Podcasts about Lisinopril

Pierre was born and lived in the UK until 1970, when he moved to Rio de Janeiro, Brazil, where he stayed for 15 years. He returned to the UK from 1985 to 1992, then moved back to São Paulo, Brazil, until 1998. In 1998, he relocated to Fort Lauderdale, USA, and became a US citizen in 2006. He is now retired and lives near Fort Lauderdale, Florida.   Pierre's wife is Brazilian. They married in Rio in January 1972 and recently celebrated their 53rd anniversary. They have three sons: the oldest are identical twins (45), and the youngest is 41. His youngest son served in the US Army Reserve and later in the US Airborne. They have five grandchildren so far.   Pierre developed psoriasis in his early twenties, which worsened over time. He also experienced minor intestinal issues that gradually became more severe, leading to serious inflammation and infections. In 1993, he was diagnosed with diverticulitis, which he assumes is linked to autoimmune disorders.   In 1999, Pierre underwent a successful sigmoid colon resection in the USA for diverticulitis. Post-surgery, he was diagnosed with Type 2 Diabetes (T2D). For 19 years, he followed ADA guidelines under the care of an endocrinologist, but his T2D progressed to the point where he required insulin. At his peak, he was taking 240 units of insulin daily, which contributed to his weight reaching 280 lbs (he is 5'7”).   In November 2018, after watching videos by Dr. Jason Fung, Pierre adopted a low-carb, healthy fats diet, primarily keto, with intermittent fasting (16:8). Last year, he transitioned to a 98% carnivore diet, eliminating most plants. The results have been remarkable.   Over the years, Pierre has lost approximately 98 lbs (with about 20 lbs left to lose), improved his eGFR, stabilized his psoriasis, and reduced his medications from 7-9 to just two: 10 mg Lisinopril and insulin as needed. His Triglyceride/HDL ratio improved from 4.78 to under 1, with triglycerides dropping from 220 to under 75 and HDL rising from 46 to the high 90s.   Recently, Pierre struggled to keep his A1c below 6% without 50 units of insulin daily, which caused weight gain. Determined to reduce his insulin dependency, he joined Revero and is now under the care of Dr. Jarrouge, who has been incredibly supportive. While he has successfully reversed some weight gain, it's clear that his pancreas has suffered over the years and can no longer produce sufficient insulin. As a result, he needs a baseline insulin dose to maintain an A1c of 6% or below. Timestamps: 00:00 Trailer and introduction   05:03 Keto and psoriasis   07:46 Keto after health scare   12:23 Health improvements post-hospital recovery   13:01 Stopping statins   16:08 Health issues and nutrition   22:20 Influenced by Ivor Cummins   22:54 Unexpectedly high calcium score concerns   26:38 Scan results   29:19 Improved mobility for life quality   33:28 Keto journey without doctor's guidance   38:07 Optimizing triglyceride-HDL ratio   42:00 Navigating healthcare with online support   43:01 Low carb-savvy physicians   47:42 Low carb for marathon stamina   49:21 Where to find Pierre Join Revero now to regain your health: https://revero.com/YT Revero.com is an online medical clinic for treating chronic diseases with this root-cause approach of nutrition therapy. You can get access to medical providers, personalized nutrition therapy, biomarker tracking, lab testing, ongoing clinical care, and daily coaching. You will also learn everything you need with educational videos, hundreds of recipes, and articles to make this easy for you. Join the Revero team (medical providers, etc): https://revero.com/jobs ‪#Revero #ReveroHealth #shawnbaker  #Carnivorediet #MeatHeals #AnimalBased #ZeroCarb #DietCoach  #FatAdapted #Carnivore #sugarfree Disclaimer: The content on this channel is not medical advice. Please consult your healthcare provider.

This week, I talk about my jump to the Dark Side. Well, not really. Hey, did you know that the term “going to the Dark Side” was popularized by Star Wars? I’m going to try another BLOOD PRESSURE MEDICATION, and hopefully this time I can take it and stay on it! We’re going to try […]

See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog In general, I spend my time defending women and the fact that our problems and sexual physiology is ignored, by the governmental powers and physician organizations in the US, so I try to do my part to bring information to women about their hormones and the aging process. Today I am changing my focus to men and the way men's normal sexual function is considered a “normal” and rarely discussed outside the men's locker room and or porn sites. So here goes…The fact is that men's sexuality isn't just the act of sex, but men spend a lot of their sexual energy on fantasies and just thinking about having sex.  Men's ability to have an orgasm is not just a wham- bam—thank you…well you know the phrase…and there are many physiologic factors that must work, in the background to bring a man from thinking about sex or desire, to an orgasm. Sadly, in the current environment couples don't talk about sex….they don't tell their partner what makes them excited or even what they want…. because none of us can read minds, too many of us don't get what we want when it comes to sex. With lack of communication between partners, leads couples to trial and error without a map.  Neither sex knows how the other sex “works”.  I decided to describe the normal series of what men go through on their way to orgasm to educate them and their partners.  In addition, the process is not always the same in each person and as men age the time between the first sexual thought to completion gets longer and longer…sometimes these detours include episodes of losing an erection, sometimes getting it back and sometimes not which leads to frustration of both partners. In youth when a man's free testosterone is high and his arteries are free of plaque, between puberty and age 35, erections may occur often, and they last a long time if the man is stimulated for a long period of time. At this point sex is automatic and easy to complete to orgasm and ejaculation. As time goes on, free Testosterone starts to decrease with age, as does the diameter of a man's arteries…blood flow doesn't rush to the pelvis to create an erection like it did in youth. The things that lower free testosterone.  What happens with age that cause erections and ejaculation to be less and less automatic and easy? T and free T drops after age 35 in most men and becomes critical by age 55, even in healthy men. Ejaculate decreases due to lowering of free T Vasectomies decrease the volume of ejaculate by 1/3 Stress causes free T to decrease. Hypertension causes arteries to contract and deliver less blood to the pelvis for an erection. High blood sugar and diabetes destroys the arteries in the pelvis making blood have a more difficult time getting to the penis. Stress causes Cortisol to rise and free T decreases, Obesity increases the estrogens in men and that decreases free T by binding it with sex hormone protein and inactivating it. Any medication the constricts blood vessels (ADD medicine, Phentermine, speed, etc) decreases blood flow to the pelvis. Some medications that lower blood pressure lower It in the pelvis too low so that men are impotent (e.g. Lisinopril). For men who don't know all these medical, aging changes that happen to most men, these changes cause fear and anxiety which of course makes it worse.  Men who have this issue (most men) are even reticent to talk to me about it and they haven't talked to their spouse either. So here is what I tell them:  You are aging like everyone else, and that fact can't be changed, however, your lifestyle and your medical health, or poor health is affecting your orgasms and your ability to have sex.  These factors CAN be changed.  You can change your BP medicine to one that doesn't impair erections.  You can get your diabetes or obesity under control, and you can improve your erections.  However, to get it all back you will need testosterone replacement if your free T is under 129 ng/dl. The safest way to accomplish this is with my practice BioBalance® Health…we do it better and know all the tricks to making you healthy productive and potent! What is in the ejaculate? mature sperm are mixed with whitish, protein-rich fluids with prostaglandins are produced by the prostate. These fluids nourish and support the sperm so they can live after ejaculation for a limited time to fertilize an egg.  This mixture of fluid and sperm, known as semen, and is what is moves through the urethra in the form of ejaculate. Sensory stimulation travels from the skin to the brain and stimulates dopamine and endorphins which are neurotransmitters that make a man fee happily ecstatic during and after an ejaculation.  These neurotransmitters also stimulate the Hypothalamus to make oxytocin, a bonding hormone that binds couples together. Many nerves, vessels and the brain are involved in a successful sexual encounter. The culmination of a sexual encounter is complex and involves the whole body. I find it interesting that the “medical view” of orgasm is still divided into 4 different steps when, if you are a male (or even a female who has had sex with a male) the divisions seem very arbitrary and is ALWAYS connected to ejaculation. It is a fact that men and women can have sexual intercourse and orgasm without ejaculation. The following is how the practice of medicine describes the male sexual act.   In contrast I have educated my patients by comparing sex to a on the fact that men can have orgasms which occur in the brain when endorphins flood the neurons, even without ejaculation.  So I will discuss, the male sexual experience to them, not with the “4 easy steps of male sexual response”, but as a “process” of achieving orgasm in men.  It is more like a recipe, that requires each ingredient to be added in order, but sometimes you can stop in the middle and start again.  It is not always a straight line from sexual desire to orgasm. In general, all men need testosterone to have sexual desire, and sexual desire to have sex, however both men and women can be physically or visually stimulated to be aroused without true sexual desire. If the man has a long history of having sex often, then the habit of having a sexual response can be achieved without enough testosterone, however the erection will not necessarily last long enough.   Continued physical stimulation can bypass desire, and therefore testosterone, and a man can be stimulated into having an erection of sorts and into having an orgasm with or without ejaculate An erection requires testosterone to become fully erect, however there is a “work around” now and men without testosterone can have an erection with Viagra, Cialis pills, or prostaglandin injections into the penis itself. Men can also have a penile implant placed so they can have sex without testosterone or Viagra/Cialis. However, let's talk about sex with testosterone in men who have good pelvic blood flow who don't require medication to become erect. The second necessary ingredient after testosterone is stimulation, which can be with touch, visual stimulation, auditory stimulation or even imagination that causes a man to be stimulated. The sexual response to any of these stimulations send messages through the nerves from the brain to the pelvis that dilates his veins and arteries. This sends blood to the penis from the arteries and blocks the veins from draining the blood out.  This creates an erection. Testosterone's role is to cause the arteries to dilate by stimulating the production of nitric oxide from the arterial walls. Remember the stimulation? The ongoing stimulation (mental, visual, auditory or imaginary) keeps the erection hard with vascular dilation. At this point stimulation can be changed or paused and other stimulation can prolong this part of the process.  Holding the base of the penis can keep it hard, or any tight encircling toy can keep the erection from proceeding to orgasm for some time or the erection can go away without continued stimulation. The third step is the preparation for orgasm which can last from as long as 30 minutes and as short as 2 minutes. A clear “pre-ejaculate” is produced that lubricates the penis for intercourse, and if ejaculation is to take place there is a “loading of semen” that takes place from the seminal vesicles readying the man for ejaculation.  At this point the penis contracts the muscles quickly in rapid repeating emissions that shoot the semen out of the urethra. This is the orgasm and ejaculation that occur together, which is typical of normal youthful ejaculation.  As men get older the force at which they ejaculate decreases. After ejaculation/orgasm the brain is flooded in endorphins, the feel-good neurotransmitters, that make a human feel happy and satisfied.  This is solely the result of the orgasm after a sexual encounter. The feeling of ejaculation does relieve pelvic pressure but is not needed to experience orgasm in most men. Medical science has been able supply an assist for desire (testosterone) and erectile function (vasodilation and release of nitric oxide but they have not discovered the “pill” to make ejaculations occur or to improve their volume.  It is important for an aging man to accept that orgasm doesn't require ejaculation since we don't have an answer to recreating the youthful ejaculation.  Besides age, vasectomy can also limit ejaculation.  dehydration, vasoconstrictors, anti-hypertensive drugs and diuretics can limit the volume of the ejaculate as well. After the “process of sexual orgasm” the penis loses tumescence, blood leaves the pelvis and overall relaxation occurs throughout the body. Then a period of time must pass before another erection can occur.  Over time some “twice a day men” can turn into once every week…..this can be changed by practicing…..having sex more often. The sexual response in both men and women is more like a symphony with several movements, than a recipe, but it is definitely not a series of steps that is followed in every human in every circumstance. It is the job of the physician to help patients both understand and live with any variations in the sexual process.  Much of what I do is act as a teacher to my patients who need to understand their own bodies and any dysfunctions thereof.  Understanding becomes treatment over time.

