct a human challenge trial to test the client's antiviral product. (Click here to read the RNS) 1. Cineworld Group plc - Response to media speculation The strategic options through which Cineworld may achieve its restructuring objectives include a possible voluntary Chapter 11 filing in the United States and associated ancillary proceedings in other jurisdictions as part of an orderly implementation process. Cineworld is in discussions with many of its major stakeholders including its secured lenders and their legal and financial advisers. (Click here to read the RNS)

Peripheral Artery Disease (PAD) Treatment Guest: Robert D. McBane, II M.D. Host: Stephen Kopecky, M.D. (@DrSteveKopecky) Most patients, who have Peripheral Artery Disease, do not experience the symptoms right away. However, patients affected with PAD will likely experience symptoms such as pain in the legs during walking and loss of hair. PAD limits the blood flow from the vessels to the heart. Without the proper treatment, the effects of PAD can lead to amputation of the foot or legs. Major amputation can potentially lower the life expectancy of patients that are affected with PAD. Joining us today to discuss Peripheral Artery Disease (PAD) Treatment is Robert D. McBane, II M.D. professor of medicine in the department of cardiovascular medicine at Mayo Clinic in Rochester, Minnesota. Specific topics discussed: How do you define PAD? Is invasive or noninvasive imaging diagnosis required? Or can be based on ABI?  Or is physical exam adequate with a bruit in the carotids, renals, or femorals? In PAD, are risk factors the same as in cardiovascular or cerebrovascular disease? Why is having PAD a greater risk factor for cardiovascular morbidity and mortality than coronary artery disease or cerebrovascular disease? Do any risk factors predominate in PAD? (e.g., is smoking more prevalent?) Are you checking lipoprotein a in patients with PAD at an early age? Has treatment of risk factors been shown to significantly reduce CV morbidity or mortality in patients with PAD? When is ABI indicated and when is toe-brachial index indicated? (What is the definition of noncompressible vessels?) When should we do exercise ABI? For treatment, other than treating the risk factors of lipids, smoking, hypertension, diabetes, or other treatments indicated such as anti-platelet and if so his aspirin adequate, what dose, or other anti-platelet agents indicated? Clopidogrel should be added when? Can be given in place of aspirin? When is cilostazol recommended? Can you give with heart failure-HFpEF and HFrEF?  Does this improve outcomes-walking distance or also overall morbidity and mortality? What home walking program is best to recommend for patients with PAD? Do patients with PAD get as aggressive treatment for risk factor control as do CV or cerebrovascular disease patients? Why are patients with PAD less often treated aggressively for risk factor control? Is that the patient or the caregiver? Any other new drugs available that are beneficial? When is revascularization helpful to consider? There is emerging evidence that lower LDL cholesterol (LDL less than 60) significantly benefits patients with CAD-is there any evidence lower LDL is beneficial in PAD? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV. NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.  

WarfarinTrade: CoumadinUse: Anticoagulant Glipizide Trade: GlucotrolUse: Diabetes Clopidogrel bisulfate Trade: Plavix Use: Platelet inhibitor 

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/ClopidogrelPlavixNursingConsiderations    Generic Name Clopidogrel Trade Name Plavix Indication Atherosclerotic events, MI, CVA, PVD, acute coronary syndrome Action Inhibits platelet aggregation Therapeutic Class Antiplatelet agent Pharmacologic Class Platelet aggregation inhibitors Nursing Considerations • May cause GI bleeding, neutropenia, hypercholesterolemia • May increase risk for bleeding in warfarin, aspirin, heparin • Can increase risk for bleeding with garlic, ginkgo, ginger • Monitor for signs of bleeding • Monitor bleeding times • Monitor CBC and platelet count • Discontinue use 5-7 days before surgery

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)00572-9/fulltextOld calculators use old studies and can over exaggerate the calculated effecthttps://pubmed.ncbi.nlm.nih.gov/33970197/We know when to start medication but it is so hard to prospectively know when to stop medication like anticoagulationhttps://pubmed.ncbi.nlm.nih.gov/34074830/2 Kiwi a day will increase your bowel movementshttps://pubmed.ncbi.nlm.nih.gov/34100866/We want to believe routine checkups work but realistically they don't work for patient oriented outcomes--but they make people 'feel good'-- what we do isn't always the doing, it's just being therehttps://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01063-1/fulltextDAPT following a stent-- but then just maybe we should stay with plavix and not aspirin

