Podcasts about Losartan

Today's sponsor is Freed AI! Freed's AI medical scribe listens, transcribes, and writes notes for you. Over 15,000 healthcare professionals use Freed and you should too! Learn more here! Clopidogrel (Plavix) is an antiplatelet medication. You need to understand the pharmacokinetics of clopidogrel and how CYP2C19 affects this medication. Doxycycline is a tetracycline antibiotic. Calcium, iron, and other metal cations can bind doxycycline and reduce the absorption of the medication. Hyzaar is a combination of losartan and hydrochlorothiazide. Losartan is an ARB and hydrochlorothiazide is a thiazide diuretic. Kytril (granisetron) is an antiemetic medication. It is from the same class of medication as the more commonly used ondansetron. Restoril (temazepam) is a benzodiazepine. It is primarily used to treat insomnia as it has a much shorter half-life than many of the other benzodiazepines.

In this episode, I divide losartan and Cozaar into syllables, tell you which syllables to emphasize, and share my sources. The written pronunciations can be helpful, so you can see them below and in the show notes on thepharmacistsvoice.com.   The purpose of my pronunciation episodes is to provide the intended pronunciations of drug names from reliable sources so you feel more confident saying them and less frustrated learning them.    Losartan = loe-SAR-tan, emphasize SAR (source: USP Dictionary Online)   Cozaar = CO-zar, emphasize CO (patient information on Organon's website)   If you know someone who needs to learn how to say losartan and Cozaar, please share this episode with them. Subscribe to/follow this podcast for all future episodes.    Thank you for listening to episode 272 of The Pharmacist's Voice ® Podcast!   To read the FULL show notes, visit https://www.thepharmacistsvoice.com.  Click the Podcast tab, and select episode 272.   Subscribe to or follow The Pharmacist's Voice ® Podcast to get each new episode delivered to your podcast player and YouTube every time a new one comes out!     Apple Podcasts   https://apple.co/42yqXOG  Spotify  https://spoti.fi/3qAk3uY  Amazon/Audible  https://adbl.co/43tM45P YouTube https://bit.ly/43Rnrjt   Links from this episode USP Dictionary Online (aka “USAN”)  **Subscription-based resource USP Dictionary's (USAN) pronunciation guide (Free resource on the American Medical Association's website) Patient Information for Cozaar ® via Organon's website accessed April 1, 2024 The Pharmacist's Voice Podcast Episode 269, pronunciation series episode 28 (tirzepatide) The Pharmacist's Voice Podcast Episode 267, pronunciation series episode 27 (atorvastatin)  The Pharmacist's Voice Podcast Episode 265, pronunciation series episode 26 (omeprazole) The Pharmacist's Voice Podcast Episode 263, pronunciation series episode 25 (PDE-5 inhibitors) The Pharmacist's Voice Podcast Episode 259, pronunciation series episode 24 (ketorolac) The Pharmacist's Voice ® Podcast episode 254, pronunciation series episode 23 (Paxlovid) The Pharmacist's Voice ® Podcast episode 250, pronunciation series episode 22 (metformin/Glucophage) The Pharmacist's Voice Podcast ® episode 245, pronunciation series episode 21 (naltrexone/Vivitrol) The Pharmacist's Voice ® Podcast episode 240, pronunciation series episode 20 (levalbuterol) The Pharmacist's Voice ® Podcast episode 236, pronunciation series episode 19 (phentermine)  The Pharmacist's Voice ® Podcast episode 228, pronunciation series episode 18 (ezetimibe) The Pharmacist's Voice ® Podcast episode 219, pronunciation series episode 17 (semaglutide) The Pharmacist's Voice ® Podcast episode 215, pronunciation series episode 16 (mifepristone and misoprostol) The Pharmacist's Voice ® Podcast episode 211, pronunciation series episode 15 (Humira®) The Pharmacist's Voice ® Podcast episode 202, pronunciation series episode 14 (SMZ-TMP) The Pharmacist's Voice ® Podcast episode 198, pronunciation series episode 13 (carisoprodol) The Pharmacist's Voice ® Podcast episode 194, pronunciation series episode 12 (tianeptine) The Pharmacist's Voice ® Podcast episode 188, pronunciation series episode 11 (insulin icodec)  The Pharmacist's Voice ® Podcast episode 184, pronunciation series episode 10 (phenytoin and isotretinoin) The Pharmacist's Voice ® Podcast episode 180, pronunciation series episode 9 Apretude® (cabotegravir) The Pharmacist's Voice ® Podcast episode 177, pronunciation series episode 8 (metoprolol)  The Pharmacist's Voice ® Podcast episode 164, pronunciation series episode 7 (levetiracetam) The Pharmacist's Voice ® Podcast episode 159, pronunciation series episode 6 (talimogene laherparepvec or T-VEC)  The Pharmacist's Voice ® Podcast episode 155, pronunciation series episode 5 Trulicity® (dulaglutide)  The Pharmacist's Voice ® Podcast episode 148, pronunciation series episode 4 Besponsa® (inotuzumab ozogamicin) The Pharmacist's Voice ® Podcast episode 142, pronunciation series episode 3 Zolmitriptan and Zokinvy The Pharmacist's Voice ® Podcast episode 138, pronunciation series episode 2 Molnupiravir and Taltz The Pharmacist's Voice ® Podcast episode 134, pronunciation series episode 1 Eszopiclone and Qulipta

Below is the patient case information: 63-year-old white male. Problem List Bipolar II disorder Insomnia Epilepsy (tonic-clonic seizures) Dyslipidemia/hypertriglyceridemia Hypertension Recent weight gain History of hyponatremia  Diabetes type 2(controlled) Medications Clonazepam 2 mg QHS Risperdal 2 mg twice daily Carbamazepine 200 mg twice daily Divalproex DR 500 mg three times daily Levetiracetam 1000 mg twice daily Losartan 100 mg daily HCTZ 25 mg daily Atorvastatin 40 mg daily Fenofibrate 48 mg daily Metformin ER 500 mg twice daily Vitals: Blood pressure is currently 144/86 mmHg Lipids: LDL-C: 98 Triglycerides: 245 (down from 423 4 months ago) CMP: Na+: 133 K+: 4.1 eGFR: 95 All others WNL as well CBC: Hgb: 10:1 g/dL MCV: 73 Ferritin: 17 A1c: 6.9% Current Appointment The patient has seen multiple neuro and psych providers over the last year.  The R­­isperdal and divalproex were for the bipolar II disorder. The patient is experiencing depression symptoms. His family notes that he has also been uncharacteristically aggressive lately and becomes agitated over minor issues. His family has recently noticed that while talking with him, his face is grimacing, his tongue will randomly protrude from his lips, as well as other facial movements. The clonazepam for insomnia. It helped with insomnia symptoms for a few weeks, but the symptoms are back to pre-treatment baseline. He was taking clonazepam 1 mg 2 hours prior to bed and zopidem 5 mg 30 minutes prior to bedtime. He didn't feel like the zolpidem was working. The clonazepam was increased to 2 mg and the zolpidem was DC'd. He is also complaining of daytime fatigue He was recently hospitalized due to hyponatremia. The carbamazepine and levetiracetam were for seizure control. However, the patient has experienced multiple seizures per month for at least the last 3 months. Needs better blood pressure and triglyceride control Thanks for listening! We want to give a big thanks to our main sponsor Pyrls. Try out their drug information app today. Visit the website below for a free trial: www.pyrls.com/corconsultrx If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. You can find our account at the website below:  www.patreon.com/corconsultrx If you have any questions for Cole or me, reach out to us on any of the following: Text - 415-943-6116 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.