This episode of Vitality Radio is Part 3 of a 5 part series in which Jen St. Clair, Jared's wife, shares her very personal story of triumph over addiction, bipolar, severe IBS, fibromyalgia, chronic pain, and many other health issues. On this part, Jen describes her experience having been started on Prozac at 13 years old and the decades of diagnoses and prescription drugs that followed. You'll hear how she went from feeling tied to those drugs for life to weaning off of them, only to feel better than she had in years. This episode is not suggesting that others stop taking their meds, but to share what is possible. Jen's story provides a roadmap to recovery for anyone dealing with these issues, but most of all, we hope it gives you hope and the belief that you too can heal.Products Mentioned (throughout this series)For CBD and THC Products - call to order 801-292-6662Additional Information:#264: Emotional Vitality: Jen's Story Part 1 - From Addiction and Mental Illness to Vitality#423: Emotional Vitality: Jen's Story Part 2 - Rebalancing Mind and Body Through Supplementation***Be sure to listen to all episodes of the “Emotional Vitality” series to learn more tools for achieving emotional vitality.Visit the podcast website here: VitalityRadio.comYou can follow @vitalityradio and @vitalitynutritionbountiful on Instagram, or Vitality Radio and Vitality Nutrition on Facebook. Join us also in the Vitality Radio Podcast Listener Community on Facebook. Shop the products that Jared mentions at vitalitynutrition.com. Let us know your thoughts about this episode using the hashtag #vitalityradio and please rate and review us on Apple Podcasts. Thank you!Please also join us on the Dearly Discarded Podcast with Jared St. Clair.Just a reminder that this podcast is for educational purposes only. The FDA has not evaluated the podcast. The information is not intended to diagnose, treat, cure, or prevent any disease. The advice given is not intended to replace the advice of your medical professional.

On this episode of the Real Life Pharmacology Podcast, I start my journey on summarizing the most highly testable pearls with the top 200 medications. I'm going through the top 200 medications, 5 drugs at a time, and sharing my experience and clinically relevant information about these medications. Escitalopram is an SSRI that can cause serotonin syndrome, sexual dysfunction, and SIADH. Simvastatin is a cholesterol medication that can cause myopathy and rhabdomyolysis. Levothyroxine is a thyroid hormone replacement medication that has numerous binding drug interactions. Vicodin is a brand name combination of hydrocodone and acetaminophen. It is an opioid combined with and OTC analgesic. Lisinopril is an ACE inhibitor used for hypertension that can cause a chronic dry cough and hyperkalemia.

In today's episode, we're shining a spotlight on Lisinopril, a true ally for your heart health. From regulating blood pressure to supporting cardiac function, Lisinopril is the unsung hero in the world of medications. Join me as we uncover the secrets behind Lisinopril's superpowers and learn how it can be your heart's best friend.

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:    Shelly: Hello. Could you explain the long term effects of using Benadryl especially with the gut? I have been using this for so many years due to sleep issues which I believe is due to histamine issues.   Terese: Hello and thank you ahead of time for all that you all do. I was diagnosed about 7 years ago with MAC. I did listen to your podcast on lung issues which was helpful but in wondering if you have anything additional to ask to help. I am presently using a nebutilizer with colloidal silver. Wondering if you have helped clients before with Mac. I do not want to do the antibiotic protocol that they have for 15 months with three high-powered antibiotics a day as I know that will wreck the immune system. The bacteria in my lungs has grown the past 3 years. I work part-time M 69 years old and take a low dose of Lisinopril for blood pressure as well. I am 165 lb and in 5 ft 10. I work part-time in my own gardening business but get tired and wear out faster than what I would like.   Ify: Hello Dr. Cabral. Thank you for everything you do. I wish I had submitted this question when I first found you but I'm okay with the wait. I have had hyperthyroidism for a number of years now and I have had scans confirming it is caused by graves disease. After being on Tapazole for 2 years and a bit I was advised to take radioactive iodine but decided that wasn't for me and ended up taking herbal teas to mitigate my symptoms. I had decided I wasn't damaging my liver anymore and got off my drugs. Since then my symptoms have been non-existent, resting hear rate averaging 80-90 BPM, no sweating or shaking or any expected symptoms. My new endo says I'm still hyper with THS at

Dr. Jeffrey James discusses Hypothyroidism with Dr. Ben Weitz. [If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.]    Podcast Highlights 3:17  Hashimoto's thyroiditis is the most common form of low functioning thyroid or hypothyroidism.  Dr. James noted that he has seen hundreds of women suffering with hypothyroidism and most of these women don't even get tested for Hashimoto's, since from the perspective of conventional medicine, if the woman has low functioning thyroid/high TSH levels, they will be treated with Synthroid or levothyroxine, which is synthetic thyroid hormone.  If it has an autoimmune origin, it doesn't change the pharmaceutical outcome.  But if you have Hashimoto's thyroiditis you have an immune system problem rather than a primary thyroid problem. We need to try to understand what would cause your immune system to dysregulate and want to attack your own body tissues?  Unfortunately, once you have one autoimmune disorder, you're 50% more likely to develop another one.  Dr. James explained that a lot of women complain that they're exhausted, they're putting on weight, they've got brain fog, they're losing their hair, they're constipated, their skin is dry, they've got brain fog, they have this constellation of symptoms, and they're cold.  When they go to their doctor, out comes the prescription for Synthroid.  Unfortunately a majority of women end up back in their doctor's office after a few months or a few years and they don't feel any better.  Their primary MD or endocrinologist then tries to dial in their TSH.  If they are depressed, then they get prescribed an antidepressant like Effexor or Cymbalta. If they have headaches, they get prescribed Imitrex.  If their blood pressure goes up, they are prescribed antihypertensive medications like Lisinopril or Amlopidipine or hydrochlorothiazide.  Dr. James sees a lot of these women who feel like they are not being seen or their complaints are not being addressed by their physician.  9:10  Functional Medicine practitioners are not simply treating each symptom with a pharmaceutical drug to ameliorate that symptom but are looking at your underlying metabolism, physiology, endocrinology as well as the root causes of the autoimmunity that is often driving these imbalances that can often be corrected with diet and lifestyle changes.  The patient with hypothyroidism could have an underlying GI infection or a biotoxin illness. They could have a genetic susceptibility to not being able to process mycotoxins that are either in their environment or that are in their foods that they're eating. They could have a Lyme infection. They could have a viral infection or a gut infection, a parasite or a bacterial infection in their gut that's driving an immunological response.  Any of these things can create a low level inflammatory response that can affect thyroid production, conversion, or uptake, all of which create symptoms that are very similar.  From a Functional Medicine perspective we want to see which way the physiology is tilting and we want to see if their lab values are optimal and not just normal or not.  11:05  The medical system in our country where once per year you go in for a physical exam with very minimal testing only to look for a pharmaceutical intervention is a failed system. Just look at how poor the health of our country is.  We need to test more widely to see how well our bodies are functioning.  For thyroid, we need to look at not just TSH but total T4 and T3, free T4 and Free T3, and reverse T3 as well as the thyroid antibodies. We need to trace everything back to the mitochondria of the cell and how our bodies produce energy.  We eat a meal and breathe some oxygen in and that glucose and oxygen mashes up against the mitochondria to produce ATP.

Episode 23:41 Natural Alternatives For The 10 Most Prescribed Drugs: Part 2 The following are the ten most prescribed drugs in the United States: Lipitor Lisinopril Albuterol Synthroid Norvasc Gabapentin Prilosec Metformin Amoxicillin Prednisone While the use of prescription drugs certainly has its place, NONE of the drugs listed above do anything to correct the underlying CAUSE. Not only that, ALL of these drugs have side-effects… some quite dangerous. There HAS TO be a better way. Fortunately, there IS. A safer, more natural alternative to drugs. On the last episode we discussed natural alternatives to three of the drugs on the list (Lipitor, Lisinopril and Norvasc). On this episode we address natural alternatives for the remaining seven. Please give it a good listen and then share it with a friend. Thanks! ———————- Want to learn more? Continue the conversation regarding this episode, and all future episodes, by signing up for our daily emails. Simply visit: GetHealthyAlabama.com  Once there, download the “Symptom Survey” and you will automatically added to our email list. ———————- Also, if you haven't already, we'd appreciate it if you'd subscribe to the podcast, leave a comment and give us a rating. (Thanks!!!) 

On Facebook? Connect with us at Facebook.com/GetHealthyAlabama

           * This podcast is for informational and educational purposes only. It is not intended to diagnose or treat any disease. Please consult with your health care provider before making any health-related changes.

In this follow up episode to #352, Jared discusses the clinically proven power of several nutrients and other natural compounds that may work for the same conditions that Gabapentin and Lisinopril are prescribed for. With the significant risk profile of these drugs, many patients are looking for effective alternatives without the risk. Jared shares natural alternatives for nerve pain, neuropathy, neuralgia, and high blood pressure. You'll learn the ins and outs of each of the ingredients and how they could potentially benefit you.Products:N.O. Cardio BoostKyolic Aged Garlic ExtractNatural Factors BerberineVital 5 Magnesium BisglycinateVital 5 Omega3 + AntioxidantsNerve ReverseNatural Factors L-TheanineCBD - call to order 801-292-6662Life-Flo Magnesium Oil Night SprayLife-Flo Magnesium GelAdditional Information:Episode #260: Prescribing Poisons. Commonly Prescribed Drugs; Are the Risks Worth the Benefits? Part 1Episode #266: Prescribing Poisons Part 2. Ibuprofen, PPI's, and Flouroquinalone AntibioticsEpisode #352: Prescribing Poisons Part 3: Gabapentin and LisinoprilEpisode #278: The Incredible Benefits of Aged Garlic ExtractEpisode #227 VR Vintage: There is an Herbal Supplement that Works for Diabetes, Blood Pressure and Cholesterol Better than Drugs! Berberine is that Powerful!Episode #242: The Vital Five How To: Your User's Guide to Filling the Gaps in Your DietEpisode #186 The Powerful Effect of 10:1 ratio CBD + THC with Stuart TomcEpisode #159 VR Vintage: CBD; the Central Nervous System, Gut Health, Immunity and How It All Interrelates an Interview with Maggie FrankResearch:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888748/https://www.healthline.com/nutrition/garlic-for-blood-pressure#dosages-formshttps://www.sciencedirect.com/science/article/abs/pii/S1530891X23003828https://www.chiroeco.com/uncommon-nutrients-carpal-tunnel/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836194/Visit the podcast website here: VitalityRadio.comYou can follow @vitalityradio and @vitalitynutritionbountiful on Instagram, or Vitality Radio and Vitality Nutrition on Facebook. Join us also in the Vitality Radio Podcast Listener Community on Facebook. Shop the products that Jared mentions at vitalitynutrition.com. Let us know your thoughts about this episode using the hashtag #vitalityradio and please rate and review us on Apple Podcasts. Thank you!Please also join us on the Dearly Discarded Podcast with Jared St. Clair.Just a reminder that this podcast is for educational purposes only. The FDA has not evaluated the podcast. The information is not intended to diagnose, treat, cure, or prevent any disease. The advice given is not intended to replace the advice of your medical professional.