Dr. Ebell and Dr. Wilkes discuss the POEM titled ' DAPT with aspirin plus clopidogrel for 30 days is the best option after minor stroke or TIA '

Marcos Meniconi, Maria Julia Souto e Manuela Gomes analisam os fatores que devem influenciar o cardiologista a definir quais antiagregantes plaquetários e quanto tempo de terapia dupla deve ser indicado para o paciente submetido a angioplastia coronária percutânea. Acompanhe para recordar os “landmark trials” e novidades sobre o tema. Minutagem: (01:45): tipos de antiagregantes plaquetários (03:15): resistência genética ao clopidogrel? (05:45): quando o segundo antiagregante deve ser o clopidogrel (07:16): ataque do antiagregante na emergência (12:45): por quanto tempo manter a DAPT? (18:22): da para reduzir o tempo de DAPT? (21:20): o que vem por aí (NEO-MINDSET trial) (23:00): mensagens finais (24:30): resposta aos dozers REFERÊNCIAS: 1. Bittl JA, Baber U, Bradley SM, Wijeysundera DN. Duration of dual antiplatelet therapy: a systematic review for the 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease. Circulation. 2016;134:e156–e178 2. Mauri L, Kereiakes DJ, Yeh RW, et al. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. N Engl J Med. 2014;371(23):2155-2166. 3. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet. 2001;358(9281):527-533.

The comparison of Clopidogrel and Aspirin monotherapy after PCI (HOST-EXAM trial)

DAPT after ischemic stroke or TIA

Drs Harrington and Gibson provide their annual roundup of what they consider the key cardiovascular trials of 2021. This podcast is intended for healthcare professionals only. To read a transcript or to comment, visit This podcast is intended for US healthcare professionals only. To read a full transcript of this episode or to comment please visit: https://www.medscape.com/viewarticle/963475 https://www.medscape.com/author/bob-harrington Antiplatelet Therapy Comparative Effectiveness of Aspirin Dosing in Cardiovascular Disease https://doi.org/10.1056/NEJMoa2102137 Dual Antiplatelet Therapy after PCI in Patients at High Bleeding Risk https://doi.org/10.1056/NEJMoa2108749 Effect of 1-Month Dual Antiplatelet Therapy Followed by Clopidogrel vs 12-Month Dual Antiplatelet Therapy on Cardiovascular and Bleeding Events in Patients Receiving PCI https://doi.org/10.1001/jama.2019.8145 Aspirin Versus Clopidogrel for Chronic Maintenance Monotherapy After Percutaneous Coronary Intervention (HOST-EXAM): An Investigator-Initiated, Prospective, Randomised, Open-Label, Multicentre Trial https://doi.org/10.1016/S0140-6736(21)01063-1 SGLT2 Inhibitors and GLP-1 Agonists Empagliflozin in Heart Failure with a Preserved Ejection Fraction https://www.nejm.org/doi/full/10.1056/NEJMoa2107038 Once-Weekly Semaglutide in Adults with Overweight or Obesity https://www.nejm.org/doi/full/10.1056/NEJMoa2032183 Cardiac Surgery and PCI Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke https://doi.org/10.1056/NEJMoa2101897 Concomitant Tricuspid Repair in Patients with Degenerative Mitral Regurgitation https://doi.org/10.1056/NEJMoa2115961 Fractional Flow Reserve–Guided PCI as Compared with Coronary Bypass Surgery https://doi.org/10.1056/NEJMoa2112299 You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine Hear John Mandrola, MD's summary and perspective on the top cardiology news each week, on This Week in Cardiology https://www.medscape.com/twic Questions or feedback? Please contact news@medscape.net

This episode covers clopidogrel and ticlopidine!