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

Dr. Dan Regan discusses his OutSmarting Osteosarcoma funded work on Focal Adhesion Kinase (FAK) inhibition to improve losartan-sunitinib immunotherapy in metastatic osteosarcoma. - Dr. Dan Regan is an Assistant Professor at the Flint Animal Cancer Center at Colorado State University and he is one of our OutSmarting Osteosarcoma 2022 grant recipients. Dr. Regan received his DVM degree from the University of Georgia and subsequently completed his residency training in veterinary anatomic pathology and PhD in the Department of Microbiology, Immunology, and Pathology (MIP) at Colorado State University. In 2018 he joined the Flint Animal Cancer Center and MIP in the College of Veterinary Medicine and Biomedical Sciences at Colorado State University. The focus of Dr. Regan's laboratory is to increase our understanding of the interplay between the immune system and (non-immune) tumor stroma, and how these compartments of the tumor microenvironment promote metastasis as well as respond to and mediate extrinsic mechanisms of resistance to anti-cancer therapy. To investigate this area of cancer biology, his laboratory utilizes a combination of in vitro 3-dimensional tumor co-culture models and animal models, focusing on breast and bone cancer (osteosarcoma). Dr. Regan also has a strong interest in comparative oncology and leveraging naturally occurring cancers in dogs as both a surrogate and intermediary model to evaluate and validate his laboratory's investigations into the tumor microenvironment. In collaboration with the laboratory of Dr. Steve Dow, his lab conducted immunotherapy clinical studies in dogs with spontaneous osteosarcoma and these study results have led to a phase I clinical trial in children with osteosarcoma. His lab's continued long-term research goal is to fully elucidate the mechanisms by which tumors prime non-malignant host stromal cells of distant organs to promote their metastasis and chemo-resistance, in order to identify novel targets for host-directed stromal therapies which “poison the soil” for effective combination with conventional tumor cell targeted drugs. --- What We Do at MIB Agents: PROGRAMS: ✨ End-of-Life MISSIONS ✨ Gamer Agents ✨ Agent Writers ✨ Prayer Agents ✨ Healing Hearts - Bereaved Parent Support ✨ Ambassador Agents - Peer Support ✨ Warrior Mail ✨ Young Adult Survivorship Support Group ✨ EDUCATION for physicians, researchers and families: ✨ OsteoBites, weekly webinar & podcast with thought leaders and innovators in Osteosarcoma ✨ MIB Book: Osteosarcoma: From our Families to Yours ✨ RESEARCH: Annual MIB FACTOR Research Conference ✨ Funding $100,000 annually for OS research ✨ MIB Testing & Research Directory ✨ The Osteosarcoma Project partner with Broad Institute of MIT and Harvard ... Kids are still dying with 40+ year old treatments. Help us MakeItBetter.

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/LosartanCozaarNursingConsiderations      Generic Name losartan Trade Name Cozaar Indication hypertension, DM neuropathy, CHF Action inhibits vasoconstrictive properties of angiotensin II Therapeutic Class antihypertensives Pharmacologic Class angiotensin II receptor antagonist Nursing Considerations • may cause hypotension, tacycardia, angiodema, hyperkalemia • may increase digoxin levels • assess blood pressure and heart rate • assess fluid levels • monitor daily weights with CHF • monitor renal and liver • instruct patient on how to take blood pressure

On this episode, I discuss losartan pharmacology, adverse effects, drug interactions, and appropriate monitoring. Losartan is an ARB and can increase potassium levels. Keep an eye out for medications like spironolactone and trimethoprim which can increase this risk further. Losartan has been shown to lower uric acid levels which could potentially be helpful in patients with gout. Monitoring renal function is very important with losartan. The risk of ARF goes significantly higher when used with NSAIDs or diuretics.

Methylphenidate Trade – Concerta Use – ADHDEstradiol Trade – Climara Use – Menopaus Losartan Potasium Trade – CozaarUse – High cholesterol 

Hyzaar is the brand name for the combination of losartan and hydrochlorothiazide (HCTZ). It comes as a tablet in several strengths (losartan/HCTZ): 100 mg/25 mg, 100 mg/12.5 mg, and 50 mg/12.5 mg. The indications are for hypertension and for the prevention of stroke. Dosing is generally initiated at 50 mg/12.5 mg PO qd but if the patient has severe hypertension it is initiated at higher strengths. There is a Black Box Warning for fetal toxicity and the medication should not be used or discontinued immediately if pregnancy is detected or suspected. The most common side effects are dizziness, cough, and dyspepsia. The serious side effects are renal failure, acute angle-closure glaucoma, and non-melanoma skin cancer. Amazon Affiliate link: https://amzn.to/31OkKVe for NAPLEX Math Review: The Foundation of a Logical NAPLEX Prep Strategy. FREE Drug Card Sheet is available for this episode at DrugCardsDaily.com along with ALL past FREE drug card sheets! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on most all socials @drugcardsdaily or send an email to contact.drugcardsdaily@gmail.com to leave feedback, request a drug, or say hello! DISCLAIMER: This content may contain sponsored content or the use of affiliate links. Partnerships, sponsorships, and the use of affiliate links provide monetary commissions for Drug Cards Daily at no cost to you! This is done in order to keep providing as much free content to everyone that comes to Drug Cards Daily. Thanks for your support! Drug Cards Daily provides drug information for educational and entertainment use. The information provided is not intended to be a sole source of drug information that is to be acted upon for patient care. If there are drug-related patient care concerns please contact your primary care Physician or local Pharmacist. --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

Is There a Recall on Losartan, Ibersartan, or Valsartan? How to Find Out and What to Consider. Thanks for listening!Small-sized validated blood pressure cuff 9-17 inches here. Regular-sized validated blood pressure cuff 13-17 inches here; Large-sized validated blood pressure cuff up to 16.5 to 21.25 inches here. Extra-large validated large cuff up to 16.5-23.6 inches click here.Need a list of validated blood pressure monitors? click here.Click this link if you need a telehealth appointment with a certified medical doctor: https://text2md.com/******Vitamin D HOME TESTING KIT here (Deficiency is less than 30 ng/ml and Optimal=50-60 ng/ml for the general public, ask your doctor what's good for you.) ******COVID-19 HOME TESTING KIT here How to use the COVID-19 HOME TESTING KIT here****Ask your doctor if you would benefit from any of the following vitamins or supplements that could potentially reduce severe COVID symptoms:Vitamin C with rose hips, Zinc, D3 & K2, Magnesium or this one, B complex, Elderberry, Probiotic or this one, Melatonin, *Quercetin, Braggs Nutritional Yeast, Apple Cider Vinegar, and NAC.*Quercetin may be contraindicated in people with thyroid disease. Ask your doctor and get a TSH, FREE  T3  & T4 , and aTPO before use.****Best thermometer2nd best thermometerAn accurate Pulse oximeter (If you have COVID-19, seek medical help if less than 95% at rest after 1 minute, which could mean you have pneumonia)****Hi, I'm Dr. Tonya Breaux-Shropshire, a clinical research scientist.  I spent the past decade studying hypertension management. I am the author of six first-authored publications in scientific journals. You can read my work HERE.****Would love to hear from you! Send me a comment or question at this link (click here).****Copyright Disclaimer under section 107 of the Copyright Act 1976, allowance is made for “fair use” for purposes such as criticism, comment, news reporting, teaching, scholarship, education, and research.****Royalty-free music: Turn on My Swag 2 Intro by Mr. Willie Breaux****Disclaimer: This podcast is for educational purposes only and not intended to replace medical advice. Affiliate links support the podcast at no cost to you. Thanks for your support!