In his continuing series on serious issues with heavily prescribed drugs, Jared tackles two big ones - Gabapentin and Lisinopril. Gabapentin is used for all kinds of things in an off label capacity, but does it work? And is it safe? Lisinopril is prescribed as the number one option for high blood pressure but it has come under significant scrutiny and seems to cause more problems the longer someone is using it. Learn the truth about these iffy prescriptions! Also the follow up episode #354 will give you some safer and still very proven natural alternatives to consider. Additional Information:Episode #260: Prescribing Poisons. Commonly Prescribed Drugs; Are the Risks Worth the Benefits? Part 1Episode #266: Prescribing Poisons Part 2. Ibuprofen, PPI's, and Flouroquinalone AntibioticsEpisode #354: Prescribing Poisons Part 3 Follow Up: Natural Alternatives to Gabapentin and Lisinopril (coming soon!)Visit the podcast website here: VitalityRadio.comYou can follow @vitalityradio and @vitalitynutritionbountiful on Instagram, or Vitality Radio and Vitality Nutrition on Facebook. Join us also in the Vitality Radio Podcast Listener Community on Facebook. Shop the products that Jared mentions at vitalitynutrition.com. Let us know your thoughts about this episode using the hashtag #vitalityradio and please rate and review us on Apple Podcasts. Thank you!Please also join us on the Dearly Discarded Podcast with Jared St. Clair.Just a reminder that this podcast is for educational purposes only. The FDA has not evaluated the podcast. The information is not intended to diagnose, treat, cure, or prevent any disease. The advice given is not intended to replace the advice of your medical professional.

In this episode, Dave speaks mainly about his most recent DOT exam. During the show he's traveling southbound on the New York State Thruway I-87 under mostly sunny skies and cold temperatures with dry roads. The point of the show is what now?

Join me with integrative pharmacist, Dr. Trang Nguyen, as we dig deep on Deprescribing, what it is and how to do it.  Anyone who is on a journey to feeling healthier and is taking medications needs a strategy to start coming off medications, which is deprescribing. In this episode, we'll cover how the following medications can be prescribed and how you can approach this with your doctor and pharmacist.How to Deprescribe Medications for High Blood pressure such as:Lisinopril, Losartan, Amlodipine and MetoprololYou can download my downloadable Blood Pressure Journal Here:Blood Pressure Checklist and LogHow to Deprescribe Medications for Cholesterol Medications, including:Statins-Atorvastatin, Simvastatin RosuvastatinWant to calculate your cardiovascular risk?https://www.mdcalc.com/calc/3398/ascvd-atherosclerotic-cardiovascular-disease-2013-risk-calculator-aha-accDr. Trang Nguyen is a Board-Certified Geriatric Pharmacist. In 2017, she found Mimosa Health LLC. Her mission is to provide expert advice on the use of medications by older adults, promote healthy aging, and educate seniors about polypharmacy as well as medication safety. Currently, she is a consultant pharmacist for Skilled Nursing Facilities and a fellow-in-training at the Academy of Integrative Health and Medicine.She is a radio host of “The Medicine Cabinet” show which is broadcast every other Saturday at 5:30 pm Central Time from The Vietnamese Public Radio Station in Oklahoma City. She is the author of “Medication Management for 50+” book .I have some great content coming!  Have you been interested in mindfulness as a practice or a way or life?Try my course (for free) Mindfulness Mastery to learn about mindfulness and get updates when my 6 week Mindfulness course is live.My book “Heart of Being” will be out next year.  Interested in a preview?I'll be sharing a free chapter to those that sign up here:Welcome to the Art of Healing Podcast.Let's explore your mind, body and spirit through Integrative Medicine, Meditation and Reiki.Don't miss the latest episodes. Sign up to get the weekly newsletters and get the Art of Healing Podcast in your inbox:Healing Arts Weekly Newsletter Thank you for listening to the Art of Healing Podcast.Ready to start your journey into Meditation, Mindfulness or Reiki?Learn about the Programs at Healing Arts here.Want to make sure you catch every episode of the Art of Healing? Click here for my weekly newsletter.Never miss an episode of Art of Healing Podcast...the podcast devoted to helping you heal your mind, body and spirit.Sign up for my weekly newsletter, and never miss an episode along with other great content:Art of Healing PodcastStay in touch socially here:Healing Arts Link in BioLearn more about me and my offerings here:Healing Arts Health and Wellness

The dangers of late night coffee, Gabe overdoses on Lisinopril, Vegas stuffGabe plays drums on the first new song in 25 years from Gabe's old (current?) band. Get full access to The Drive Home with Gabriel Rutledge at gabrielrutledge.substack.com/subscribe

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/LisinoprilPrinivilNursingConsiderations      Generic Name lisinopril Trade Name Prinivil Indication hypertension, management of CHF Action block conversion of angiotensin I to angiotensin II, increases renin levels and decreases aldosterone leading to vasodilation Therapeutic Class antihypertensives Pharmacologic Class ACE Inhibitor Nursing Considerations • dry cough • first dose hypotension • use cautiously with potassium supplements and potassium sparing diuretics • use cautiously with diuretic therapy • administer 1 hour before meals • monitor blood pressure often • monitor weight and fluid status • monitor renal profile • monitor liver function tests • may cause angioedema

Nearly 50% of all American adults may have elevated blood pressure, but the unfortunate truth is that many may not even know it. This is why high blood pressure is often referred to as the “silent killer” because the symptoms can be so subtle that most people don't even notice them.In this week's episode, we dive deep into high blood pressure, the causes and effects, how to know you have blood pressure, and how to lower blood pressure using natural means. We also talk about the side effects of LISINOPRIL,  a high blood pressure medication, on black people. Do you have questions about your wellness routine and boundaries?We are all about community and wellness in this episode so let's jump right into it.[01:20] Lisinopril: side effects and why you shouldn't take the drug if you're black.[02:45] Causes of high blood pressure[05:11] Natural ways to lower your blood pressure[05:24] Herbs for cooking that lowers blood pressure[06:22] Foods and diets that lower high blood pressure[07:32] Some signs to know you have high blood pressure[09:13] Foods and diets that lower high blood pressure cont.[14:36] Foods to stay away from if you have high blood pressure [19:54] Food swap: great swap for pancakes  instead of Hungry Jack that is full of bleached flour[23:13] More About Us & Our Mission & How to Be featured on our podcastBlended Banana Oatmeal pancake recipe:Ingredients 2 medium very ripe bananas (where the peel has a ton of brown specs or even solid black is great!) 2 large eggs 1/2 cup unsweetened almond milk 1 teaspoon vanilla 1 1/2 cups old-fashioned rolled oats 2 teaspoons baking powder 1/2 teaspoon cinnamon 1/4 teaspoon salt pinch of nutmeg unsalted butter, for the pan maple syrup, for serving, if desired Instructions Add all of the ingredients to a blender and blend on high until completely smooth (30-60 seconds.) Let the batter sit while you heat up a pan or griddle. Place pan or griddle over medium heat and lightly coat with a little butter. Once the surface is hot, add a 1/3 cup of the batter and cook until the pancakes puff up and bubbles form and begin to pop about 2-3 minutes. Gently flip pancakes over and cook another 2 minutes until golden brown on the underside. (NOTE: If you find the pancakes are browning too quickly, lower the heat so that the pancakes don't over-brown or burn.) Wipe the pan clean and repeat with more butter, as needed with the remaining batter. Serve with a little drizzle of maple syrup and a couple slices of banana, if desired. LINKS MENTIONED IN THIS EPISODEDownload the Recipe and instructions for the homemade formula here+ @WellHonestlyPodcast on Instagram+ Join the Facebook Community+ Buy Our Tea+ Subscribe on youtubeSUBSCRIBE + REVIEW ON APPLE PODCASTSThank you for listening. We hope this podcast has been informative & an inspiring resource to create the kind of life you want with your health in mind.To help get this podcast in front of more women like you, please consider leaving us a rating and review on Apple Podcasts here! The 10 seconds you take doing this means the WORLD to us and the women who will be helped by this show.Click here to go to our Podcast Website

In this episode, Dr. Christopher Tookey and Dr. Rose Wolbrink discuss a relatively new goal for blood pressure shown to reduce risk of heart disease and stroke.    We're providing general guidance but everyone is different and you should always discuss with your health care professional management of any disease and therapy before trying anything you discover from a source on the internet (including this podcast). This podcast does not reflect the opinion of our employer. 

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. Question #7 While you are on holiday break visiting your family, your aunt pulls you aside during the family gathering to ask a few questions about your 70-year-old uncle. He has hypertension, hyperlipidemia, type 2 diabetes mellitus, and moderate chronic obstructive pulmonary disease. His medications include Fluticasone/Salmeterol, Tiotropium, Albuterol, Lisinopril, Simvastatin, and Metformin. She is very concerned about his risk for heart disease as he has never had his “heart checked out.” She asks if the presence of COPD increases his chance of having heart disease. Which of the following statements would best answer her question? A. Systemic inflammation and oxidative stress caused by COPD promote vascular remodeling and a paradoxical ‘anticoagulant' state affecting all vasculature types. B. Although chronic COPD is associated with increased cardiovascular events, individual exacerbations have no impact on risk of cardiovascular events. C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. D. Cardiovascular mortality increases proportionally with an increase in forced expiratory volume in 1 second (FEV1) Answer #7 The correct answer is C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. Patients with COPD have a 2-3-fold increased risk of CV events compared to age-matched controls even when adjusted for tobacco smoking, a shared risk factor. This can be partly explained by other common risk factors including aging, hypertension, hyperlipidemia, and low physical activity. Interestingly, CVD mortality increases proportionally with a decrease (rather than increase) in FEV1, making answer choice D wrong (28% increase CVD mortality for every 10% decrease in FEV1). Additionally, COPD exacerbations and related infections are associated with a 4x increase in CVD events, making answer choice B incorrect. COPD has several effects on the vasculature which creates a ‘procoagulant' not ‘anticoagulant' effect on all vascular beds. This is associated with increased risk of cognitive impairment due to cerebral microvascular damage as well as increased risk of ischemic and hemorrhagic stroke. Main Takeaway The presence of COPD (even mild to moderate) has a significant impact on the incidence of non-fatal coronary events, stroke, and cardiovascular mortality mediated by inherent disease process and progression, risk factors (smoking, aging, hypertension, and hyperlipidemia), and systemic inflammation altering vasculature creating a ‘procoagulant' effect. The ESC gives a Class I indication (LOE C) to investigate for ASCVD and ASCVD risk factors in patients with COPD. Guideline Location 3.4.5, Page 3264. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Preventing the cardiotoxicity of Trastuzumab

Dermatology memes – Collagenase for cellulite – Upadacitinib for AD – Lisinopril for COVID-induced filler swelling Luke and Michelle report no conflicts of interest http://www.dermaspherepodcast.com