FDA 批准颈动脉窦压力反射刺激疗法治疗心衰Lancet 血ACE2水平与心血管疾病及死亡的关系Science子刊 一种具有几何适应性的人工心脏瓣膜BAROSTIM NEO系统BAROSTIM NEO系统包括一个植入式脉冲发生器（IPG）、一个颈动脉窦含铅套件和一个程序。医生将BAROSTIM NEO脉冲发生器植入晚期心力衰竭患者的左或右锁骨下方，并在患者的左或右颈动脉窦处放置颈动脉窦导线，然后将脉冲发生器连接到颈动脉窦导线上。医生根据病人的个人需求制定脉冲发生器程序，然后向颈动脉的压力感受器传递电脉冲。压力反射激活（BAT）疗法的目的是激活颈动脉壁的压力感受器，刺激自主神经系统的传入和传出神经，大脑接收到神经信号作出相应反应：松弛血管、降低心率、并通过改善肾功能来减少液体储留。2019年8月，FDA批准BAROSTIM NEO系统用于药物治疗无效的、不符合心脏再同步化治疗适应症的、难治性心力衰竭患者。《BeAT-HF研究：这项研究证明了压力反射刺激疗法（BAT）对射血分数降低的心力衰竭患者的安全性和有效性》Journal of American College of Cardiology，2020年7月 (1) BeAT-HF研究是一项多中心、前瞻性、随机对照研究，纳入408名射血分数降低的心力衰竭（HFrEF）患者中，入组要求：纽约心功能分级II-III级、射血分数≤35%、药物治疗方案稳定≥4周、不符合心脏再同步化治疗的I类指征。这篇报告重点汇报了D队列中、NT-proBNP

Clopidogrel is an antiplatelet drug. When I was in school it was the “classic” example of a prodrug. The brand name is Plavix. This drug works by irreversibly blocking the P2Y12 component of ADP receptors which prevents GPIIb/IIIa activation causing a reduction in platelet aggregation. Based on indications and diagnosis there may be a loading dose of 300 mg to 600 mg with the general treatment dosing of 75 mg po qd. The active form of this drug relies on the Cytochrome P450 CYP2C10 oxidation to active thiol. Common side effects include bleeding, bruising, rash. There is a black box warning for CYP2C19 metabolism and diminished efficacy in poor CYP2C19 metabolizer. Go to DrugCardsDaily.com for episode show notes which consist of the drug summary, quiz, and link to the drug card for FREE! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. The main goal is to go over the Top 200 Drugs with the occasional drug of interest. Also, if you'd like to say hello, suggest a drug, or leave some feedback I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

  Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Our feature discussion today is about the validation of a novel biomarker-based stroke risk score for atrial fibrillation, the ABC stroke score. But first, here's your summary of this week's journal.     The first paper provides experimental insights into endothelial nitric oxide synthase uncoupling in endothelial dysfunction. In this paper by first author Dr. Lee, corresponding author Dr. Wong and colleagues from Qilu Hospital of Shandong University in China, authors assessed endothelial function in animal models of hyperglycemia, hyperhomocysteinemia, and a dyslipidemia. They demonstrated that GTP cyclohydrolase 1 is the target of the microRNA-133a and that it's a topic expression and endothelial cells mediates endothelial dysfunction.     Furthermore, Lovastatin up-regulated GTP cyclohydrolase 1 and tetrahydrobiopterin and re-coupled endothelial nitric oxide synthase in stress endothelial cells. These actions of Lovastatin were abolished by enforced micro RNA 133A expression and mirrored by a mir-133a-antagomir. Finally, the beneficial effect of Lovastatin in mice were abrogated by in vivo mir-133A over-expression or by GTP cyclohydrolase 1 knockdown. In summary, this paper offers a mechanistic basis for targeting micro RNA 133A as a therapeutic approach to correct endothelial nitric oxide synthase dysfunction. It also provides further support to the role of statins in combating endothelial dysfunction.     The next study shows us that in hypertrophic cardiomyopathy, calcium mishandling may be the potential link between the primary genetic cause and downstream signaling cascade that leads to hypertrophy and arrythmias. In this study, Dr. Helms and colleagues from University of Michigan analyzed gene expression, protein levels and functional essays for calcium regulatory pathways in 35 human hypertrophic cardiomyopathy surgical samples with and without sarcomere mutations and compared that with 8 control hearts. They found a marked reduction in circa2 abundance, which correlated with reduced circa2 function in hypertrophic cardiomyopathy compared to controlled hearts regardless of the underlying genetic etiology.     However, calcium calmodulin depend protein kinase type 2 or cam2, which is a calcium sensing kinase, was deferentially activated only in the sarcomere gene mutation positive samples. Activation of chem kinase 2 was associated with an increase in phospholamb and phosphorylation in hypertrophic cardiomyopathy. However, neither calcineurin MRNA nor MEF2 activity was increased, suggesting that calcineurin pathway activation was not an upstream cause of increased chem kinase 2 protein abundance or activation.     In summary, this paper demonstrated that calcium mishandling occurs through both genotype specific and common pathways in human hypertrophic cardiomyopathy. Post-translational activation of chem kinase 2 pathway is specific to sarcomere mutation positive hypertrophic cardiomyopathy. While Sarco 2 abundance and sarcoplasmic reticulum calcium uptake are depressed in both sarcomere positive and negative hypertrophic cardiomyopathy. Thus, chem kinase pathway inhibition may improve aberrant calcium cycling in hypertrophic cardiomyopathy. This is discussed further in an accompanying editorial by Dr. Jill Tardiff.     The third study suggests that in patients with a dilated aortic route and trileaflet aortic valve, a ratio of aortic route area to height provides independent and improved stratification for prediction of death. First author Dr. Masry, corresponding author Dr. Desai and colleagues from the Center for Aortic Disease, Heart and Vascular Institute of Cleveland Clinic, studied consecutive patients with a dilated aortic route of greater or equal to 4 centimeters who underwent echocardiography and gated contrast enhanced thoracic aortic computer tomography or magnetic resonance and geography between 2003 and 2007.     A ratio of aortic route area over height was calculated on tomography and a cutoff of 10 squared centimeters per meter of height was chosen as abnormal. In 771 patients with trileaflet aortic valve and concomitant aortopathy, there was incremental prognostic value for indexing aortic route or ascending aortic area to patient height rather than using an unindexed aortic diameter. Incorporation of the ratio significantly and independently reclassified the risk for death and at normal ratio was independently associated with higher long-term mortality while cardiovascular surgery was associated with improved survival. Importantly, a sizable minority of patients with aortic route diameters between 4.5 and 5.5 centimeters had an abnormal aortic route when indexed to height ratio. 78 percent of deaths in this subgroup occurred in those with an abnormal aortic route area to height ratio. Findings were similar when ascending aortic measurements were considered. The take home message is that an aortic route area to height ratio above 10 squared centimeters per meter of height has significant and independent prognostic utility and may be used to re-stratify patients with trileaflet aortic valve and a dilated aorta.     The final study provides pre-clinical data to show that Ticagrelor reduces cardio damage post myocardial infarction to a greater extent than Clopidogrel by an adenosine induced organ protective response. First author Dr. Villaher, corresponding author Dr. Bademan and colleagues from the Cardiovascular Research Center in Barcelona, Spain studied a close-chest swine model of ischemia reperfusion in which myocardial infarction was induced by 1 hour balloon occlusion of the mid-left anterior descending coronary artery followed by 24 hours of re-flow. Prior to occlusion, the animals were randomly assigned to receive either placebo, a loading does of Clopidogrel, a loading does of Ticagrelor or a loading does of Ticagrelor followed by an A1 A2 receptor antagonist. Edema infarc size left ventricular size and left ventricular function were assessed by three T cardiomagnetic resonance imaging. Inhibition of platelet aggregation was the same between the groups receiving a P2Y-12 inhibitor.     Yet, Ticagrelor reduced infarc size to a significantly greater extent than Clopidogrel, reducing it by a further 23.5 percent, an effect supported by troponin eye assessment and histopathological analysis. Furthermore, compared to Clopidogrel, Ticagrelor significantly diminished myocardial edema by 24.5 percent, which correlated with infarced mass. Administration of an adenosine A1 A2 antagonist abolished the cardio protective effects of Ticagrelor over Clopidogrel. At a molecular level, aquaporin 4 expression decreased and the expression and activation of AMP kinase cyclin and COX-2 increased in the ischemic myocardium of Ticagrelor versus Clopidogrel treated animals. In summary, this study shows that Ticagrelor exerts cardio protective effects beyond its anti-platelet efficacy by adenosine dependent mechanisms, which reduce necrotic injury and edema formation. This is discussed in an accompanying editorial by Drs. Gerbel, Jung and Tantry. That wraps it up for the summaries. Now for our feature discussion.     Today, we are going to be discussing the performance of the ABC score for stroke in atrial fibrillation. And as a reminder for all our listeners there, ABC stands for A for age, B for biomarkers, that's NT-proBNP and high-sensitivity troponin, and C for clinical history of prior stroke. And again as a reminder, this risk score was originally derived in the Aristotle trial. However, we have new results about its performance and validation today from first and corresponding author Dr. Jonas Oldgren from Uppsala Clinical Research Center in Sweden. Welcome, Jonas.   Speaker 2: Thank you very much.   Carolyn Lam: We also have today the associate editor who managed this paper, Dr. Sandeep Das from UT Southwestern. Hi Sandeep.   Speaker 3: Hi Carolyn, thanks for having me.   Carolyn Lam: So Jonas, could you start off by telling us why you did this study and what you found?   