In this episode Jonathan Rosenfeld chats with Martin D. Gould an Attorney at Romanucci & Blandin, LLC. Here, they discuss: Zantac Lawsuits Update   Read the Transcript Download the PDF Jonathan Rosenfeld : Hi, I am Jonathan Rosenfeld and I am an attorney, and I am with my good friend and colleague Marty Gould today. We are here to talk about probably one of the largest and most prolific drug recalls in the United States ever, certainly in recent history, and that involves the popular heartburn medication Zantac. Jonathan Rosenfeld : Marty is very active with the Zantac litigation, and he is here today to discuss the status of the litigation who qualifies for this and to sort of give us some insight as to how these cases may play out. Jonathan Rosenfeld : Marty, first off, thank you for joining me today. I appreciate it, and could you just briefly introduce yourself, and let us know a little bit about the background and just what Zantac is and bring us up to date with the current status of the recall on Zantac? Marty Gould: John, thanks for the introduction. I'm of counsel with Rosenfeld Injury Lawyers. Our team represents hundreds and hundreds of individuals that have cancer that we believe was caused by a Zantac consumption or generic. Zantac was a very popular heartburn and acid reflux medication. Marty Gould: Millions and millions of people have used Zantac for those purposes, and recent studies have shown that there's a connection between an ingredient in Zantac, ranitidine, and cancer. It's the chemical structure of the Zantac tablet that once it's consumed, and once it's mixed with water in your body, it causes what's called NDMA, a very toxic substance that is linked to cancer. Marty Gould: For that reason, people that have been taking Zantac, many of these people for years and years on a frequent basis, are now getting cancer. Typically, it's a stomach cancer, bladder cancer, stomach cancer, but also the blood-based cancers such as liver cancer. Right now, there's a litigation that's being handled, a multi-district litigation, where all the Zantac cases are being filed in the Southern District of Florida. Marty Gould: Anyone who has a case, they're filing their claims there, and the lawyers are litigating those cases now. We're still in the earlier stages, and there's trials that are expected to start going in probably 2022. Jonathan Rosenfeld : Now, you mentioned that these cases are filed in what's called a multi-district litigation or MDL. I want to talk with you about the differences between an MDL that some people may not be familiar with and a traditional lawsuit. First off, I guess, as a starting point, I guess, what is an MDL case? Marty Gould: Sure. Multi-district litigation is essentially a type of case where all the cases may be a little bit different, so if you've been taking Zantac for one year, several times a week, and somebody else has been taking Zantac for 10 years on a daily basis, you may have a different type of case because your exposure was different. If you have a family history of cancer, that may be a relevant facts. Marty Gould: Everyone's case is a little bit different. Everyone's injuries are a little different. Some people tragically are filing a case on behalf of a loved one who's deceased, who has died because of cancer linked to Zantac. Others may just have an early diagnosis, so the injuries are different every case. Marty Gould: A multi-district litigation, essentially, consolidates all the different cases into one courtroom for efficiency purposes. It's typically done in a federal courthouse. In this case, it's a federal courthouse in the Southern District of Florida. Marty Gould: To avoid having rulings in many different states, in many different jurisdictions that could be conflicting, you'll have one judge who will oversee the litigation. Will set various deadlines, and essentially, the cases are litigated in a fashion where there's bellwether cases. The steering committee that's litigating most of these cases will choose a certain number of cases, that will be the first cases to be litigated, the first cases to go to trial. Marty Gould: Once these bellwether cases are concluded, that usually allows the rest of the plaintiffs to know what the potential value of these zantac cases are, and it usually drives settlements. If there's successful results at trial, it usually results in a settlement agreements or settlement discussions on other people that have cancer that was linked to Zantac. Jonathan Rosenfeld : Right now, we have this MDL that's been filed in Florida, but we also have a recall that was issued by the food and Drug Administration, the FDA, related to Zantac, and that would happen in 2000... I'm sorry, in September 13, 2019, the FDA issued that recall. Why, I guess, did the FDA issued this recall, and what is the impact that you see in terms of the recall on the pending litigation? Marty Gould: There are studies going back to the '80s that linked NDMA and Zantac to cancer, and as of late, because lawsuits were filed, the US Food and Drug Administration started its own investigation, and September 13, 2019, they essentially published a public warning about the link. There was additional research and lab testing. Marty Gould: The levels of NDMA found were significantly higher than which was deemed to be safe for a body to consume, certainly very alarming. The FDA certainly announced that this was a potential health hazard. Marty Gould: In the wake of the FDA safety warnings, the drug manufacturers for Zantac and its generic brands pulled off the drug from shelves across the country. Walmart, Walgreens, CVS, many of the big retailers pulled the drug because the consensus was it wasn't safe to be consumed. Marty Gould: The unfortunate reality is that, while people now aren't being exposed to Zantac and the cancer-causing substances within the tablets, we still have thousands and thousands of people that have been using Zantac for years and have existing injuries. That's what these cases are about. It's about compensating people for their past harms and for their current harms. Jonathan Rosenfeld : Let me ask you this, so you mentioned that, first off, Zantac has been on the market since the 1980s, so this has been on the market for a long time. I guess as a consequence of the patents are on the original drug expiring, now we have different manufacturers and generic versions of this that were on the market. Is that correct? Marty Gould: That's correct. You had various drug manufacturers that were producing Zantac or a generic version of it, ranitidine, Sanofi, GlaxoSmithKline, [Oringer 00:09:03], and the claims are essentially falling into two categories, defective design or manufacturer of that drug, that it was defective. It was harmful. It shouldn't have been sold to the public in the first place. Marty Gould: The second part of that is the failure to warn consumers, because people are taking these drugs because the advertisements are saying, look, this is a safe drug, and I can remember some of the Zantac commercials. They had somebody with a fire extinguisher, and he's using it and it's, "Hey, this is going to extinguish your heartburn and your acid reflux. It's a safe drug to use." That was the message, and that wasn't the case. Marty Gould: I think through the discovery process, we'll get more specifics. When did these drug manufacturers first know that it wasn't harmful? If there's studies out there from the '80s saying that there was that potential harmful cancer-causing link, there's good reason to believe that the manufacturers had that information, and because they were selling it to millions and millions of consumers, they didn't act on that information. Jonathan Rosenfeld : I guess at this point, if you took Zantac or the generic equivalent, first off, does it make any difference in terms of pursuing a legal claim? In other words, if I took Zantac manufactured by Sanofi or by Glaxo, does it make any difference in terms of my legal rights, in terms of filing a lawsuit at this point? Marty Gould: Well, John, as you know, we represent hundreds and hundreds of plaintiffs who have used either the name brand or the generic. There are legal differences, and that's why I think it's important for people to speak with a lawyer to understand what the potential legal ramifications are if you were only consuming a generic, but there's a few things to keep in mind. Marty Gould: When we sign a case, the first thing we tell people is, for one, do you have any Zantac in the house? Do you have any ranitidine in the house? Were you prescribed it? We've had many clients that still have the bottle, preserved the bottle. That's going to be evidence in the case. It's something we certainly want to hold on to. Marty Gould: Then, I guess, the next part of that is proving the use of the drug, medical records. Some people were prescribed it. Other people maybe, because it was sold over the counter, weren't prescribed it, but had reported to other primary care physician or other doctors when they were asked, are you on any drugs prescribed or over counter? They mentioned Zantac. Marty Gould: Those are some things to keep in mind, but there is a difference in terms of the cases, if it's generic versus name brand. That's why it's important to speak to a lawyer about that. Jonathan Rosenfeld : Now, these cases are filed, and they're pending in this MDL in Southern District of Florida. Can you give us a little insight as to how these cases are handled in terms of an MDL, what the court really does to sort of get a grasp of these cases? Jonathan Rosenfeld : We have people from really all over the country who have been impacted and what the court is doing in terms of unifying these cases and getting a grasp as to how people have been impacted. Logistically, it seems like a little bit of a nightmare to have all these different people and all these different cases and everything else. Jonathan Rosenfeld : As a person who has been impacted, either individually or if I have a family member who may have been impacted, and I'm looking at this and saying like, oh boy, do I even want to get involved? Can you just give some insight as to what a plaintiff could expect if they were to get involved with the case? Marty Gould: Sure. Step one is, we have an internal questionnaire that we have potential clients fill out, which asks a lot of the questions that the court is going to want to know, the type of cancer the individual has, when they used the drug, how often they use it, are they still using it, and that's essentially the information that we're going to have to submit to the court. Marty Gould: Judge Rosenberg from the Southern District of Florida, the federal judge who's overseeing the case, has essentially issued a questionnaire. It's called a census plus form that all claimants have to complete and file in the Zantac case. Those questions are the questions that we have our clients answer, when they used it, how often, for how long, what's their diagnosis. Marty Gould: From there, that allows the court, the defense and the lawyers, to have a better idea of each individual's claim. It provides a basis to verify the claims and make sure that the ones we have are legitimate claims that we can ideally get compensation for. Marty Gould: With that, there may be a second phase to the case, where after the census plus form is submitted, we may have a more detailed questionnaire that we have to submit to the court, sometimes with you attached medical records, verifying your cancer diagnosis and any medical records that list Zantac as a drug that you use, whether it was prescribed, or perhaps you referenced it to a doctor. Marty Gould: That's not the only way you can prove use. Your testimony is evidence, so many people don't keep receipts. Maybe they didn't tell their doctors they're taking it because it's over the counter. You can still have a case, even if you don't have that. Your testimony is evidence. If you have family members that knew you were taking it, their witnesses, they can provide evidence. Marty Gould: There's many ways in which we go about proving your use and litigating your case. It starts with that initial intake to find out whether you meet the certain criteria that we believe would put you in a position to file a claim. Jonathan Rosenfeld : Now, before you even get to the point where you're filing a claim, I guess the first step is, hey, are you eligible? When I'm talking about eligible, I'm talking about the timeframe for bringing a case. Every single case is governed by a statute of limitations, and the statute of limitations in these cases, it varies by where the person lives. Is that correct? Marty Gould: That's correct. Even though there is a multi-district litigation in Florida, that doesn't mean that Florida law is controlling here. Every case, every claim in every client's case can be a little bit different, because you're applying laws often from that state in which the individual had experienced the harm, where they were consuming the Zantac. Marty Gould: If you were consuming the Zantac while you were living in Illinois and then you were diagnosed with cancer, and then you move to Michigan or Florida, the law that would apply in terms of the statute of limitations would likely be Illinois law, but every case is a little bit different. It's important to speak with a lawyer to help you find out whether there's an issue with the statute limitations. Marty Gould: With cases against drug companies, such as this or Roundup or Losartan, many people have consumed the drug decades earlier, and they consumed it for a long period of time. It's not like being in a car accident where if you were hit by a car, you knew that you were injured the day of the accident. There is a period of time, a latency period, where you may not be diagnosed with cancer. Marty Gould: It's the worst news to get. It's a very traumatic situation, but you may not get that diagnosis until 10 years after you had been taking Zantac. There's something called the discovery rule in many states, a point in time where you discovered that you were injured and discovered why you were injured. That could trigger the running of the statute of limitations. Marty Gould: Every case is a little bit different, but if you had consumed it a long time ago, that may not close the door to pursue a case, and you should certainly call lawyer and find out if you still can. Jonathan Rosenfeld : Interesting. One of the ancillary issues here is we have a whole nother group of potential plaintiffs who may have taken Zantac or the generic equivalent, and they may have developed a cancer and they may have have died from that cancer. Jonathan Rosenfeld : In those situations, can the family of the deceased pursue a claim at this point? Can they pursue a wrongful death claim if their loved one took Zantac in the past? They may not have been aware of the connection between their cancer and the NDMA in Zantac. Marty Gould: In many cases, you can. A family can file a wrongful death case on behalf of a loved one who was taking Zantac and, unfortunately, died of cancer. There's still the same process is involved, where we file a census plus form. We try and retrieve as many of the medical records as we can, although you can still pursue it. Marty Gould: Then there's also something to note is, sometimes, because we're dealing with cancer cases, we have clients that file lawsuits while they're still alive, and then tragically, they died during litigation. The family can then step in and pursue that litigation for the loss of that loved one, for the wrongful death and survival damages. Marty Gould: Courts recognize the sad reality that many claimants may not survive to see the under this case or really any of these cases, and because of that, in some of those circumstances, we can fight to have a deposition of the individual before they pass away. It varies from case to case, and it varies in terms of the health of the plaintiff. Marty Gould: But it's certainly something we've done in many cases where we've taken a deposition of our client before he passed away, and judges understand that, and the defense attorneys understand that. Then they're sensitive to the situation and the emotional difficulties surrounding giving testimony in that circumstance. Jonathan Rosenfeld : Now these, the pending Zantac cases, they're civil lawsuits, and I want to talk with you about damages in a case like this. Now you and I, we don't have a crystal ball. We have no way of anticipating how these cases may play out. There's still a lot of evidence that needs to be disclosed by all parties involved, but obviously, when you file a civil lawsuit, your sole recourse really is to get economic compensation. Jonathan Rosenfeld : Obviously, we have no way of predicting the value of these cases, but can you just talk through the available damages in a civil case, such as Zantac, where someone at home may be thinking, well, I don't know if it's worth bringing a case. It may not be that much, which I hear pretty consistently. Can you just sort of explain the potential damages available in these cases? Marty Gould: Yes. We're talking about cancer lawsuits here. The damages are catastrophic. It's the worst news for anybody to hear that they were diagnosed with cancer, and we're also talking about a case where the allegation is that these drug manufacturers were creating a drug that was dangerous, was cancer-causing. Marty Gould: People were consuming this, and it was essentially like putting gunpowder and a fuse in somebody's body. It was being lit once it's mixed with water and other substances within your body and causing a very toxic cancer-causing substance, NDMA. The types of recoveries in a situation like that, where somebody's wrongful conduct caused somebody else to get cancer, in some cases to die. Marty Gould: You can get what's called loss of consortium. The family can get a recovery and survival claim, family can get a recovery for the loss of love, the loss of having that person around, pain and suffering for when the person was alive, emotional trauma, emotional distress, economic damages, lost income that the person could have earned, past and future lost income. If they weren't able to work for a period of time, because of the cancer treatment. Marty Gould: You can also get punitive damages in these cases. At this stage, we don't know yet whether we will, but there's certainly going, in many of these cases, we do get punitive damages. Those are additional damages, which can be significant, as a way to punish the drug manufacturers if they in fact knew about the harms and didn't warn people, or didn't take the necessary actions to protect the consumers. Jonathan Rosenfeld : Well, it certainly seems like these are cases which really are going to be an emerging area of litigation. I really appreciate you sharing your insight with us. Jonathan Rosenfeld : If someone is sitting on the sideline, sitting at home, is there anything you would tell them to do at this point in terms of moving forward? If they're sitting on the sideline and they're a little hesitant at this point, do you have any suggestions for them? Marty Gould: They should immediately contact a lawyer to understand their rights, because they don't have to make a decision whether they want to file a claim or not just yet. But they should understand are there any deadlines that could apply to them, is there any statute limitations that may be expiring soon, and speak with a lawyer and find out what their rights are and also whether they have a potential claim. Marty Gould: Maybe they don't, but it would probably give them some peace of mind to know that they had asked the lawyer. They had spoken to a lawyer, and they did not meet the criteria, but you don't want to sit around and do nothing if there's a chance that your Zantac consumption did cause serious injuries up to and including cancer. Marty Gould: If you were taking Zantac for a long period of time and you don't have cancer, you should still be monitoring their health. I would speak to a doctor about it, just to get their opinions on whether you are at risk, and more importantly, to make sure that you don't take any other substances like Zantac that have this toxic substance, and that you switched to alternative drugs that are safer for heartburn or acid reflux. Jonathan Rosenfeld : This is great information, Marty. I really appreciate you sharing your expertise with us today. I look forward to talking with you about this again as these cases proceed towards trial. Thanks again, and I'm going to put your contact information in our show notes, but we appreciate your time. Thank you.