  Click here for a machine-generated transcript   AFOs (Ankle-Foot Orthotics) offer many stroke survivors freedom by letting us safely walk. They lift our affected feet as we take our steps so our toes don't drag on the ground and trip us. They give us the mobility that foot drop threatens to take. But they're not usually very attractive. And finding shoes that work with them is a challenge because they need to be bigger and wider so we can squeeze a weak foot and brace into the show. A common question I hear from survivors is, "Where can I get shoes that aren't so ugly?" Well, I don't always have great answers to that, but Lainie Ishbia does. Laine runs the Trend-Able blog and is one half of the emBRACE IT podcast. She's an expert on finding and making accessible fashion, and she joins us this week to share her story. Bio Lainie Ishbia is a blogger and podcaster helping people with invisible and visible disabilities look good and feel good. Her website at Trend-Able.com offers tips and strategies for literally and metaphorically  balancing fashion and physical needs. She develops tips for find accessible clothing options. If you can't find it, she offers tips on modifying clothes to make them work. Lainie lives with Charcot-Marie-Tooth disease. It's a hereditary, degenerative nerve condition that today impacts her hands and feet. She began wearing AFOs on each foot at age 30 and mourned the loss of sleek heels at the time. Since then, she's turned around her perspective, leveraged skills acquired through a career in social work and now helps folks with disabilities live their best lives with confidence, self esteem, and passion. You can find more details of Lainie's story here. Disability and Lifestyle Living with disability (visible or not) is a lifestyle. It shapes what we wear, the careers we pursue if able, and the social activities we pursue. And we learn so much along the way. I often say I now know way more about neurology and neuroplasticity than any marketing guy should ever know. And now I know the foot bed in a shoe may be removal. And I know there is a thing in a shoe called a foot bed. Lainie's fashion blog goes well beyond just the particulars of clothing and includes tips and strategies on how to navigate the world, like 5 Cocktail Survival Tips for Unsteady Girls or A Girlfriend's Guide to Dating with an Invisible Disability. Disability Pride Month July is Disability Pride Month. I'm a little fuzzy on the origins and scope of the celebration, but my understanding is it started in 2015 in New York City to recognize the importance of the Americans with Disabilities Act. How ought we celebrate it in 2021? It will depend largely on your personal comfort level. Don't let anyone tell you you're doing it wrong. The first thing is to recognize, accept, and believe with all your heart (original, mechanical, acquired from someone else, etc.) that there is no shame in being disabled. Say it out loud if you can. There is no shame in disability. We are people with lives to live. Sure, those lives may be different from the lives of the temporarily abled, but they are no less valuable. Second, you can celebrate disability pride by simply being visible. By being a part of the world, participating in it and taking up space in it just like any temporarily-abled person. Don't let people pretend we don't exist. Don't hide from people just because our presence makes them uncomfortable. Third, when someone talks about diversity and inclusion, make sure they are talking about disability in that, too. A diverse organization with no disabled people is not a diverse organization. Fourth, share your story with folks. You don't have to share it with the world in a podcast, blog or YouTube channel if you don't want to. But you can share it with people in your community and family.  The woman who hosted the graduation party Lainie talked about in our interview (probably) wasn't trying to keep disabled people from having a good time at the party. It's likely the challenges Lainie faced never even occurred to her. The more we tell our stories, the more people will think about accessibility. That's just a few ideas to consider. Ultimately, you can celebrate in the manner that feels most comfortable to you. If that means you walk, roll, or hobble down the street in a parade or protest, great. If it means all you can do is remind yourself there is no shame in disability, that's great, too. Disabled is not a bad word. There is no shame in it. Have a fantastic Disability Pride Month! Hack of the Week. Lainie suggests picking up (no pun intended) mini-lint-rollers, like these.* These have sticky sheets used for getting lint or pet hair off your clothes. If you struggle with manual dexterity, though, they can also be great for picking up change at a store counter. They can also be a nice solution when that pill box spills on the floor and Plaxix and Lisinopril go everywhere! "But, Bill, why wouldn't I just pick things up with my unaffected hand?" There are a few reasons. First, a toned or spastic hand can probably still hold a lint roller, and if you have some shoulder control, you can move it. One of the most important tools in recovery is to use your affected limb as much as possible in practical way. Just because it's no longer fully connected to your brain is no reason not to make it work. Second, especially when I need to get something on the floor, I often need to use my unaffected arm to balance or stabilize myself. If I get in an awkward position and my unaffected hand is busy, it's much more difficult to not fall. Everything in life can be therapy! Links Where do we go from here? Check out the Trend-Able website here and the emBRACE It podcast in your favorite podcast app. The first issue of the Strokecast Newsletter goes out this week. If you haven't already signed up you can do so at http://Strokecast.com/news Share this episode with an Occupational Therapist or someone else you care about by giving them the link http://Strokecast.com/Trends Don't get best…get better.

Ob nach einer Hyaluron Behandlung die Corona Impfung dazu führen kann, dass Schwellungen auftreten oder ob nach einer Corona Impfung eine Hyaluron Behandlung stattfinden kann, erklärt Dr. med. Robert Kasten auf Basis aktuellster Daten in diesem Video.

