Ruth Chen

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Ruth Chen

Ruth Chen

@chenruth

Cardiologist & Intensivist. #critcarecards #APICS #echo

Singapore Katılım Ocak 2010
883 Takip Edilen368 Takipçiler
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Siyab Panhwar, MD
Siyab Panhwar, MD@DrSiyabMD·
I am an interventional cardiologist who treats heart disease for a living, including by putting stents. This is my opinion on my tweet above. This is aimed at the general public. Long but worth the read: First, some basics: Atherosclerosis (plaque formation) is a NATURAL PROCESS of life that begins in childhood. It progresses or can accelerate as you get older - as you live more life, due to genetics, and as you accumulate medical conditions such as high blood pressure, diabetes, live the "American" diet and lifestyle, etc. Just like the plumbing in your home - a brand new house has clean, new pipes. Over 30, 40, 50 years of use, the pipes accumulate junk on the inside and can get clogged over time. EVERYONE has some degree of plaque, some more than others. You cannot STOP the process. The goal of prevention is to find stuff BEFORE it causes problems, and to initiate measures to SLOW progression of plaque and to STABILIZE what you already have so it doesn't cause problems, i.e. a heart attack. The goal is to control it, live a long, good life, and die WITH heart disease and not BECAUSE of it. 1. CAC is a great SCREENING, preventive tool in APPROPRIATE patients to get a sense of how much coronary artery plaque one might have, to then better assess their RISK of future adverse outcomes like a heart attack. The result of this test is NOT USED IN ISOLATION, rather it is used with OTHER tests, clinical history, etc to determine the best strategy to LOWER risk. But in reality, a lot of people do not really *understand* RISK. They use this test, or are told by others to, as a way to "predict" *if* they will have a heart attack. I have lost count of the number of people who tell me "I have a CAC of 0 that means I won't have a heart attack, right?" or "I have a CAC of 1000! I was told I'm at imminent risk of a heart attack and I'm freaking out". NO. There is NO test in the world, and no human being that can tell you, if you are going to have a heart attack tomorrow, next week, next month, etc. Anyone who says they can is lying to you. You can't tell the future. If you want an ETA on if/when, ask God because only God knows. But we CAN do is estimate RISK. A low CAC or CAC of 0 is great, and low risk, but not ZERO risk. A high CAC is indicates higher risk but does not mean 100% probability. Some people with low/Zero CAC have heart attacks and some people with CACs of 1000s never have a heart attack. 2. CAC measures CALCIFIED plaque - the advanced stage of plaque formation by which time plaque tends to become calcified and hard. It does NOT measure soft plaque - young plaque that has not had time to calcify yet. Therefore, while a CAC of 0 is reassuring, it DOES NOT MEAN YOU DON'T HAVE HEART DISEASE OR PLAQUE. Generally, soft plaque can be "unstable" or "vulnerable" plaque which is often responsible for heart attacks, instead of the more stable, calcified type. Carnivore bros in their early 30s and LDLs of 180 will often flaunt their CAC of 0 and say look! I’m good! No. Doing a CAC on an average, healthy 30 year old with no family history is silly because the CAC will LIKELY BE ZERO. THEY HAVE NOT HAD ENOUGH TIME FOR PLAQUE TO CALCIFY YET. In fact, they can be layering soft plaque because of their LDL of 200 and have no clue. It can give people a false sense of security. I have put stents in enough 40 year olds with heart attacks with a 0 CAC score in the past to know this. It would also be silly to think that if you have a CAC of 0 you can continue to smoke and you're good - I don't think anyone thinks that. Which is why when I have 30 year olds in my clinic with uncontrolled lipids, hypertension etc, I don’t do a CAC score. It will likely be 0. But i’m not going to just let them accumulate plaque until they get a CAC years later and finally they have a positive test and then we talk about risk factor control. That’s silly. I aggressively control all these risk factors EARLY in life. 3. The calcification *itself* does not necessarily cause a heart attack or stroke - like I mentioned earlier, these are typically very stable, hard plaques and less likely to cause a heart attack than unstable, vulnerable soft plaque. A CAC is still very useful because it helps you assess overall plaque *burden* and therefore, risk. Compared to someone with a lower CAC score, someone with a higher CAC may have an overall higher BURDEN of atherosclerosis (including both calcified and non calcified). And a higher burden of plaque indicates higher risk. 3. CAC is not always = blocked artery. A common misconception is that if you have a high CAC score that automatically means you have significant percentage blockage (50, 60, 70+ %) in your arteries. No. CAC should be seen as a marker of atherosclerosis and not blockage. A CAC test *cannot* tell you if you have a 70% blockage. You need a coronary CT or a coronary angiogram for that. Plaque can accumulate in many ways, and the arteries of the heart often adapt (“remodeling”) to accommodate that plaque WITHOUT causing a significant obstruction of the actual lumen of the artery, so blood flow is still relatively unimpacted. Obviously this is only to a limit, and eventually the plaque starts to protrude into the lumen and causes a significant blockage. Don’t get me wrong, obviously a high score increases the chances of a significant blockage but this is not gospel. There are people with scores in the 1000s and all their plaque is in the wall of the artery, and the artery itself is wide open - there is no need for a stent or bypass for that. Conversely, people with low scores can have a significant blockage in an artery. Life is unpredictable and bizarre shit happens all the time. 4. A higher CAC does not automatically = further testing or a stent This is another big misconception that people struggle with. For a lot of people who get this test - the average, *asymptomatic* person with a higher CAC score, the answer is to STOP further testing, and just manage risk factors aggressively. That’s it. People say "but doc what if I have a heart attack? Why don't we look for an actual BLOCKAGE?" You don’t typically need a stress test if you are asymptomatic. You don’t need a coronary angiogram or CCTA to look to see if there is a percentage blockage. Why? Because whatever plaque you do have has been