This week, your hosts Steve Lowry and Yvonne Godfrey interview Adam Slater of Mazie Slater Katz & Freeman (https://www.mazieslater.com/).   Remember to rate and review GTP in iTunes: Click Here To Rate and Review   Episode Details: New Jersey trial lawyer Adam Slater of Mazie Slater Katz & Freeman shares how he successfully represented Mary McGinnis, a 70-year-old woman who underwent numerous surgeries after C.R. Bard's defective transvaginal mesh products eroded within her body, causing chronic inflammation, severe pain, and debilitating physical injuries. In March 2009, Mary's doctor implanted the Avaulta Solo and Align TO mesh products to treat her pelvic prolapse. Due to recurrent mesh erosion, Mary later endured multiple mesh removal surgeries and a complex vaginal wall reconstruction. Today, she still suffers from severe pain and is unable to sit comfortably or be intimate with her husband. Despite the defense's attempts to blame Mary's pain on pre-existing medical issues or her surgeon's techniques, a Bergen County, New Jersey jury found that the Avaulta Solo and Align TO were defective in its design, and that Bard failed to warn of the defects, and awarded $33 million in compensatory damages to Mary and her husband, Thomas.  In a separate punitive damages phase, Attorney Adam Slater obtained a punitive damages award of an additional $35 million against Bard.. Click Here to Read/Download the Complete Trial Documents   Guest Bio: Adam Slater Adam Slater is certified as a civil trial attorney by the Supreme Court of New Jersey, and a partner in the law firm of Mazie Slater Katz & Freeman, LLC in Roseland, New Jersey.  Mr. Slater specializes in the handling of complex civil litigation including product liability, malpractice, catastrophic injury cases, class actions, and mass litigations. He has obtained many jury verdicts and settlements in excess of $1 million, with a number in the nine figures.  He also has argued appeals in the New Jersey Supreme Court, New Jersey Appellate Division, and the Third Circuit Court of Appeals, in his own cases and as Amicus, with numerous published decisions. Mr. Slater also has been appointed as lead counsel in numerous mass torts and class actions, including for example the coordinated litigation of more than 10,000 pelvic mesh cases against Johnson & Johnson, Ethicon, and C.R. Bard in New Jersey State Court, the In Re Benicar Federal MDL in the District of New Jersey which resulted in a global settlement for $358 million, the In Re Valsartan, Losartan, and Irbesartan Federal MDL in the District of New Jersey, the New Jersey State Court consolidation of the Allergan breast implant litigation, and a member of the Executive Committee for the Federal MDL of the Allergan breast implant litigation, Federal class actions against Volkswagen and Audi for breach of warranty (settlement with $84 million value), and a Federal class action against Sanofi-Aventis, on behalf of a class of pharmaceutical sales representatives. Mr. Slater filed the first pelvic mesh case in the country against Ethicon, Inc. and Johnson & Johnson in early 2008, and he was lead trial counsel for the first trial in the United States against Ethicon and Johnson & Johnson, held in the New Jersey Superior Court.  The trial resulted in a verdict for the plaintiffs, with compensatory damages of $3.35 million, and punitive damages of $7.76 million, and the Judgment was affirmed by the New Jersey Appellate Division, with certification denied by the New Jersey Supreme Court.  Mr. Slater has been trial counsel in numerous other pelvic mesh cases against Ethicon and Johnson & Johnson around the country, including in Philadelphia in December, 2015 ($12.5 million verdict including punitive damages of $7 million), New Jersey in December, 2017 ($15 million verdict including punitive damages of $10 million) the MDL Court in West Virginia (settled during trial), and Missouri State Court (settled during trial).  He also obtained the largest pelvic mesh verdict ever obtained against C.R. Bard, in March 2018, in the amount of $68 million, including punitive damages of $35 million.  Of note, Mr. Slater testified in 2015 to the Scottish Parliament, at the invitation of a Parliamentary subcommittee, with regard to the dangers of pelvic mesh, aiding the successful effort to have pelvic mesh banned in Scotland. Read Full Bio   Show Sponsors: Legal Technology Services - LTSatlanta.com Digital Law Marketing - DigitalLawMarketing.com Harris, Lowry, and Manton - hlmlawfirm.com   Free Resources: Stages Of A Jury Trial - Part 1 Stages Of A Jury Trial - Part 2