This week’s episode features author Emma Birks and Associate Editor Hesham Sadek as they discuss the article " Prospective Multicentre Study of Myocardial Recovery Using Left Ventricular Assist Devices (REmission from Stage D Heart Failure: RESTAGE-HF): Medium Term and Primary Endpoint Results." TRANSCRIPT BELOW: Dr. 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. Dr. Greg Hundley: And I'm Dr. Greg Hundley, associate editor, director of the Pauley Heart Center of VCU Health in Richmond, Virginia. Carolyn, our feature article this week, we're going to examine myocardial recovery using left ventricular assist devices, getting some early results from the RESTAGE-HF study. But before we jump to the feature discussion, how about we discuss some of the papers in the issue? Would you like to go first? Dr. Carolyn Lam: Yes I would. Have you thought about what's the benefit of emergent coronary angiography after resuscitation from out of hospital cardiac arrest for patients without ST elevation? It's an important question. Well, the portal study was reported by Dr. Kern from University of Arizona and colleagues, and this was designed to evaluate the efficacy and safety of early coronary angiography and to determine the prevalence of acute coronary occlusion in resuscitated out of hospital cardiac arrest in patients without ST elevation. So adult comatose survivors without ST elevation after resuscitation, were prospectively randomized to early coronary angiography versus no early coronary angiography, where early was defined as less than 120 minutes from arrival at the PCI capable facility. The primary endpoint was a composite of efficacy and safety measures, including efficacy parameters of survival to discharge favorable neurological status at discharge echo measures of left ventricular ejection fraction, more than 50% and a normal regional wall motion score within 24 hours of admission. Dr. Greg Hundley: So, lots of data here. What did they find? Dr. Carolyn Lam: So, unfortunately the study was prematurely terminated before enrolling the target numbers of patients. A total of 99 patients were enrolled from 2015 to 2018 and 49 were randomized to early coronary angiography. The primary endpoint of efficacy and safety was not different between the two groups. Early coronary angiography was not associated with any significant increase in survival or adverse events. And early coronary angiography revealed a culprit vessel in 47% with a total of 14% of patients undergoing early coronary angiography, having an acutely occluded culprit coronary artery. So while this was an underpowered study, when considered together with previous clinical trials, it does not support early coronary angiography, comatose survivors of cardiac arrest without ST elevation, whether early detection of occluded potential culprit arteries leads to interventions that improve outcomes does require additional study. And this is discussed in an editorial by Dr. Lemkes from Amsterdam university medical center. Dr. Greg Hundley: Very nice Carolyn. So at least the study that points us toward the next study that has to be performed and also does with other studies provide a little more clarity. Well, my next paper is from Professor Sanjiv Shah and--oh, wait a minute! And also from you as a co-author. Well, Carolyn, how about we have a little mini feature discussion where I can ask you some questions and then you can tell us all about your paper. Dr. Carolyn Lam: Happy to. Dr. Greg Hundley: Great. So Carolyn, what hypotheses were you testing and what was your study design and who was included in your study population? Dr. Carolyn Lam: Okay. So the question was we wanted to answer was thus a systemic pro-inflammatory state as indicated by proteomic profiling. Does that mediate the association between comorbidities and normal cardiac structure and function in HFpEF. To answer that we studied 228 patients with HFpEF from our multicenter promis HFpEF study. And these patients had 248 unique circulating proteins quantified using the old link multiplex immunoassay. Now I'm going to describe a complex analysis, but we basically had to first perform principal component analysis. And we did this to summarize 47 proteins known a priori to be involved in inflammation, and then used unbiased network analysis of all the 248 proteins to identify clusters of proteins that over-represented inflammatory pathways. We then used a mediation analysis to determine whether and to what extent inflammation mediates the association of comorbidity burdens with abnormal cardiac structure and function. And finally, we externally validated our findings in an independent cohort of 117 HFpEF cases and 30 comorbidity controls without HFpEF. Dr. Greg Hundley: Wow Carolyn, such a great design and an app machine learning mediation analyses, and then validation in an independent cohort. So tell us, what did you find? Dr. Carolyn Lam: So first, comorbidity burden was associated with abnormal cardiac function and structure and with these principle components of clusters of inflammation proteins. Second, systemic inflammation was associated with echo indicators of worse hemodynamics, like higher EDE' ratio and worse, right ventricular function. And third, inflammation indeed mediated the association between comorbidity burden and many of these echo parameters with, and I'm going to name a couple of routines. So TNF-R1, uPAR, IGFBP-7 and GDF-15 being the top individual mediating proteins. In the validation cohort inflammation was up-regulated in HFpEF compared to controls and the most prominent inflammation protein cluster identified was also the same one as in PROMIS-HFpEF. Dr. Greg Hundley: Beautiful Carolyn. So with these new proteins identified, what's the take home message here? Dr. Carolyn Lam: Here it is. Proteins involved in inflammation form a conserved network in HFpEF. And this was found across two independent cohorts. This may mediate the association between comorbidity burden and echo indicators of worst hemodynamics and right ventricular dysfunction. In totality, these findings support the comorbidity inflammation paradigm in HFpEF. Dr. Greg Hundley: Great job Carolyn, I liked the mini feature. That was so nice having one of the authors of the study here to explain kind of a two for one here, because we're going to get a feature and a mini feature. Have you got another paper you want to tell us about? Dr. Carolyn Lam: Thanks Greg and that works both ways. This next paper provides insights into the identity origin and function of many cells that make up late stage atherosclerotic lesions. It also identifies the mechanisms by which these control plucks stability. So corresponding author, Dr. Owens from Virginia School of Medicine and colleagues conducted a comprehensive single cell RNA sequencing of advanced human carotid endarterectomy samples, and compared these with murine micro dissected advanced atherosclerotic lesions with smooth muscle cell and endothelial lineage tracing to survey all plaque cell types and to rigorously determine their origins. Dr. Greg Hundley: Carolyn you know, this is another great study where we have both human subjects research and small animals. What were their results? Dr. Carolyn Lam: They provided evidence that smooth muscle cell specific knockout of transcription factors, KLF4 versus Oct-4 showed virtually opposite genomic signatures and their putative target genes played an important role, regulating smooth muscle cells phenotypic changes. They also provided evidence that smooth muscle cell derived cells within advanced mouse and human atherosclerotic lesions exhibited far greater phenotypic plasticity than generally believed, with KLF4 regulating the transition to multiple phenotypes, including LGALS 3 plus osteogenic cells likely to be detrimental for late stage atherosclerosis plaque pathogenesis. So in summary, smooth cell phenotypic switching produces cells that can be beneficial or detrimental to lesion stability and may be an important mechanism controlling the risk of unstable atherosclerotic plaque and myocardial infarction or stroke. Dr. Greg Hundley: Oh, great job, Carolyn. Well, the next paper I have is from Professor Muredach Reilly from Columbia University. And Carolyn smooth muscle cells play significant roles in atherosclerosis via phenotypic switching, a pathological process and with smooth muscle cell D differentiation, migration and trans differentiation into other cell types yet how smooth muscle cells contribute completely to the pathophysiology of atherosclerosis remain somewhat illicit. So the authors sought to reveal the trajectories of smooth muscle cell trans differentiation during atherosclerosis, and to identify molecular targets for disease therapy by combining smooth muscle cell fate mapping and single cell RNA sequencing of both mouse and human atherosclerotic plaques. Dr. Carolyn Lam: Echoing what you said earlier, Greg, both animal and human data. Terrific. So what were the results? Dr. Greg Hundley: The authors found that smooth muscle cells transitioned to an intermediate cell state during atherosclerosis, which was also found in human atherosclerotic plaques of carotid and coronary arteries. Smooth muscle cell derived intermediate cells termed stem cells were multiphoton and could differentiate into macrophage like and fibro chondrocyte like cells as well as returned towards the smooth muscle cell phenotype. Retinoic acid signaling was identified as a regulator of the transition of smooth muscle cells to stem cells and RA signaling was dysregulated in symptomatic human atherosclerosis. Finally Carolyn, human genomics revealed enrichment of genome-wide association study signals for coronary artery disease in RA signaling target gene low PSI and correlated between coronary artery disease risk levels and repressed expression of these genes. Now, activation of RA signaling by all trans retinoic acid and the anticancer drug for acute promyelocytic leukemia blocked the smooth muscle cell transition to stem cells, and that also reduced atherosclerotic burden and then promoted fibrous cap stability. So a lot of clarification of the role of smooth muscle cells, trans differentiation and the development of atherosclerotic disease Dr. Carolyn Lam: Indeed and translational implications. Interesting. Now let's review some of the other papers in this issue. Shall we? First as an, on my mind paper by Dr. Kullo on familial hypercholesterolemia, a reportable disorder. There's an exchange of letters between doctors Lazzerini and Li regarding the article autoantibody signature in cardiac arrest. Dr. Greg Hundley: Thanks Carolyn. Well, I've got a couple other papers to tell you about really a series of research letters from the mailbag. So first Daniel Modin has a Research Letter entitled “Acute COVID-19 and the Incidents of Ischemic Stroke and Acute Myocardial Infarction.” Dr. Christian Mueller has a Research Letter entitled “Effect of a Proposed Modification of the Type 1 and Type 2 Myocardial Infarction Definitions on Incidents and Prognosis.” And finally Carolyn a Research letter from Dr. Jizheng Wang involving an East Asian-specific common variant in TNNI3 that appears to predispose to hypertrophic cardiomyopathy. Well, Carolyn, what a great issue and thank you for that many feature, but how about we proceed on next to our feature discussion? Dr. Carolyn Lam: Let's go, Greg. Today's feature paper is one of those that I think is going to change clinical practice. So please listen up. It's about the RESTAGE-HF study. So pleased to have with us the first and corresponding author, Dr. Emma Birks from University of Kentucky Gill Heart and Vascular Institute, as well as our associate editor, Dr. Hesham Sadek from UT Southwestern to discuss this very important paper. Emma, could you please describe the RESTAGE heart failure study? Dr. Emma Birks: Let's say prospective study of patients getting left ventricular assist devices. So patients with very advanced heart failure are receiving left ventricular assist devices as either a bridge to transplant or as destination therapy. And they're seeing them for chronic heart failure because really all other medical therapy has failed and we use the pump to try and recover their own heart. So when the pump's implanted, we optimize the LVAD unloading, the maximum loading, and we give them a very aggressive medical therapy regime, unless they may not have tolerated these medications before because of poor blood pressure and renal dysfunction, we find they do tolerate them. So we give them in very aggressive doses and then we monitor their underlying function at regular intervals and try and promote recovery. So with that, we had done this in England in the past, in a single center study, but it had not yet been reproduced, which was obviously essential to have a bigger impact. Dr. Emma Birks: So we did a prospective study of six big US centers. We found that we've created a primary endpoint that was statistically powered in advance. And the primary endpoint was the number of patients that recovered within an 18 month period, that were explanted and remained off the pump and alive without transplant over for one year. So overall we found that of the 40 patients we recruited in the centers with chronic heart failure, we were able to explore 19. Of those that satisfied the primary endpoint, that was actually 40% of patients, with 52.3% being explanted overall. And importantly, patients were explanted in all six centers, so we found that the protocol was reproducible under the how much higher rate of recovery that you would otherwise see. Normally there is a database in the US that tracks outcomes from bad patients. And generally only 1-2% seemed to recover enough to be explanted generally. So this was a much bigger percentage. Dr. Carolyn Lam: Emma, first of all, congratulations, what an important trial and what stunning results. More than half of patients receiving that protocol were explanted. That's just remarkable. Now, could I just ask, what is it that you did that was different? I noticed you spent a lot of time saying this was an aggressive pharmacological protocol that was along with the LVAD unloading. Could you maybe elaborate on that a little bit more? Dr. Emma Birks: Yeah, I think that was a very important part of it. So generally I think when the LVAD goes in most centers, the patients are very sick, so most of those patients wouldn't then try and recover them or look at underlying functions. I think that was the first thing that was different was to try very hard. And then we had centers, the experience, I had done this before, it was also very helpful, all agreeing to do the same thing. We use a very aggressive regime of ACE inhibitors, Beta blockers, auto serotonin antagonists and ARBs. And that was also an unusual thing. We use the fact that they're supported with the pump to use both an ACE and an ARB together, but the idea that they have better blood flow in the cranial is way more tolerant and we give very high doses. So we use Lisinopril with the target dose of 40 milligrams, Coreg with a target dose of 50 BID, Aldactone 25 milligrams daily. Dr. Emma Birks: And then we add in losartan if they tolerate it and actually aim for 150 milligrams daily, so those doses are very high. And I think not normally given to people on LVADs. So you must've had the LVAD that don't tolerate the medical therapy and stop it. They might just have blood pressure control, etc. There is now also another INTERMACS trial, a sort of big study that's come out that actually shows benefit of neurohormonal antagonists in general. So that goes together with our study to show that they should already be given and then the regular testing. So we had quite thorough testing. So first of all, we do echos on the pump and then we do echos with the LVAD turned down to a speed at which is not contributing. So we do that and we do an echo at five minutes with it down 15 minutes, and then we walk the patient, distress them. Once we show that the hearts come down in size and improved function, then we do an exercise test, right heart cath on an off pump to look at the hemodynamics. Dr. Carolyn Lam: Wow. So tremendous effort and really the protocol is unique in and of itself, not just the pharmacological therapy, also the way this is monitored and decisions are made really, really amazing. Just one last question for me, because it's a humbling reminder of the importance of neurohormonal blockade in these patients. Do you continue that after they're explanted? Dr. Emma Birks: Yes, we do. And we continue aggressively and that's slightly different as well in that normally you wouldn't give a patient a nascent an up of course, but given that they've already tolerated it on the pump in that same patient. So we restart the same drug regime afterwards, and we actually like to get them to quite along that dosage before we discharge them from the XPLAN, we don't want to do that slowly. We get them back on it quite quickly. And then we follow them very carefully because we don't really know the long-term durability. Dr. Carolyn Lam: Wow, thank you. Hesham. I would love your thoughts on this paper. I mean, it really, really is remarkable results. Dr. Hesham Sadek: Yeah. I mean, I was very happy that we received this paper to review, frankly I've been following that work for a long time since the first new England paper that came out and I'd like to congratulate you for an amazing work. I think this will change the field. First, how was this trial different from the first trial, other than the fact that it's multicenter, what would you say are the major changes that you made to the protocol and what you've learned since the first trial? Dr. Emma Birks: Yes, you're absolutely right. We did make some changes. So first of all, it was six sites instead of one site. I think it was very important to reproduce it in the US but we changed the protocol itself as well. The first trial had optimization of the LVAD speed, really just by echo looking at the reduction in the ventricle size. It had the aggressive medical regime was very similar except this time we increased the Losartan dose from 100 to 150 after the Hill's trial came out. The testing was very frequent in the original English Sheffield study, probably a little bit too frequent to be able to be adopted on a wide scale. So we tried to reduce it down a little bit. So we decrease the frequency of the low-speed echos. I think we had them at six weeks, four months, six months, nine months in a year. Dr. Emma Birks: And after that, we saw if they were already improving and started and only did them at a year to 18 months, if they were improving. And then we also cut down the number of exercise tests. So we didn't do the exercise test until the echo was already showing significant improvement. For two reasons, one, we didn't find it very reliable and two, it was just too much testing for the patient. So it was more of a confirmatory test. In fact, it wasn't a requisite for a pump explantation. We didn't do a left heart catheter, which we did before. Previously we tried to measure LVEDP, this time we decided which was enough. So we just did a right heart cath on and off pump. And we did that once the echo was improved as well. So we rationalized that a little bit. And then the other important thing was before in hayfield study, once we saw the ventricular size come down and injection fraction start to improve, we actually added in Clenbuterol, which was a Beta-2 agonist. Dr. Emma Birks: And the idea with that was to cause a kind of physiological hypertrophy so that when you took the pump out, the heart didn't just dilate. We were worried about atrophy at the heart on the pump long-term. So we did that to try and improve the durability of recovery. So the reason we left off this time was really the previous protocol was very good, but was very complicated. So we wanted to see what rate of recovery we could get just with the aggressive reverse remodeling, neurohormonal drugs, plus the aggressive testing and the optimum loading with the idea that later on, we could add on either Clenbuterol or something later to improve the durability of recovery, if the ability of recovery is not good enough, but actually so far it's proven to be pretty good because the study itself takes quite a long time. It was sort of to recruit them. We had an 18 month period than the follow-ups. It was already a multi-year study. So we wanted to establish a regime that many centers could use to try and promote recovery. Dr. Hesham Sadek: I want to follow up on that last point, because as you know, I've looked at some of these Heights as well in our center, and we looked at the results with you and Stavros and others. So the myocytes size is expected to change, decrease with unloading, right with sufficient unloading. So how would you prepare the Myocardium to take on the normal afterload if you are not going to induce by a beta agonist, for example, Dr. Emma Birks: What I would like to do in the future is try using the pump itself actually. Sometimes there's heart recovers, the heart shrinks and actually start opening their own valve and working in the heart. Of course, when you have the HeartMate one, actually, sometimes wasn't synchronous with the heart. So sometimes the heart will beat against the pump anyway. Once you go to the continuous flow pumps, you've got continuous unloading. So I think it'd be very interesting to intermittently turn down the pump speed and load the heart to work it before you take the pump out. So I would really like to do that. I think that might be the next interesting phase of the study to improve your ability to.. So I guess once you've got maximum reverse remodeling and improvement in function, you could just turn the pump speed down to let the valve open. Dr. Hesham Sadek: Do you think perhaps if you do that, you will increase the percentage of patients that can be explanted? Do you think that could be a factor in the percentage of patient that can be explained? Dr. Emma Birks: I think it might be, it might more improve the, to your ability to make sure we have for a long, good echo function afterwards. Dr. Hesham Sadek: That's great. So another question this was limited to not ischemic cardiomyopathy patients. Can you elaborate a bit on why not include, for example, revascularized ischemic cardiomyopathy patients. Dr. Emma Birks: Yeah, so we did that really just because we didn't want to change too much from the original protocol. We also stuck with one device because we thought if you have multiple pumps, multiple diagnosis, it does get hard to analyze in a multicenter trial. So we did that on purpose and we were always trying to simulate the bridge to transplant population in the age group too. But actually interestingly, most of the patients recruited in the trial were destination therapy patients in the end. Dr. Emma Birks: I think this could be done with ischemic cardiomyopathy. I think we don't have enough data on ischemic cardiomyopathy to know whether it does or it doesn't recover. So I don't think our results say that it's only known as ischemics. I think it just means we haven't studied ischemics sufficiently. Logically they might have more scarred. It might be harder to get such a good percentage to recover. I think all of us in our individual centers have seen a few and we've sort of seen the on pump echo improved, and we've tested them and then taken some out. But most of these cases are anecdotal. So I think that is another important study that needs to be done, obviously a large group of patients. Dr. Hesham Sadek: I agree. So given that they're not ischemic cardiomyopathy, do you know how many of them had genetic testing or what is the percentage of monogenic cardiomyopathys or how do you think these patients would respond to this protocol? Dr. Emma Birks: But if you had a familiar history and actually found it didn't make any difference, whether they recovered or not. I think some of us have personally seen actually those were the familial cardiomyopathy tend to recover more actually again, anecdotally. We published a people before looking at the Titin gene saying that that did recover. I think actually only five of these patients, 12% of them had a family history, but some of them recovered Dr. Hesham Sadek: One final question, as you know, I'm a basic scientist. So ultimately the question I'm going to ask, what do you think the mechanism is? Is it that these hearts are just in a vicious cycle of remodeling and validation, increased pressure, and you were sort of giving it a chance for actual structural reverse remodeling where you changed the geometry of the myocardium and perhaps rest of myocardium, allow for improvement of calcium cycling dynamics, or do you think, is something more exciting? Like three-generation for example. Dr. Emma Birks: Yeah, that's very interesting because I think the LVAD doesn't unload, so it shrinks the ventricles. I think it does improve the geometry and the dynamics. And then you use the drugs where they may have felt before you almost put them from class four, heart failure into class three with the bad to give that chance to work again. And then I think various cellular and fibrotic factors have been looked at and it's hard because there was so many factors have been looked at that. You were going to find some that go up and some that go down and what's important. But the impression I get overall is that you do get improvement, the matrix limits, the recovery on the fibrosis and the matrix. Whereas you do get improvements of myocardial function and cellular function. The cells will tend to reverse the dysfunction and it's really whether that happens or not. It's probably limited a lot by the matrix Dr. Carolyn Lam: That is amazing here. Hesham, I'm going to put you on the spot. Do you have your own hypothesis about this Dr. Hesham Sadek: Based on the work that they did initially in the new England paper, we did actually a small pathology study looking at cell cycle of cardiomyocytes from the core samples and from the explanted hearts post-transplant and we saw evidence of increased cardiomyocytes cell cycle in these patients along with decreased DNA damage and some metabolic remodeling as well with mitochondria. So, you can't really tell much from tissue whether you regenerated it or not, but as you know myocytes don't divide and this is the basis for the lack of spontaneous regeneration of the myocardium. So if this in fact removes the block to cardiomyocyte cell cycle, then this might be a regenerative therapy mechanism. Dr. Carolyn Lam: Well, this is amazing. I wish we had all day to discuss this more. I mean, this is the only place you can get a discussion that goes from clinical to basic signs and back to clinical. Thank you so much, Emma and Hesham for sharing today. Thank you audience for joining us today. You've been listening to circulation on the run on behalf of Greg as well. Don't forget to tune in again next week. Speaker 1: Program is copyright the American heart association, 2020.  