ACCUMULATED OVER YOUR LIFETIME and is STABLE. You had it 2 months ago, even 6 months ago. If you are ASYMPTOMATIC, it is just sitting there, NOT CAUSING PROBLEMS (yet). We found it, great, now we do things to reduce the risk that it causes problems 10, 20, 30 years down the line. Again, no one can predict if/when a heart attack happens. You could have had a heart attack months ago, when you had all this plaque but didn't even know about it. Like I said earlier, atherosclerosis is a NATURAL process of life and EVERYONE has some degree of plaque. There are many people in your life, just walking around with severe plaque but they have no idea because it hasn’t caused problems for them, YET. They are at risk, of course. If I did a coronary angiogram procedure for everyone (with or without a positive CAC), I would find some degree of blockage in most people. Even a significant blockage! But if this is STABLE and CHRONIC, generally there is no need to put a stent to open it up. Because in stable heart disease, the heart often adapts in many ways. Stents generally do NOT help you live longer, they do not reduce the chance of a heart attack in the future. They really only just make people FEEL better, IF they have symptoms and IF their symptoms are caused by the blockage. If you’re asymptomatic, a stent is likely not going to do anything for you and you’re probably just incurring the risk of an invasive procedure without any significant meaningful benefit. Opening up a stable blockage won't necessarily stop a heart attack in the future because you may have some soft, vulnerable unstable plaque somewhere else in the arteries that is not causing a significant % blockage in the artery, but decides to act up one day and cause a heart attack. Obviously a heart attack is an acute condition with sudden 100% closure, and stents help save lives, and your heart muscle. But many people with heart attacks ALSO have chronic (even significant %) blockages in other arteries that were just bystanders. These blockages didn't cause problems and were found incidentally. They were present months, years ago, and the person probably didn't even know Consider this analogy: the drain under your kitchen sink. When it clogs, it doesn't happen overnight. It happens over weeks and months. There may be a 50% clog but the drain works fine. But then as the clog progresses, the flow slows down over time and finally stops. That is STABLE. A heart attack is like someone throwing something in to your toilet and now you have a clogged toilet and an emergency. Obviously, there are caveats to this - some people with high CAC need further testing, and may even need bypass surgery, depending on how high the score is, their risk factors, their history, and the type/severity of blockages. But *generally* speaking, this is not true for the AVERAGE person. I have done no further testing for people with high calcium scores, and conversely the full shebang for people with low scores. It depends. All this sounds great in theory, but in practice, reality is very different. Influencers peddling CAC scores have meant that people are now getting these who may not be appropriate for them, and then they are getting a lot of downstream testing and unnecessary procedures (ie stent) that they DO NOT NEED. People also, understandably, have anxiety. It can be hard to accept that they have a high calcium score and I do not recommend any further testing. This is all understandable of course. No one wants to have a heart attack. I obviously think everyone should educate themselves and their loved ones about heart disease and take an active role to prevent disease, but we have to recognize there can be significant harm with indiscriminate, inappropriate use. Bottom line: Prevention is KEY, and we need to do a LOT MORE of it. CAC scores are great tools, but need to be used and interpreted appropriately. Disclaimer: Very simplified explanation, written quickly, educational only, and not medical advice. Discuss your specific case with your doctor. your doctor may disagree with me, and that's fine too! Do what is best for you! Thanks for reading!
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UC San Diego Cardiology Fellows
UC San Diego Cardiology Fellows@UCSDCardFellows·
Emerging Therapies: Levosimendan 🧪 Calcium sensitizer + vasodilator 🫁 Improves hemodynamics in PH-HFpEF 📚 Studied in small trials (HELP trial) Still investigational — may be considered in advanced PH phenotype
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UC San Diego Cardiology Fellows
UC San Diego Cardiology Fellows@UCSDCardFellows·
GLP-1 agonists = Metabolic Game Changers 📚 STEP-HFpEF (semaglutide) → ↓ weight, ↑ 6MWT, ↑ KCCQ score 📚 SUMMIT trial (tirzepatide) → ↓ HF events, weight, and improved QoL ⚠️ Not in guidelines yet — but compelling and practice-influencing
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UC San Diego Cardiology Fellows
UC San Diego Cardiology Fellows@UCSDCardFellows·
HFpEF ≠ “nothing to do” — we have therapies There’s no Class I therapy for HFpEF yet. But we do have options that work — and are guideline-endorsed. 2022 AHA/ACC/HFSA HF Guidelines: •SGLT2 inhibitors = Class 2a •ARNi / ARB / ACEi = Class 2b •MRAs = Class 2b
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UC San Diego Cardiology Fellows
UC San Diego Cardiology Fellows@UCSDCardFellows·
How do we diagnose it? 🧪 BNP/NT-proBNP → may be lower in obese patients 🩺 Echo: •LA enlargement •E/e′ >15 •TR velocity >2.8 •LV mass index ↑ 🏃 Exercise echo or cath → reveals latent ↑ filling pressures 🧠 Consider: H₂FpEF score (Mayo) or ESC diagnostic algorithm
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M Velia Antonini
M Velia Antonini@FOAMecmo·
CI, SvO2 & pCO2 in #ECMO for cardiogenic shock? 🔍 post-hoc analysis of ECMO-CS trial: immediate #ECLS initiation vs early conservative strategy in CS The presence of any of following criteria: 🫀 low cardiac index 🫁 high PCO2 gap 🩸 low SvO2 may indicate poor prognosis with conservative therapy & substantial mortality benefit from mechanical circulatory support. Measurement of these parameters could improve CS management. @Crit_Care #FOAMcc #FOAMecmo 🔓 rdcu.be/ewxc9
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Jan Verwerft
Jan Verwerft@VerwerftJan·
1/ Agree that reduced O₂ utilization in HFpEF mirrors COPD — likely driven by inactivity & deconditioning 🛋️. But if A-VO₂Diff is similar in HFpEF vs controls despite lower CO 🫀— and longer capillary transit time — that suggests impaired 🦵peripheral extraction (Ref ➡️6/)
Jan Verwerft tweet media
Yogesh Reddy@yreddyhf