Brad and Chris the Pharmacist discuss a popular high blood pressure medication called Losartan. They will discuss the side effects and risks to know about this medication. In this video Brad will play as the patient, while Chris gives his pharmacsit point of view. Medical Disclaimer All information, content, and material of this website is for informational purposes only and are not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. Affiliate disclaimer: Keep in mind that we may receive commissions when you click our links and make purchases. However, this does not impact our reviews and comparisons. We are highly selective in our products and try our best to keep things fair and balanced in order to help you make the best choice for you.

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.  

Volvemos con otro programa repleto de miseria a raudales. El señor zyloric no puede dejar de ver tacaños extremos y nos trae lo peor de lo peor y sin honores. El Dr Civeta exprime sus archivos words repletos de datos innecesarios para verter un elixir en vuestros oídos para que subáis un peldaño las conversaciones triviales de ascensor y el Dr Losartan nos trae noticas miserables para vuestro deleite. email: lamiseriameencanta@gmail.com twister: @lagrimas_lluvia

SORTEO (lee hasta el final para saber cómo participar) Hoy os traemos una oda al hater estudiándolo cual félix Rodríguez de la Fuente en "El Hombre y la Miseria" conducida por el Sr Zyloric. El Dr Civeta viene a tirarnos por el suelo unos cuantos mitos y el Dr. Losartan nos traerá situaciones históricas donde la jodienda ha tenido mucho que decir. Email: lamiseriameencanta@gmail.com twitter: @lagrimas_lluvia SORTEO: para saber qué tienes que hacer y optar al premio que visteis en la portada del programa anterior, tendréis que escuchar el programa. Que cabrones que somos 😁

Programa cargado de temas transcendentales repondiendo vuestras peticiones, las del respetable. Lo único respetable que hay en el Lágrimas. El menú del programa es el que sigue: masculinidad en el trail running y tacaños extremos por el Sr Zyloric, Comidas e ingredientes del mundo por el Dr Civeta y novias Rusas por el Dr Losartan. En la portada podíéis ver el próximo premio que sortearemos en el lágrimas, aunque todavía no sabemos cómo será el concurso. Esto lo sabremos en la próxima entrega de miseria Si tienes dudas existenciales, temas a sugerir o cualquier otra visicitud. Puedes encontrarnos en twitter: @lagrimas_lluvia email: lamiseriameencanta@gmail.com

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. 

In fighting this virus we have two paths to pursue, curative therapies and suppressing spread. Which path we travel will dicate much of the future. Today we run down some of the changes already upon us.

Sorry for the week off, everyone. We needed a minute to mourn the loss of Luke Perry. We're back and this week we discuss Baywatch episodes, early Nickelodeon tv shows, and Josh might have cancer (oops). Follow us on Instagram @wcbfpodcast, Twitter @wcbfpodcast1, and email us about the time you were almost abudcted at wcbfpodcast@gmail.com. Check if your Losartan prescription was recalled here

Sorry for the week off, everyone. We needed a minute to mourn the loss of Luke Perry. We're back and this week we discuss Baywatch episodes, early Nickelodeon tv shows, and Josh might have cancer (oops). Follow us on Instagram @wcbfpodcast, Twitter @wcbfpodcast1, and email us about the time you were almost abudcted at wcbfpodcast@gmail.com. Check if your Losartan prescription was recalled here

I met with Dr. Alan Braverman to talk about aortic diseases (aka aortopathies) such as Marfan’s disease, Ehlers-Danlos and Loeys-Dietz. We discuss everything from clinical presentations and genetics to treatments. Articles referenced: NEJM Atenolol vs Losartan in Marfan’s

This week from MDedge Cardiology, a biodegradable polymer shows no long-term benefit in heart stents, appropriate use criteria for imaging in nonvalvular heart disease are released, ACOG updates guidance on hypertension in pregnancy, and more losartan lots are recalled.

The post Losartan (Cozaar) Nursing Pharmacology Considerations appeared first on NURSING.com.