This episode of Drug Cards Daily is on the drug lisinopril. The name brands are Zestril, Prinivil, Qbrelis (Solution). Lisinopril is an Angiotensin-Converting Enzyme (ACE) inhibitor that is most known for treatment of hypertension. Other indications are for heart failure and ST-elevation myocardial infarction. Tablets come in a variety of doses. Initial dosing for hypertension begins at 5-10 mg once daily and is evaluated every 4-5 weeks. The dose is then doubled with the goal of 40 mg/day is achieved or until the patient's tolerance is reached. This drug is not metabolized with any unused unchanged drug being excreted through the urine. The hallmark side effect to watch for is cough. Other side effects are syncope, chest pain, headache, and change in the sense of smell. This drug is not to be used if the patient is or may be pregnant due to fetal toxicity. 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

Have you been trying to keep up with the medical literature, but its eat out to help out, and nothing is getting in the way of 50% your favourite pizza joint?In this months episode:..How to use D-dimers to diagnose cerebral venous thrombosis...(04:17)Heldner, Mirjam R et al. “Prediction of cerebral venous thrombosis with a new clinical score and D-dimer levels.” Neurology vol. 95,7 (2020): e898-e909. doi:10.1212/WNL.0000000000009998...Do we still need metronidazole for pneumonia?...(07:13) Marin-Corral, Judith et al. “Aspiration risk factors, microbiology and empiric antibiotics for patients hospitalized with community-acquired pneumonia.” Chest, S0012-3692(20)31905-X. 17 Jul. 2020, doi:10.1016/j.chest.2020.06.079...Ambulatory pneumothorax management...(09:45) Hallifax, Rob J et al. “Ambulatory management of primary spontaneous pneumothorax: an open-label, randomised controlled trial.” Lancet (London, England) vol. 396,10243 (2020): 39-49. doi:10.1016/S0140-6736(20)31043-6...SIADH management: more to it than just fluid restriction?... (16:37)Krisanapan, Pajaree et al. “Efficacy of Furosemide, Oral Sodium Chloride, and Fluid Restriction for Treatment of Syndrome of Inappropriate Antidiuresis (SIAD): An Open-label Randomized Controlled Study (The EFFUSE-FLUID Trial).” American journal of kidney diseases : the official journal of the National Kidney Foundation vol. 76,2 (2020): 203-212. doi:10.1053/j.ajkd.2019.11.012...How harmful are steroid bursts?... (22:15)Yao, Tsung-Chieh et al. “Association Between Oral Corticosteroid Bursts and Severe Adverse Events : A Nationwide Population-Based Cohort Study.” Annals of internal medicine vol. 173,5 (2020): 325-330. doi:10.7326/M20-0432...Candesartan's role in cognitive decline... (25:11)Hajjar, Ihab et al. “Effects of Candesartan vs Lisinopril on Neurocognitive Function in Older Adults With Executive Mild Cognitive Impairment: A Randomized Clinical Trial.” JAMA network open vol. 3,8 e2012252. 3 Aug. 2020, doi:10.1001/jamanetworkopen.2020.12252...Weight loss: when do you go hunting for cancer?... (29:16)Nicholson, Brian D et al. “Prioritising primary care patients with unexpected weight loss for cancer investigation: diagnostic accuracy study.” BMJ (Clinical research ed.) vol. 370 m2651. 13 Aug. 2020, doi:10.1136/bmj.m2651...Baloxavir: the antiviral no ones talking about...yet...(33:15)Ikematsu, Hideyuki et al. “Baloxavir Marboxil for Prophylaxis against Influenza in Household Contacts.” The New England journal of medicine vol. 383,4 (2020): 309-320. doi:10.1056/NEJMoa1915341...Is race/ethnicity a factor in physician burnout?... (29:16)Garcia, Luis C et al. “Burnout, Depression, Career Satisfaction, and Work-Life Integration by Physician Race/Ethnicity.” JAMA network open vol. 3,8 e2012762. 3 Aug. 2020, doi:10.1001/jamanetworkopen.2020.12762

This week on the pod we look at results from a COVID-19 prevention trial of hydroxychloroquine; A vaccine arrival date prediction by Dr Fauci; A FDA notification regarding vial caps; A look into prescription patterns during COVID-19; And an antibody treatment trial begins. 

Damon Young is writer, critic, humorist, satirist, and professional Black person. He's a co-founder and editor in chief of VerySmartBrothas -- coined "the blackest thing that ever happened to the internet" by The Washington Post -- and a columnist for GQ. Damon's writing -- which vacillates from anthropological satire and absurdist racial insights to razor sharp cultural critique and unflinching indictments of privilege and bias -- has often generated praise from from his peers. Ava DuVernay called his voice "clear and critical." Michael Eric Dyson said he's "one of the most important young voices in humor writing today." And Kiese Laymon called his work "the best of American twenty-first century writing." Damon's debut memoir -- What Doesn't Kill You Makes You Blacker: A Memoir In Essays (Ecco/HarperCollins) -- is a tragicomic exploration of the angsts, anxieties, and absurdities of existing while black in America, and won Barnes & Noble's 2019 Discover Award. It was also longlisted for the PEN America Diamonstein-Spielvogel Award, nominated for an NAACP Image Award, and is a Krause Essay Prize nominee. NPR, which named it one of the best books of 2019, called it an "outstanding collection of nonfiction." Damon currently resides in Pittsburgh's Northside, with his wife, two children, and his faithful bottles of Nexium and Lisinopril. Find Damon on social media: @damonyoungvsb @verysmartbros and @damonyoungvsb (twitter) damonjyoung.com ----- DiDi Delgado is creating change (unapologetically). http://linktr.ee/thedididelgado https://thedididelgado.com/ --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/the-full-set-podcast/support

Lisinopril is an ace-inhibitor blood pressure medication that lowers blood pressure, and it is used to protect your kidneys. It is also used in heart failure and after a heart attack. Captopril, enalapril, fosinopril and other medications that end in "pril" have similar effects and side effects as lisinopril.Cough is one of the most aggravating things that most patients complain of when taking lisinopril.But lisinopril can cause a life-threatening side effect called angioedema. Dr. Tonya explains both and shares suggestions to avoid these two side effects. She also tells you about the ace inhibitor losartan.In light of the Coronavirus pandemic, I will highlight experts who will give updated information on lisinopril (Ace inhibitors) and the potential for worsening COVID-19 symptoms on hypertensioresistanttotreatment.com. The short answer is that no one knows the answer to this question at this time. Read the American College of Cardiology and leading researchers recommendations at hypertensioresistanttotreatment.com.Ready, let’s do this!For more information about Lisinopril side effects go to https://www.mayoclinic.org/drugs-supplements/lisinopril-oral-route/side-effects/drg-20069129View the video about Epipen administration and storage at https://hypertensionresistanttotreatment.com/what-about-lisinopril-losartan-may-be-best-if-you-african-american/About the host: Dr. Tonya is a clinical research scientist at the University of Alabama at Birmingham, Alabama, where she holds various positions. She spent the past decade studying home blood pressure monitoring and tracking, medication adherence, readiness, and confidence to change lifestyle behaviors. She is the author of six first-authored publications in scientific journals. She has collaborated with her colleagues on three published studies with the finding from the landmark Systolic Blood Pressure Intervention (SPRINT) Trial. You can read her peer-reviewed research studies at https://www.ncbi.nlm.nih.gov/pubmed/?term=TONYA+BREAUX-SHROPSHIRE.About the podcast: Dr. Tonya has created this blog and podcast for everyday people to learn what everybody ought to know about hypertension. Uncontrolled hypertension is a leading cause of stroke, kidney failure, heart attack, congestive heart failure, and other poor cardiovascular outcomes. Before you can take control of your health and health care costs, you have to invest your time in learning what you ought to know about hypertension. Hit the subscribe button to get upcoming episodes immediately when released. Share Hypertension Resistant to Treatment blog and podcast with any one person who would benefit from it.If you enjoyed the podcast, please consider leaving a 5-star rating and leave a short review below.Voiceover Intro and soon to be outro done by Mr. Willie Breaux, Jr.Song: Forget Your Feet; Artist: Tayler Watts; Licensed to YouTube by Epidemic Sound; Epidemic Sound PublishingDisclaimer: This podcast is for information purposes only and should not be used as medical advice. It is for educational purposes only and was not intended to replace medical advice. Dr. Tonya has provided this content based on her research training and clinical and research knowledge. Consult your health care provider for medical advice and treatment and

Jave is treating a patient in cardiac rehabilitation who is taking Spironolactone, Lisinopril, and Aricept. The physical therapist is challenged with determining the most appropriate action when viewing possible abnormalities on an EKG. How good are you at reading EKG's? Let's test your skills in this excellent episode about EKG reading. Are you looking for an awesome cheatsheet that reviews the facts to know about lower extremity EKG interpretation? Look no further: https://www.kylericeprep.com/EKG2 Do you want all of the cheatsheets in one place: https://www.kylericeprep.com/nptecheatsheetdrive Click to listen now: iTunes:http://bit.ly/NPTECLINICALFILES Libsyn: http://bit.ly/LIBSYNFILES Did you get this question wrong?! If you were stuck between two answers and selected the wrong one, then you need to visit www.DestroytheNPTE.com, to learn about the #1 solution to STOP getting stuck.