Speaker 2: We did this study to validate the recently derived ABC stroke risk score. We have had risk scores for predicting stroke in patients with atrial fibrillation derived since the late 1990's and refined later on. But those risk scores have only used clinical markers for risk. We have for several years developed new risk prediction models with biomarkers and now we are combine them in a very simple biomarker based risk score, taking into account age as a clinical variable and the clinical history of prior stroke and only two common used biomarkers. And by that we can predict the risk of stroke with better precision than previous clinical risk scores.   Carolyn Lam: Yeah, I like what you said. I mean it is literally as simple as ABC. So tell us how you validated it and what you found.   Speaker 2: It was derived in a large cohort of patients participating in a clinical trial with new or relapsed coagulant compared to Warfarin and we now validated in almost a full size group participating it another clinical trial. So we have large data sets of very well described patients where we have good outcome data. Very solid data to rely on. Now we can see that the ABC risk score is now validated but the good precision and good collaboration of the discriminatory abilities is high and better than the previously used clinical risk scores.   Carolyn Lam: Could you give us some numbers behind that that are clinically meaningful? Everyone's going to be wondering compared to the chads-vasc score for example, how does this ABC score perform in that validation test set?   Speaker 2: We can adjust that by several different aspects. One is of course to calculate the C index which is a statistical method to see how good we can predict risk and the C indices for the ABC stroke score both in the duration and now in the validation cohort is higher than for the chads-vasc and atrial risk scores. But we can also look at what we have in this paper in circulation ... we can look at predicted outcome rates and observed outcome rates and can see that they clearly overlap both in the duration and validation court. So if you predict a risk that is less than 1 percent per year, it is observed also a risk that is less than 1 percent a year. Does this always ... the thing is when you derive risk or but when you validate it in another cohort, you need to show that it's a similar result.   Carolyn Lam: Yeah, that's true. Sandeep, you are managing this paper. It's very important. How do you think that clinicians should be taking the results?   Speaker 3: I think that clearly using anticoagulation and selected patients at high risk for stroke with atrial fibrillation is one of the best things we do in cardiology. You know in terms of reducing the risk of an important harm to patients. I think there's a fair bit of dissatisfaction out there with currently sort of standard, which is chads-vasc. Especially in people with a chads-vasc ... men with a chads-vasc of 1 or women with a chads-vasc of 1 to 2 where there's a bit of struggling over how to decide. So I think that one real advantage of this score in addition to the fact that it predicts better by the higher C statistic, which is fantastic and pretty uncommon, right? Lars sort of buried the lead a little bit by not emphasizing that it's relatively rare that we're able to move a c statistic by a point of 5 in the modern era.     But the other thing is that it helps give us an ability to come up with good estimates in people at low risk, which I think has been a challenge and something that people are a little concerned clinically. So I think that this is easily available, biomarkers that we routinely check all the time and it doesn't have the sort of gender challenge with chads-vasc where you're trying to figure out whether your low risk woman really needs to be on Warfarin or anticoagulation. So I think that it has a lot of clinical utility right out of the box, which is nice.   Carolyn Lam: Actually, Jonas could you let us know is there any sex differences in the performance of the score?   [00:14:46] Speaker 2:   There are no differences in the performance of the score. So we looked ... the advantage of this score is when we derived it in the original model, we looked at all important clinical and biomarker risk factors and we can see that these were the foremost interesting markers. So we only used those. So we can predict much better and as pointed out so nicely by Sandeep, for patients at the lower end of the risk spectrum, we can find patients or have higher or lower risk even within patients with chads-vasc 1 or chads-vasc 2. And I think it's also important to see what about patients at higher risk despite proper anticoagulation. We did not know how to treat them but in the future we might perhaps tailor treatment also for those patients with residual high risk of stroke despite proper anticoagulation treatment. For instance, if the left atrial appendage occluded devices are shown in the future to be a good option for those patients, we can find them also by this risk score. So both in the higher and lower end of the risk spectrum.   Carolyn Lam: That's a really good point. On that note, I'm just curious. What do you think is in the future? What more knowledge do we need to address before we put this into practice or are you already using this? Or do you think it should enter guidelines for example? Maybe Sandeep, I could ask for your opinion first.   Speaker 3: We see a lot of biomarkers associated with increased risk kind of studies come out in the literature. You know probably every week you see several of these things come out. So what's really interesting about this is that it's obviously methodologically extremely well done but its been derived and validated in two large cohorts, which is pretty much best practice right? You want to see people validate these risk scores in large and distinct cohorts of patients to build up sort of clinical validity to the reader or consumer. So I think, from my standpoint, this is ready for prime time. I'm really intrigued by the fact that biomarkers, especially troponin, are predicting stroke in this population and there have been some observational reports out there that have showed an association between troponin and increased risk of stroke or worse outcomes after stroke. So I'd be really curious as to what Jonas thinks about why troponin would be predictive of stroke in this population.   Speaker 2: We were extremely intrigued by the finding when we first did those single observations of only troponin as a risk marker because we know that troponin is a very specific protein found in the myocardium. But the clinic predicts risk for stroke also and there are several explanations but they are mainly hypotheses about aging and myocardial function really to identify patients of risk. But the clear cut explanation is still not there.   Carolyn Lam: It's likely that these biomarkers are incorporating aspects that we don't fully understand, which is why they are better predictors isn't it? I mean to your point Sandeep.   Speaker 3: Yeah, no absolutely. And I think that's great.   Carolyn Lam: Exactly. It really opens a lot of other questions that need to be answered in the meantime. Jonas, any other last words about how you may be applying this clinically in your own patients?   Speaker 2: We have no solid data supporting the use of this clinical risk score and as already pointed out, which I think is very good, all clinic risk scores should of course be in the best world validated as useful decision support truth and really in clinics trial seeing that they improve outcomes. This is to my knowledge never been down with a clinical risk scores. We have never used them prospectively to guide treatment and to improve outcomes. Actually, we are aiming to do that. We hope to start a clinical trial next year with ABC score guided treatment compared to standard of care. But it's a very huge undertake of course to that we can improve treatment by risk or guided management.   Carolyn Lam: That's excellent. So remember everyone, you heard it right here. A new trial that they're engaging. I really congratulate you first for this study, as well as this future efforts which are clearly going to be very important.     Thank you very much both of you for joining us today and thank you listeners for listening. Don't forget to tune in next week.  