Commentary by Dr. Valentin Fuster

This week we delve into the world of Marfan Syndrome and review a recent report from the Pediatric Heart Network with the first author of this work, Dr. Seda Selamet Tierney - Associate Professor of Pediatrics, Stanford University. Why does stiffness of the aortic wall predict dilation and need for surgery? Does the use of atenolol or losartan affect aortic growth or dilation? Which agent is preferable? Dr. Selamet Tierney shares her insights this week on the podcast. DOI: 10.1016/j.amjcard.2018.01.016

This week we delve into the world of Marfan Syndrome and review a recent report from the Pediatric Heart Network with the first author of this work, Dr. Seda Selamet Tierney - Associate Professor of Pediatrics, Stanford University. Why does stiffness of the aortic wall predict dilation and need for surgery? Does the use of atenolol or losartan affect aortic growth or dilation? Which agent is preferable? Dr. Selamet Tierney shares her insights this week on the podcast. DOI: 10.1016/j.amjcard.2018.01.016

I can't believe it's already time for another Cabral HouseCall - the weeks have been flying by! I'm really looking forward to today's show and here are our community's questions: Vicky: Dr. Cabral, I would like to start using your Daily Nutritional Support. I had my gallbladder removed about 10 years ago. So I'm wondering if this Support is safe for me to use. Also take 50 mg Losartan for high blood pressure. Recently diagnosed with a hernia. With the above, would the product be ok for me to start using. Always look forward every morning to listening to your podcast. Thank you so much for your help and time. Vicky   Maggie: my son has been battling a very rare form of cancer since he was five. He has been sick a lot due to all the chemo wiping out his immune system. We almost lost him around December 2016. He is now almost seven and has recently been sick with a virus in his blood that the doctors cannot control. I want to build up his immune system and help him fight his cancer in as natural way as possible. Could you please recommend how I can go about this. Thank you so much for all your advise and help. You are a blessing to us all. Maggie   Cindy: Hello Dr Stephen Cabral, I have a question. Thanks again for all your podcasts and for all the information you provide to us. May God bless you , your team and your family. My question is... why is my uterus low? How can I fix this issue? Thanks again.    Michele: Hi Dr. Cabral, So many people I know are looking for recommendations for comfortable mattresses that aren't toxic. Can you recommend a couple of brands? Curious what you use? I have one all cotton one for my child and my husband and I are due for a new one. Ours is not a "clean" mattress and not particularly comfortable. Any input would be greatly appreciated! Thanks! Michele    Sotirios: Greetings I read about your work with great interest. I specifically read that some consumer groups have send to different labs ( I don't know which ones ) same blood samples and they receive different and not overlapping results. Or that food sensitivity testing has not been studied systematically so we have no reliable evidence that it is meaningful. For instance - How you make sure the tears are accurate ? Do you run them twice ? We were thinking of purchasing some of the tests in my family but I would like to read more about that in detail if it is possible . Many thanks best wishes Thank you for tuning in and I can't wait to share with you a brand new set of Q&As tomorrow! - - - Show Notes & Resources: http://StephenCabral.com/554 - - - Get Your Question Answered: http://StephenCabral.com/askcabral    