In this Live Friday CME Series recap, Dr. Todd Holcomb, an Internist and hospitalist with Lakeview Clinic and Ridgeview Medical Center, presents an interesting Internal Medicine case that is sure to scratch some heads, and remind us of the need to go back to the beginning, if it's not making sense after several attempts. Dr. Holcomb is accompanied by cardiologist Dr. Joshua Buckler, with Minneapolis Heart Institute, Dr. Jonathan Larson, family physician at Lakeview Clinic, Dr. Carl Dean, nephrologist with Kidney Specialists of Minnesota, and Dr. David Gross, radiologist with Consulting Radiologists.  So put on your thinking caps, listen closely and ask yourself what you would do as Dr. Holcomb guides us through this interesting case. Enjoy the podcast! OBJECTIVES:    Upon completion of this podcast, participants should be able to: Identify secondary causes of hypertension. Identify when further testing is warranted. Discuss newer treatments available for cholesterol related conditions. CME credit is only offered to Ridgeview Providers for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org.   CLICK ON THE FOLLOWING LINK FOR YOUR CME CREDIT: CME Evaluation: "2019 Internal Medicine Case Conference" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition.   FACULTY DISCLOSURE ANNOUNCEMENT  It is our intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: PART 1: Alright, let's break down the first portion of this case discussion. This is a 60 yo male with chest pain for over a year. Intermittent aching and burning in right anterior chest, worse with activity and lately has worsened overall with a stressful job and strong family hx of heart disease. General exam ins unremarkable. ECG normal. HDL is 60 and LDL slightly up at 137. PFTs and CXR are normal.  Stress echo is normal.  Cardiology referral results in a low Ca++ score but some plaque in the LAD. Dr. Buckler, the cardiologist, feels this is ischemic heart disease until proven otherwise. Therefore, a coronary angiogram is necessary. Imaging has its limitations, as do stress tests. When the history still doesn't point in another explicable direction, we must follow the logic and most likely etiology, which is till coronary artery disease and ACS. One of the problems with stress tests in general, is there are limitations inherent. It's hard to miss the big stuff, but the more minor findings can be missed. With a high pretest probability, he could have perhaps gone straight to angio. In this case, though, he was started on a statin and aspirin. Per Dr. Buckler, Imdur could also have been given. Two year later, he comes in with headaches in the same area of the head since his wife recently passed away. He takes Advil for this. BP has been elevated at home. Dr. Jonathan Larson, family physician, questions the type of headache, it's location and possible etiologies. Is the Advil causing rebound headaches or contributing to the headaches? The elevated home blood pressures also need further investigation. His kidney function is temporarily normal. NSAIDs are d/c'd and Lisinopril is started. A month later, the headaches have improved. BP improved, but not tremendously. In addition, his chest pain has gone away. A new antihypertensive, a combo HCTZ/Lisinopril regimen is started. Although Amlodipine would have been a reasonable choice. A year later, he returns with the same chest pain on exertion. Normal ECG. Normal renal function too. He now goes back to a CT angiogram showing multi-vessel disease. Per Dr. Buckler, one of the reasons he has worsened on a statin is that we may have limited understanding of his pathology, or potentially the CTA was not accurate the first time. Virtual FFT now can show the flow and how significant the lesion is, which is an advancement in this technology. Unfortunately, despite aggressive lipid therapy, sometimes people progress. A few days after the CTA, his Creatinine goes up a bit and GFR goes to 43. This is also after years of Lisinopril. Dr. Carl Dean comments on this alteration in renal function. He feels this is not entirely unexpected, but the data doesn't really reflect CIN (contrast induced nephropathy). Yet intuitively and experientially, we sometimes see this. The amount of contrast used is significantly more on a CTA than on an invasive angio. At this point, the ACE inhibitor is held and Amlodipine is started. Renal function now has improved. The angiogram demonstrates significant 3 vessel disease, with good downstream targets. The SYNTAX surgical risk score directs the cardiologist toward CABG instead of PCI. Post angio, he develops some lower extremity edema, and he is discontinues on Amlodipine, resumed on the HCTZ, Lisinopril. The creatinine is now 2.4. Did he receive enough fluids for the angiogram? Or was the few hundred cc's he obtained during the angio okay? Again, hindsight is 20/20, but the data doesn't support a causality for AKI due to CIN, nor is there a true preventable measure, including n-acetylcysteine or bicarbonate. Perhaps, in this case, CIN as a possibility in the past as discussed, that many would not argue with overhydrating. Ultimately it was felt the ACE and contrast contributed to his creatinine elevation. The ACE combo is now stopped and he is started on Hydralazine and Metoprolol. Creatinine improves, and he goes into CABG surgery. He is discharged and he continues on aspirin and Plavix for 3 months, and Carvedilol and Hydralazine. Atorvastatin is increased to 80 mg daily, a more aggressive dose. EF is normal on echo.  Do statins affect kidney function positively or negatively? According to Dr. Dean, there is no trial that supports either. His BP starts to increase, and Lisinopril is once again added, along with an increase of creatinine, and the ACE is again d/c'd. HCTZ was added. Then spironolactone for ongoing HTN. He's still running high though. Labetalol is replacing carvedilol now. And the pressure is still running high. What is happening here? What to do next? Do we try Lisinopril again? It is attempted, and he once again fails the creatinine test. It goes up again. PART 2: What we do now for this patient? It seems he can only improve on Lisinopril for blood pressure, but his creatinine continues to go up. According to Dr. Dean, in this patient, Lisinopril may not be a great option going forward, not only due to creatinine increase, but it will not help him in terms of mortality outcome. renal artery stenosis is a concern in this case. Dr. Tara McMichael interjects the question, could a loop diuretic have been tried? With a creatinine of 2.3, a loop diuretic could have been an option, since volume and sodium retention could be contributing to the hypertension. Isosorbide with hydralazine is also an option if more meds were to be added. Per Dr. Buckler, however, a four drug regimen that is poorly controlling blood pressure doesn't necessarily indicate adding a fifth drug. We need to know if there is a secondary cause of HTN. Sometimes, even in the setting of renal artery stenosis, patients still require significant anti-HTN drug regimens. Also, per Dr. Dean, the pretest probability in this type of patient for renal artery disease is high. And will an intervention be desirable if it is found? The ASTRAL trial demonstrated no improvement in outcomes. The CORAL trial was also done and considered to be a negative trial. One of the trial criticisms though was that it didn't include patients with severe enough disease. According to Dr. Dean, refractory hypertension should cause screening for this and an intervention should be done if it is seen.  Our patient has a renal u/s that shows bilateral RAS. Dr. David Gross, radiologist discussed the results of the MRA. The aorta, SMA and celiac trunk show atherosclerosis. The renal arteries are paired bilaterally. They have moderate to high grade narrowing of the arteries. Dr. Buckler asks the question of the safety of gadolinium in renal disease. In the setting of low GFR, in other words, less than 30, the risk for nephrogenic systemic fibrosis exists, although very rare. This is usually fatal, though. Basically, he has 4 out of 4 arteries occluded. Dr. Dean feels referral to a center of excellence for this unique issue is best for the patient. He undergoes transaortic endarterectomy, as his creatinine is rapidly going up. A significant plaque is resected from the aorta which was extending into the renal arteries. Post-procedure, he is placed on metoprolol, requiring nothing further. Rosuvastatin, Zetia and baby aspirin is started. Basically, unclogging the pipes resulted in a cure. And a while later, he's no longer on any antihypertensives. Blood pressures are great now. LDL now 57 on the new cholesterol meds. Zetia has limited data, but the PcsK9 inhibitor and his LDL is now 1. Dr. Buckler states there is a lot of unknowns about the LDL levels and whether there is a point of diminishing returns, but the science is not there yet. In this case, Dr. Buckler feels that stopping the Zetia and continuing the pcksk9 inhibitor makes sense. PART 3: Renovascular HTN is more commonly found in the setting of acute, severe, refractory, very high blood pressure. Work-up is needed when there is a strong possibility of secondary cause, and in the absence of another secondary cause, like pheochromocytoma or hyperaldosteronism. Also in an acute rise in BP, a young age, elevated Cr after starting an ace inhibitor, etc. Renal asymmetry on imaging and flash pulmonary edema are other clues. If Cr and BP are stable in the setting of stenosis, no intervention is indicated. Testing can potentially worsen function, as can the interventions performed to treat the disease. Who benefits most? People with short term hx of HTN, people who fail optimal medical therapy, not tolerating medical therapy and progressive renal failure. Ultrasound and CTA or MRA are the options for work-up. US is cheaper, but time consuming and operator dependent, with modest sensitivity/specificity. CTA is accurate for atherosclerosis. Highly sensitive and better if GFR below 30. MRA is highly sens/spec. Gadolinium complications can ensue in low GFR situations. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9) will lower LDL up to 60%. 50% decease in stroke and MI risk. The PCSK9 enzyme binds to liver LDL receptors and thereby increases plasma LDL levels. so inhibiting this enzyme leads to a lower LDL level. These inhibitors also can decrease triglycerides, increase HDL somewhat and decrease the volume of atheroma. Low adverse effects are noted with the med as well. Regarding renovascular HTN, Dr. Dean also reminds us that someone who is significantly older with chronic renal ischemia in the setting of this disease, may not have improvement in renal function even after intervention. Therefore, some of these patients who suddenly reperfuse a chronically ischemic kidney may actually worsen. Renal artery stenosis is also not an absolute contraindication for ACE. Such as in low EF heart failure. If the creatinine markedly rises, it can be discontinued again. Fibromuscular dysplasia patients, unlike atherosclerosis patients, should all receive an intervention. This is more commonly found in younger patients. Dr. Buckler addresses the ease of use and cost of the PCSK9 inhibitors. It turns out the cost is high at this point, up to $14k/year. But coverage has shown promise in FH and refractory high LDL. As it was alluded to by Dr. Holcomb, the patient really doesn't exercise and has a very stressful job, as it turns out. His dies wasn't discussed. Was he managing his risk factors very well? What does that mean nowadays? We have potent medications and skillful intervention options for reacting to this sort of pathology nowadays, but where are we at with prevention? Hopefully a conversation for another day.

See all the Healthcast at https://www.biobalancehealth.com/healthcast-blog/ Erectile Dysfunction is a difficulty that many if not most men experience as they age. Often when this begins to happen in their lives, men go to their doctor and ask for the “little Blue Pill” (Viagra or its variants). What we are going to discuss this week is what you need to know about your health and lifestyle choices that may help you not need medicine to restore your erectile quality. We want to talk about several examples of things that we know that contribute to the problem of ED in men and how simple changes can improve your condition without the requirement to see a physician and to obtain medications. Usually when men come to BioBalance Health to see Dr. Maupin they often expect that testosterone pellets will solve their ED problems. While testosterone does help restore libido and can help with erections, it is the last step in the journey not the first. For many men the first step is to check your blood pressure. If you are on Lisinopril it lowers the blood pressure in the pelvis and that will negatively impact your erections. This drug and others like it are called ACE inhibitors. They are among the most common forms of blood pressure medicines. Dr. Maupin will encourage you to discuss with your doctor whether or not moving away from ACE inhibitors and into another blood pressure regulator may help you with your erection concerns, and still regulate your blood pressure. Your doctor will tell you that you have to look at your lifestyle: what is your caffeine intake? What is your weight? How much do you exercise? How much stress are you under?  Your answer to these questions will help you figure out where you need to make changes that may solve your problem without medicines. Medicines will help you if you need them, but if you can change your lifestyle, you may no longer need the medicines. It is better to be in shape and lower your stress and watch what you eat than to take these meds which may have negative side effects. Have these conversations with your doctor, ask them about anti inflammatory meds, ACE inhibitors, Beta Blockers, and ask about side effects. Your doctor may not think to speak to you about sexual side effects for these medicines. If they are of concern to you, then bring it up in the conversation with your doctor. Your doctor should be able to talk to you about work arounds that will help you limit the adverse impact of the medicines and of the ED. You are an important participant in your own health care. Be aware, be involved, and be informed.