Exercise intolerance in HFpEF is almost all about the heart, and little to do with the periphery. Skeletal muscle changes reported are similar to those in multiple other non-HFpEF diseases likely due to heart failure induced sedentariness + deconditioning rdcu.be/ewAxS

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Kiran Rikhraj
Kiran Rikhraj@KiranRikhraj·
Back to basics! I am starting a new series of videos focusing on mastering basic #POCUS concepts. Starting off with honing your ability to obtain the 4 basic cardiac views and steps on how to obtain additional/advanced views. Please give it a watch: youtube.com/watch?v=kX2s_2…
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Benoy Shah MD
Benoy Shah MD@dr_benoy_n_shah·
**VALVE CASE OF THE MONTH** Mid 40s, exertional dyspnoea Loud ESM on examination Referred for echocardiography Question - What is the severity of aortic stenosis? #CardioTwitter #MedTwitter #ACCFIT
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🇳🇴🇩🇰Asbjørn Støylen 🇬🇱🇵🇸🇺🇦
Contractility cannot be measured by cardial imaging; all imaging measures shortening (=volume reduction), which is load dependent. Myocardial contraction is not shortening, during systole there is both contraction without shortening, and shortening without contraction.
🇳🇴🇩🇰Asbjørn Støylen 🇬🇱🇵🇸🇺🇦 tweet media
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Dr G Rajesh (Gopalan Nair Rajesh).
In all ACS like presentations, look at suprasternal window for type B dissection, esp: if CAG done through right radial is normal.Type A dissection you will pick up easily from PLAX view, suprasternal may not be routine!Howmany send D-Dimer routinely in all chest pain syndromes
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Abdulla A. Damluji, MD, PhD
Reevaluating Beta-Blocker Recommendations Post-Myocardial Infarction: Perspective on the 2025 Guideline Update: @JACCJournals 🥸Commentary on the guidelines - early beta blocker use post MI - 😱@MichaelGNanna wrote extensively on this in older pts. 🥸Take a look 👇👇👇
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Novi Yanti Sari
Novi Yanti Sari@slumberbell·
Brilliant reflections about #HeartFailure in Asia by the one and only @lamcardio: 📍 Same burden, same challenges, but different⚠️ 📍 High heterogeneity across #Asian populations 📍 #COPD stands out as a key risk factor in South & East Asia 🚬 📍 Influence of traditional medicine in some regions 📍“lean diabetic” phenotype in Southeast Asia 📍 Lower rates of #AFib among South Asians #HeartFailure2025 @escardio
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Abdulla A. Damluji, MD, PhD
Abdulla A. Damluji, MD, PhD@DrDamluji·
Palliative and End-of-Life Care During Critical Cardiovascular Illness: A Scientific Statement From the American Heart Association: @AHAScience @CircAHA 🥸 Led by my friend @EBohula: the most comprehensive account on palliative care/futility during cardiac illness 😱 Summary
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