  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. Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore.                                                 In today's episode, we are discussing very important new data regarding stroke risk stratification in patients with atrial fibrillation. First though, let me give you the highlights of this week's journal.                                                 The first paper provides mechanistic evidence that endothelial-derived microparticles may play a key role in the development of endothelial dysfunction following acute coronary syndrome. In this paper from first author, Dr. Abbas, co-corresponding authors, Dr. Toti and Morel from the University of Strasbourg in France, authors expose core sign coronary artery endothelial cells to microparticles shed from senescent cells, or circulating microparticles from patients with acute coronary syndrome.                                                 They showed that exposure to these microparticles induced increase senescence-associated beta-galactosidase activity, oxidative stress, and early phosphorylation of MAP kinases and AKT, and upregulation of p53, p21 and p16. Depletion of endothelial-derived microparticles from acute coronary syndrome patients reduced the induction of senescence.                                                 On the other hand, pro-senescent microparticles promoted endothelial cell thrombogenicity. These microparticles exhibited angiotensin-converting enzyme activity and upregulated AT1 receptors and ACE in endothelial cells. Losartan and AT1 receptor antagonist and inhibitors of either MAT kinases or PI3-kinase prevented the microparticle-induced endothelial senescence.                                                  In summary, these findings indicate that endothelial-derived microparticles from acute coronary syndrome patients induce premature endothelial senescence and thrombogenicity suggesting that targeting endothil-derived microparticles and their bioactivity may be a promising therapeutic strategy to limit the development of endothelial dysfunction post-acute coronary syndrome.                                                 The next study is the first large and prospective study showing that NT-proBNP is associated with cardiovascular events in patients with adult congenital heart disease independent of multiple clinical and echocardiographic variables.                                                 This is a study from first author, Dr. Bekan; and corresponding author, Dr. Roos-Hesselink and colleagues from the Erasmus University Medical Center in Rotterdam, the Netherlands. The author studied 595 clinically stable patients with adult congenital heart disease who attended the outpatient clinic between 2011 and 2013.                                                 All patients underwent clinical assessment, electrocardiography, echocardiography and biomarker measurement, including NT-proBNP, high-sensitivity troponin T and growth differentiation factor 15. Patients were prospectively followed over a median of 42 months for the occurrence of cardiovascular events including death, heart failure, hospitalization, arrhythmia, thromboembolic events and reintervention.                                                 They found that of the three evaluated biomarkers, NT-proBNP was most strongly associated with cardiovascular events. Importantly, patients with a low-risk of death and heart failure could be accurately identified with a high negative predictive value.                                                 In patients with elevated NT-proBNP, elevations of high sensitivity troponin T and growth differentiation factor 15 identified those patients at highest risk of cardiovascular events.                                                 In summary, these biomarkers may play an important role in the monitoring and management of patients with adult congenital heart disease.                                                 The next study describes heart failure stages among older adults in the community. Dr. Shah and colleagues from the Brigham and Women's Hospital in Boston Massachusets classified more than 6,000 participants in the atherosclerosis risk and community study into heart failure stages. These were stage A; asymptomatic individuals with heart failure risk factors, but no cardiac structural or functional abnormalities. Stage B; asymptomatic individuals with structural abnormalities such as left ventricle hypertrophy, dilation, dysfunction, or valve disease. Stage C1; clinical heart failure without prior hospitalization. Stage C2; clinical heart failure with prior hospitalization.                                                 They found that only 5% of examined participants were free of heart failure risk factors or structural heart disease. 52% were categorized as stage A, 30% stage B, 7% stage C1, and 6% stage C2. Worst heart failure stage was associated with a greater risk of incident heart failure hospitalization or death at a median follow up of 608 days.                                                 Left ventricular ejection fraction was preserved in 77% of stage C1 and 65% of stage C2 respectively. In corporation of longitudinal strain measurements and diastolic dysfunction into the stage B definition, reclassified 14% of the sample from stage A to B.                                                 Abnormal LV structure, systolic function, whether based on ejection fraction of longitudinal strain, and diastolic dysfunction, were each independently and additively associated with the risk of incident heart failure hospitalization or death in stage A and B participants.                                                 The authors concluded that the majority of older adults in the community are at risk of heart failure, appreciably more compared to previous reports in younger community-based samples. The study also highlighted the burden of heart failure with preserved ejection fraction in the elderly and provided evidence that left ventricular diastolic function and longitudinal strain provide incremental prognostic value beyond conventional measures of LV structure and ejection fraction in identifying patient at risk of heart failure hospitalization or death.                                                 The next study sheds light on the association of the LPA gene, ethnicity and cardiovascular events. First author, Dr. Lee; corresponding author Dr. Tsimikas and colleagues from University of California San Diego studied 1,792 black, 1,030 white, and 597 Hispanic subjects all enrolled in the Dallas Heart Study. They measured LPA snips, apolipoprotein A isoforms, LP(a) and oxidized phospholipids on apolipoprotein B100.                                                 These individuals were also followed for a median of 9.5 years for major adverse cardiovascular events. The authors found that the prevalence of LPA snips and apolipoprotein A isoforms were very different across ethnic groups. LPA snips that were associated with elevated LP(a) in whites were associated with low LP(a) in Hispanics mainly due to differences in apoliproprotein A isoforms size.                                                 After multi-variable adjustment, LP(a) and oxidized phospholipids on apolipoprotein B were both predictors of major adverse cardiovascular events. Conversely, LPA snips and apolipoprotein A isoforms did not add predictive value to models and did not show clinical utility in this study.                                                 These data suggests that much of LP(s) mediated major adverse coronary events is driven by oxidized phospholipids. Importantly, elevated LP(a) and oxidized phospholipids on apolipoprotein B must be recognized as important predictors of major adverse cardiovascular events across racial groups.                                                 The final study addresses the question of the optimal antithrombotic regimen for longterm management of patients with symptomatic peripheral artery disease, or PAD, with a history of limb revascularization. To answer this question, Dr. Jones and colleagues from Duke Clinical Research Institute looked at the EUCLID trial, or examining use of ticagrelor in PAD trial, which randomized patients with PAD to treatment with ticagrelor 90 milligrams twice daily, or clopidogrel 75 milligrams daily.                                                 As a reminder, patients in EUCLID were enrolled based on a normal ankle-brachial index of less .8, or a prior lower extremity revascularization. The current paper really focus on the subset of 7,875 patients who were enrolled based on a prior lower extremity revascularization criterion.                                                 The authors found that after adjustment for baseline characteristics, patients enrolled based on prior revascularization for PAD had higher higher rates of myocardial infarction and acute limb ischemia with similar composite rates of cardiovascular death, myocardial infarction and stroke when compared with patients enrolled based on the ankle brachial index criterion.                                                 Overall, there were no significant differences between ticagrelor and clopidogrel for the reduction of cardiovascular or acute limb events.                                                 Those were your highlights. Now, for our featured discussion.                                                 On today's podcast, we are discussing the very, very important issue of stroke risk in patients with atrial fibrillation. Most of us use the international guidelines for anticoagulation in atrial fibrillation that mostly suggest that we use the CHADS VASc scoring system to determine the stroke risk in a particular patient and then determine whether or not this patient meets the threshold for anticoagulation.                                                 This assumes that the CHADS VASc score corresponds to a fixed stroke rate. Today, in our journal, we have very, very interesting results from a paper with corresponding author, Dr. Daniel Singer who really suggest that we may need to rethink that. Dr. Daniel Singer joins us today from Massachusets General Hospital.                                                 Welcome Daniel. Dr. Daniel Singer:             Thank you for having me. Dr. Carolyn Lam:               Great. Today, we also have Dr. Sana Al-Khatib who's the associate editor from Duke University who managed this paper. Welcome Sana. Dr. Sana Al-Khatib :         Thank you Dr. Carolyn, I'm happy to be here. Dr. Carolyn Lam:               Daniel, could we start by you letting us know what you sought to do in your study and what you found? Dr. Daniel Singer:             We all know that anticoagulants are extraordinarily effective at preventing stroke in patients with atrial fibrillation, but they also raise the risk of bleeding, and sometimes that bleeding could be quite serious and even fatal. As a result, for that past 10, 15 years, we have used a risk-based approach to the decision about whether to start a patient on anticoagulation, and that risk is the stroke risk that a patient faces if they weren't taking anticoagulants. Then we figured that anticoagulants will reduce it by about two-thirds.                                                 There are formal decision analysis and then a more informal sense that a patient has to face an anticoagulated risk of stroke of about 2%, some people might say 1% to 2% before anticoagulation results in an expected net clinical benefit that the effect in reducing ischemic stroke will exceed the risk of increasing bleeding.                                                 While the CHADs VASc score has been widely accepted as the basis for estimating that risk, it became apparent to us as we looked across the studies that were underlying that assumption, that the risk that were associated with various CHADs VASc scores were extremely variable. Many of these risks actually were less than that 1% or 2% threshold for anticoagulation.                                                 What I mean is that the stroke risk associated with CHADs VASc score of one, or two, which is the basis for the guideline threshold for anticoagulation actually corresponded to risk less than 1% in many of these very large studies. We have conducted a systematic review just to be sure that we were capturing the overall evidence base for this, and that's what we report in our paper. Dr. Carolyn Lam:               Perhaps you could start by letting us know exactly how far off are we in our stroke risk estimation. Dr. Daniel Singer:             We looked at 34 studies that were quite large and then we zeroed in on the largest one. If you looked at the rate for stroke overall, they varied enormously in terms of the overall stroke rate. Then when we focused down on CHADs VASc score of 1, or 2, we found that the majority of these studies, actually, for CHADs VASc 1, was less than 1% per year. For CHADs VASc 2 score was in the majority these studies less than 2% per year.                                                 Both of those stroke risks have raised us the question where are these patients could gain in that clinical benefit from being anti-coagulated, because those stroke risk, if they were reduced by two-thirds, would really be a very small reduction in risk and yet they'd still face the bleeding risk.                                                 Among the most interesting findings actually is that we found that a Swedish national database and the large Danish national database came up with threefold difference in their estimate of stroke rates. The Swedish database produced lower risk, and the Danish database produced substantially higher risk.                                                 If you think about it, there are probably no two countries in the world that are more similar in terms of gene, social environmental, medical care systems, and that raises the specific question of, "Is it underlying rates that vary across different cohorts and different geographies, or is it a different in methodology?"                                                 We think a lot of the differences are due to methodologic difference, and that we need to standardize these differences together, better handle on what the real stroke rate is among patients with these low CHADs VASc scores. Dr. Carolyn Lam:               The variability that you pointed on your paper is really striking, but another possibility, do you think, is that maybe stroke risk isn't static. Dr. Daniel Singer:             Yeah. If that's the case, we face a great difficulty in developing predictions rules of what the stroke risk could be. I think most people feel it's the function of their age, and whether they've had a prior stroke, and whether they have the comorbidity, hypertension, and diabetes, and so on, that are incorporated into the various stroke risk scores, in particular, CHADs VASc.                                                 We tend to think that that's pretty fixed until you get older or until you accumulated another comorbidity. I think the striking difference is that, one, that we actually anticipated in the beginning, was that the stroke rates in people with atrial fibrillation were also coming down. The stroke rates in general have been dramatically decreasing for decades now.                                                 One issue is whether that applies as well to atrial fibrillation associated stroke. There is a suggestion of that, but the variability across the cohorts is so great that you can't pick up a strong signal in terms of calendar time. Although I suspect that there is a strong calendar effect. Exactly why that is, we could speculate. I suspect a lot of it is control of blood pressure, but that's speculation. Dr. Carolyn Lam:               Daniel, congratulations again for that fascinating and really very sobering findings.                                                 Sana, you managed this paper. It's very important paper. In fact, important enough that you invited an editorial. Could you please share some of your thoughts? Dr. Sana Al-Khatib :         Oh, yeah. Absolutely. First, I'd like to start by congratulating Daniel and his team on conducting this really important study. I enjoyed reading it and managing it. Definitely, congratulations.                                                 A couple of thoughts that I have. I completely agree with this really important finding, that there is a lot of variability in the rates of stroke that come from different patient populations and databases. As you pointed out Daniel, I think this is indeed largely due to differences in methodology in terms of how the information was selected, how certain things were defined.                                                 I agree with you there. You called for standardization of this, and I wonder if you have any thoughts about how we can go about doing that. I also want to bring up some of the newer studies now that are showing some significance in terms of biomarkers. Is that really adding significantly to the predictive ability of risk prediction models? I wanted to get your thoughts on that as well. Dr. Daniel Singer:             Let me address your last question, which is simply you state that the CHADs VASc score, the CHAD score and so on, are based on very simple clinical features, and it would be unusual for them to be highly predictive. In fact, they're only mediocrely predictive, and the addition of biomarkers high-sensitivity troponin proBNP, now, people have suggested the imaging biomarkers like magnetic resonance to asses fibrosis in the left atrium. These are all very, very promising in terms of getting better models.                                                 The problem is to do that on a very scale such that we can get precise and well-calibrated predictions. We've found when we're analyzing to pair risk scores, we found that the most important issue is the underlying risk, so that, yes, you can get a great model, but if you have high variability in the underlying rate, you can have a problem specifying an individual with a stroke risk.                                                 We have to standardize and improve the quality of bringing people into these cohorts, and of interrogating the cohorts and databases and making sure that we have the same approach to assessing outcomes.                                                 This could probably be best done in very big scientific prospective registry studies, but it's tough to get all that information. There are some registry studies now ongoing, the ORBIT registries, the GARFIELD registries that may help us a lot with specifying stroke risk, but they don't have the biomarkers embedded in them. I'm hopeful that with better message, and large studies, and incorporating biomarkers, that we'll really get down to very accurate and generalizable stroke risk.                                                 I think the CHADs VASc and similar simple stroke risk scores will be in the rear-view mirror. Dr. Sana Al-Khatib :         That's great. Can I ask one other question, because I completely agree with you looking at your numbers and the data that you presented, is that when you look, especially at the CHADs VASc score 1 patient, the risk seems to be pretty low.                                                 As you very well know, the guideline documents don't really ... At least, for the American AHA/ACC guideline document, they don't really verbalize very definitively the need to anticoagulate patients with a CHADs VASc score of 1.                                                 If you look at the numbers related to a CHADs VASc score of 2, I'm not sure that I completely agree that the risk is very low. Certainly, there was 33% of the studies reported stroke rates of greater than 2% per year. I think maybe different people have different thresholds. While I completely agree with you on the CHADs VASc score of 1 patients, I find that the findings on patients with a CHADs VASc score of 2 a bit more concerning.                                                 In fact, if anything, I would want based even on your data, not on the guidelines to offer anticoagulation to patients with CHADs VASc score of 2. What would you say to that? Dr. Daniel Singer:             I'm looking at our table that has this, and a lot of the CHADs VASc 2 scores are under 2%, but they're in mid 1%. In the North American cohorts in particular, the rates tend to be lower. That said, I think the heart of the problem here is that we have focused on the threshold for anticoagulation. I think there's an argument to be made that you lay out the risks and benefits to the patients and engage them in a decision, particularly with regards to these lower CHADs VASc scores.                                                 At least you make a lot of, perhaps, even more emphasis on being sure that the higher CHADs VASc scores, that anticoagulation is the net benefits of anticoagulation are made very clear to the patient, and that we don't have large fractions of patients who can take anticoagulants not taking them.                                                 We know from the pinnacle registry and other registries, that even at high CHADs VASc scores, we have 40% plus of atrial fibrillation patients who are not getting anticoagulants. I think that's where we have a lot more assurance that the net benefit is positive and that we can make a different both in terms of a patient in front of us, and in terms of the overall public health aspects of atrial fibrillation and stroke. Dr. Sana Al-Khatib :         I do believe that this is really important, but it is also important to keep in mind that with the novel novel oral anticoagulants, I think the whole landscape has changed. Not only do patients have different options to consider, but certainly, the risk of bleeding, which is the other part of this equation, has gone down significantly with the novel agents.                                                 I think as we engage in shared decision making with patients, I think it is really important to highlight these really very remarkable features about the agents that have really changed the care of patients with atrial fibrillation.                                                 One thing to add to this whole topic is, really, all the new advances that we're seeing in this field that has been really life-changing for us and for our patients. Dr. Carolyn Lam:               Indeed Sana. I was about to bring up the bleeding risk part, the flip side of the coin as well. Also, the point that most of my patients with atrial fibrillation, they really strongly value the avoidance of stroke even more than avoidance of bleeding. Someone, that needs to be taken into consideration as well.                                                 Daniel, I'd love to give you the last words. You mentioned that you like to highlight, maybe, some more of the implications of your findings. Dr. Daniel Singer:             I guess I would say there's a scientific implication, which is what we've ben discussing, which is the importance of trying to get these rates down correctly and accurately, and maybe we have to get people together to say how they're doing these studies.                                                 The second is, for the individual patient, that we should engage them in this discussion. Maybe patients who are perfectly willing to a novel anticoagulant and CHADs VASc score of zero. That would come out of a discussion with the patient. That our emphasis at this point since we're a little unsure about the threshold level, our emphasis both at the individual patient level, and then from the public heath perspective should be on the higher CHADs VASc scores where we know that we can expect a net clinical benefit from the vast majority of patients with AF.                                                 I agree with Dr. Al-Khatib, that the novel anticoagulants post an important advantage in the sense not so much in their overall bleeding, but particularly in terms of their intercranial bleeding, which is the lethal bleeding we most want to avoid. Dr. Carolyn Lam:               Thank you both for joining us. Thank you listeners for joining us. Don't forget to tune in next week.  