Commentary by Dr. Valentin Fuster

This episode was originally supposed to be a simple topic discussion between my student and me. We ended up recording it as a podcast episode that will hopefully serve as a quick review of material that has been covered in other episodes. The patient case that we discussed during the episode: 63 y/o female with diabetes, HFrEF, hypertension. Medications: A1c = 8.9% HFrEF – EF = 30% BP = 154/84 mmHg Glargine-Lantus insulin 36 U QAM Pioglitazone 45 mg Lisinopril 10 mg HCTZ 25 mg QAM Metoprolol tartrate 50 mg BID Carvedilol 25mg BID Doxazosin 4 mg daily  èSTOP  Simvastatin 20 mg She presents for pharmacotherapy management   If you have any questions, reach out to us on any of the following: Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com Instagram and other social media platforms - @corconsultrx This podcast reviews current evidence-based medicine and pharmacy treatment options. This podcast is intended to be used for educational purposes only and is intended for healthcare professionals and students. This podcast is not for patients and not intended as advice or treatment.  

In addition to the three main classes of anti-hypertensives we already discussed, ACE Inhibitors like Lisinopril and Captopril, Beta Blockers like Metoprolol and Propranolol, and Calcium Channel Blockers like Nicardipine and Diltiazem, there are a number of other classes of… The post Cardiac Labs and Meds for Nurses appeared first on NURSING.com.

In the episode, I break down the pharmacology of lisinopril (and all ACE inhibitors).  I also outline common adverse effects, drug interactions and its role in managing hypertension.  Hope you enjoy the show and please feel free to reach out with feedback! All subscribers to the website/podcast will get access to a FREE Top 200 Drug Study Guide where I highlight the 3 most highly testable pearls from each medication (this is a 31 page PDF!)  In addition, you'll get a free 100 question pharmacology test.  Both resources are free, simply for following the podcast!  What are you waiting for? Click Here to Subscribe

2018 Medicare Part D Prescription Drug Cost Sharing It's October folks! Medicare season has begun! As of October 1st, licensed health insurance agents may begin speaking about 2018 Medicare Advantage Plans and stand-alone prescription drug plans. If you have a relationship with a licensed health insurance agent, Medicare Specialist or Medicare Consultant, they will more than likely start contacting you about your current plan. This is the time to discuss your concerns with your Medicare Specialist. You need to determine if all your prescription drugs are listed in the plan's 2018 formulary.  You also need to determine what your 2018 monthly costs will be for all your prescription medications. Ask yourself......."Have my out-of-pocket prescription drugs costs remained feasible on my current plan for 2018?" If so..... that's great! If not, it may be time to take a look at a new stand-alone-prescription drug plan. If you're on a Medicare Advantage Drug Plan, you will need to determine if your physicians are still in your plan's network and if your medical out-of-pocket costs are reasonable before you make any decisions. It is important to remember........ Medicare Specialists cannot take an enrollment application from you .......BEFORE October 15th! That is a Medicare Regulation!  If a Medicare licensed agent tries to take a signed application from you PRIOR to October 15th....... FIND A NEW AGENT! As a reminder........ NO ONE from Medicare will be knocking on your door or CALL you on the phone. Medicare will send you mail from the Social Security Administration ONLY! Any post cards or any letters with a return address from anywhere else on this Earth other than the Social Security Administration........ is not from MEDICARE!  It is most likely a solicitation from an Insurance Agent trying to get your business. Throw it out! Ok......let's take a look at the 2018 changes to Part D Prescription Drug Plans. Annual Deductible  The 2018 Maximum PDP Annual Deductible is $405.00. That's an increase of $5.00 from $400.00 in 2017. Starting January 1st of 2018....... if you are on a Medicare Advantage Prescription Drug Plan or Stand-Alone-Prescription Drug Plan...... that has a annual deductible, you will fit in one of two categories: 1. You will need to pay your annual deductible right away        prior to your plan's benefits kicking-in.  As of January 1, 2018, when you hand in a prescription for a listed drug on your plan's formulary, you will be expected to pay the full cost of that drug or the listed annual prescription deductible, whichever is less. For example, your stand-alone prescription drug plan has an annual prescription deductible of $405 on all tiers. You hand in your first prescription for lisinopril, which is listed as a Tier 1 on your plan's formulary. The listed      co-pay for a Tier 1 drug on your plan is $2.00. The total cost for a 30 day supply of lisinopril at your preferred pharmacy is $100.00. Since you have a $405.00 deductible, the cost for the 30 day supply of lisinopril  at $100.00 would be a lower out-of-pocket cost than the full $405.00 deductible. Therefore, you pay the $100.00 and deduct that amount from the $405.00 annual deductible, leaving you with a balance of $305.00. You will pay $100.00 for February, March and April for your lisinopril and in May you will pay the remaining balance of your deductible, which is $5.00. Then, your prescription drug benefits will kick in and you will also pay your $2.00 co-pay. Beginning in June, you will pay a $2.00 co-pay for your lisinopril for the remainder of the year.                                      OR 2. You will pay the annual deductible if and when you            "trigger" the deductible. As an example, You would trigger the annual deductible if you requested a prescription for a drug that was a Tier 3, Tier 4 or Tier 5 on your Medicare Advantage Drug Plan or Stand-Alone Prescription Drug Plan. If you requested a drug that was a Tier 1 or Tier 2 on that same plan, you would NOT "trigger" the annual deductible. Therefore, you would just pay the listed co-pay or co-insurance for that Tier 1 or Tier 2 prescription drug on your plan. So.....as we used lisinopril in the above example, in this case you would just pay your $2.00 co-pay for the 30 day supply of lisinopril starting right away in January. This is because lisinopril is listed as a Tier 1 drug on your plan's formulary. You wouldn't pay an annual deductible, since you haven't requested a prescription that was a Tier 3, Tier 4 or Tier 5 drug. You will continue to pay a $2.00 co-pay for your lisinopril for the remainder of 2018. The next portion of cost-sharing under prescription drug plans is called the Initial Coverage Period (ICP) During this portion of cost-sharing, the total amount spent during the Initial Coverage Period (ICP) is $3,750.00. The costs of covered drugs are shared - 25% by the beneficiary and 75% by the plan. If you do not have an annual deductible for prescription coverage, the maximum a beneficiary would spend out of pocket during the ICP is $937.50. The plan would pay the remaining balance, which is $2,812.50 ($3,750.00 - $2,812.50 = $937.50) You pay your co-pays and/or co-insurance, which is placed towards the $937.50. The plan pays the remaining balance of the Medicare negotiated price for the prescription, which is applied towards the $2,812.50. Once the total amount of your prescription drug costs (from your out of pocket costs and the plan's contributions) reach $3,750.00, you move into the next phase of cost-sharing. The next phase of Part D cost-sharing is called, The Coverage Gap, or commonly known as the "Donut Hole." During this phase, you will pay more for your prescription drugs. You will pay 35% for Brand name drugs and 44% for Generic drugs. Let's use Lisinopril again to look at the costs during the Donut Hole.  We stated a 30 day supply of Lisinopril from a preferred pharmacy is $100.00. Lisinopril is a generic drug, listed as a Tier 1 on your plan. In the Donut Hole, you are required to pay 44% of the Medicare negotiated price for Generics. In this example, you would pay $44.00 for a 30 day supply of Lisinopril in the Donut Hole. You are also paying a "Dispensing Fee," (about $1-$3 per drug) while in the Donut Hole. If you have a Brand prescription drug that is listed on a Tier 3, Tier 4 or Tier 5 on your plan, you will pay 35% of the Medicare negotiated price, while in the Donut Hole. Only True out-of-pocket (TrOOP) costs are counted toward the cost-sharing amount in the Donut Hole. TrOOP costs are - 1. The drug costs paid by the beneficiary 2. A 50% discount on Brand-Name drugs that is provided by the drug manufacturer. Payments made by the "plan" during the Donut Hole on Brand Name drugs DO NOT count toward TrOOP. If you DO have an annual deductible for your prescription drug coverage, the amount you pay out-of-pocket for your deductible is applied towards the ICP of $3,750.00. The maximum amount you would pay out-of-pocket during the Donut Hole portion of cost-sharing is $3,758.75 If the total cost-sharing amount reaches $3,758.75 in the Donut Hole phase, you will then move into the final phase of cost-sharing for 2018, which is called the "Catastrophic Stage." In the Catastrophic Stage, you will pay reduced co-pays and or co-insurance. You will pay either: A 5% co-insurance or a $3.35 co-pay for Generic drugs or a $8.35 co-pay for Brand drugs. You will pay whichever amount is greater. Let's use our example of Lisinopril one more time. With a total cost of Lisinopril being $100.00, a 5% co-insurance would be $5.00. With $5.00 being greater than $3.35 for Generic drugs, you would pay $5.00 for the 30 day supply of Lisinopril. You will remain in the "Catastrophic Phase" until January 1, 2019, when the slate is wiped clean and we start all over again.   I hope that answers your questions regarding changes to Prescription Drug Costs for 2018. If you have a question, and I can answer it in ONE paragraph or less, send me an email to - Support@TheMedicareNation.com I'll be happy to answer your question. If my answer requires more than one paragraph, or I need to research an answer....... you will need to hire me as a consultant to assist you. Go to this link and request a consultation from the "contact" tab. www.TheMedicareNation.com That's it for this week's show! I would love for you to rate & review Medicare Nation! Go to this link and tell me what you think!  https://goo.gl/sb3JXo   Have a happy, peaceful and prosperous week everyone!  

Medications and prescriptions Metformin is used with a proper diet and exercise program and possibly with other medications to control high blood sugar. It is used in patients with type 2 diabetes. Controlling high blood sugar helps prevent kidney damage, blindness, nerve problems, loss of limbs, and sexual function problems. Proper control of diabetes may also lessen your risk of a heart attack or stroke. Metformin works by helping to restore your body's proper response to the insulin you naturally produce. It also decreases the amount of sugar that your liver makes and that your stomach/intestines absorb. OTHER USES: This section contains uses of this drug that are not listed in the approved professional labeling for the drug but that may be prescribed by your health care professional. Use this drug for a condition that is listed in this section only if it has been so prescribed by your health care professional...   Lisinopril is used to treat high blood pressure. Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. It is also used to treat heart failure and to improve survival after a heart attack. Lisinopril belongs to a class of drugs known as ACE inhibitors. It works by relaxing blood vessels so blood can flow more easily. OTHER USES: This section contains uses of this drug that are not listed in the approved professional labeling for the drug but that may be prescribed by your health care professional. Use this drug for a condition that is listed in this section only if it has been so prescribed by your health care professional. This medication may also be used to help protect the kidneys from harm due to diabetes...

The post Lisinopril (Prinivil ) appeared first on NURSING.com.

Guest: Jill Rafael-Fortney, PhD, Department of Molecular and Cellular Biochemistry, The Ohio State University Access an abstract of this month’s featured research article: Early Treatment with Lisinopril and Spironolactone Preserves Cardiac and Skeletal Muscle in Duchenne Muscular Dystrophy Mice. Circulation. 2011 Aug 2;124(5):582-8.

Guest: Jill Rafael-Fortney, PhD, Department of Molecular and Cellular Biochemistry, The Ohio State University Access an abstract of this month’s featured research article: Early Treatment with Lisinopril and Spironolactone Preserves Cardiac and Skeletal Muscle in Duchenne Muscular Dystrophy Mice. Circulation. 2011 Aug 2;124(5):582-8.