This week we review delayed ICH in patients with head trauma on blood thinners and discuss the role of repeat imaging and admission. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_43_0_Final_Cut.m4a Download 2 Comments Tags: Clopidogrel, Delayed Intracranial Hemorrhage, Head Trauma, Plavix, Warfarin Show Notes Nishijima DK et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and perjury warfarin or clopidogrel use. Ann Emerge Med 2012; 59(6): 460-8. PMID: 22626015 Menditto VG et al. Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med 2012; 59(6): 451-5. PMID: 22244878 Miller J et al. Delayed intracranial hemorrhage in the anticoagulated patient: a systematic review. J Trauma Acute Care Surg 2015; 79: 310-3. PMID: 26218702 Read More

This week we review delayed ICH in patients with head trauma on blood thinners and discuss the role of repeat imaging and admission. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_43_0_Final_Cut.m4a Download 2 Comments Tags: Clopidogrel, Delayed Intracranial Hemorrhage, Head Trauma, Plavix, Warfarin Show Notes Nishijima DK et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and perjury warfarin or clopidogrel use. Ann Emerge Med 2012; 59(6): 460-8. PMID: 22626015 Menditto VG et al. Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med 2012; 59(6): 451-5. PMID: 22244878 Miller J et al. Delayed intracranial hemorrhage in the anticoagulated patient: a systematic review. J Trauma Acute Care Surg 2015; 79: 310-3. PMID: 26218702 Read More