PhysicianAssistantBoards.com - Lets talk GOUT!  Signs, symptoms, testing,and treatment.  Remember HCTZ and ASA can increase uric acid levels. Losartan, vitamin C, and fenofibrate can actually lower uric acid levels.  But, listen to the show to get all the details, so you can pass the boards, but more importantly, help those in clinical practice!

Dr Bauchner, Editor in Chief of JAMA, provides summary and commentary on the April 11, 2012 issue of JAMA, the Journal of the American Medical Association. ECG Abnormalities and CHD Event Prediction, Losartan and Heart Failure Mortality, Eliminating Waste in US Health Care, Does This Patient Have Blunt Intra-abdominal Injury?, Should healthy men take statins?, Accountable care organizations and antitrust issues.

Es wurden die hämodynamischen, biochemischen und morphologischen Effekte einer Angiotensin-II-Rezeptorblockade mit dem AT1-Blocker Losartan auf eine hypoxie-induzierte rechtsventrikuläre Hypertrophie an der Ratte untersucht. In weiblichen „Sprague Dawley“ Ratten wurde eine isolierte rechtsventrikuläre Hypertrophie durch intermittierende Hypoxie hervorgerufen. Die intermittierende Hypoxie bewirkte einen Anstieg des rechtsventrikulären Drucks und eine Erhöhung des Verhältnisses von Ventrikelgewicht zu Körpergewicht im rechten Ventrikel, die Hypoxiebehandlung hatte keinen Einfluss auf die linksventrikulären Kreislaufparameter oder das Herzzeitvolumen. Die Aktivitäten der Glukose-6-Phosphat Dehydrogenase und der 6-Phosphoglukonat-Dehydrogenase waren nach der Hypoxiebehandlung im rechten Ventrikel erhöht, jedoch nicht im linken Ventrikel. In der Hypoxiegruppe ohne Losartan war das Zellvolumen der isolierten Kardiomyozyten erhöht, die Kardiomyozytenzellänge unverändert, so dass man von einer hypoxieinduzierten rechtsventrikulären Hypertrophie vom primär konzentrischen Typ ausgehen muss. Losartan verringerte den hypoxie-induzierten Anstieg des rechtsventrikulären systolischen Druckes, die Zunahme des Verhältnisses von rechtsventrikulärem Gewicht zu Körpergewicht und die Enzymaktivitätserhöhung signifikant, wenn auch nicht vollständig. Die Zunahme des Volumens und der Querschnittsfläche der isolierten Kardiomyozyten wurde durch Losartan jedoch vollkommen verhindert.

Sorry for the week off, everyone. We needed a minute to mourn the loss of Luke Perry. We're back and this week we discuss Baywatch episodes, early Nickelodeon tv shows, and Josh might have cancer (oops). Follow us on Instagram @wcbfpodcast, Twitter @wcbfpodcast1, and email us about the time you were almost abudcted at wcbfpodcast@gmail.com. Check if your Losartan prescription was recalled [here](https://www.fda.gov/Drugs/DrugSafety/DrugRecalls/default.htm)