Jun 06 2025 This Week in Cardiology

0:00 You're listening to this week in cardiology from the heart.org Medscape Cardiology. This podcast is intended for health care professionals only. Any views expressed are the presenter's own and do not necessarily reflect the views of WebMD or Medscape. Hi everyone, this is John Mandola from the heart.org Medscape Cardiology and this is this week in cardiology for June 6, 2025. This week, listener feedback on cardiac sarcidosis, out of hospital cardiac arrest, less is more again when it comes to post stent antiplatlets, lipoprotein little a and atrial fibrillation and hepath. First up, some listener feedback. I received an email from

0:46 Finland this week. Dr. Arena Candlean from Helsinki writes that I should clarify some of my comments on the cardiac sarcidosis paper that I covered last week. The paper I spoke about was from a primarily Dutch and Minnesota group and they had compared societal professional societal recommendations for an ICD versus CMR phenotyping in patients with suspected cardiac sarcidosis. And the key word there is suspected cardiac sarcidosis. In that study that I covered last week in the European Heart Journal, CMR phenotyping by four criteria. No LG normal EF, no LG abnormal EF, pathology frequent LG, LG,

1:34 and pathology rare LG performed better than professional societal recommendations for VT. Dr. Kendallan from Helsinki pointed me to an incredible circulation EP paper from their group in Helsinki on 305 patients with either biopsy proven cardiac sarcoid which was just under half the group or findings highly suggestive of cardiac sarcidosis. Now right away this is a different population because the first study looked at patients with distant sarcidosis say in the lungs and they were being evaluated for cardiac involvement while the second study in the circ this year studied patients with proven cardiac

2:19 sarcidosis. The two main points of differences arise in patients with true cardiac saride all have pathology frequent LG. So in the circ paper if everybody has path pathology frequent LG it can't distinguish risk rather the Finnish group showed that it was the degree and somewhat the distribution of LG that predicts sudden death and VT they found that myioardial LG making up more than 9.9% of LV mass or affecting s greater than six LV segments may suggest prognostic ically significant LV involvement in a high risk of sudden cardiac death. This

3:05 analysis and its implication bears similarities to what we do for hypertrophic cardiammyopathy, doesn't it? Namely, in HCM, there is a risk score that corresponds to a yearly risk of VT. And if that 5-year threshold reaches greater than 6% for sudden cardiac death, then an ICD is recommended. The ESC also recommends a similar type risk score prediction for laminopathies as well. ICDS for criteria above a risk threshold. The Finnish authors therefore suggested in their discussion section that their CMR findings could have clinical relevance. quote, "In patients who have no other guideline-based class one or 2A indications, implantation could be considered if LG mass is

3:53 greater than 9.9% by the full width at half maximum method or the LG involves greater than six LV segments." They write less extensive LG predicted a 5-year sudden cardiac death or VT rate less than 7% with a sudden cardiac deaths risk of 0.6 per 100 patient years. And in these patients, other EP studies or close surveillance with repeated risk assessments could be discussed at shared decisionmaking. I think if you care about cardiac sarcoid and risk stratification, this is an excellent paper. it's worthy of a bookmark and I appreciate the feedback because I learned a lot reading this extra paper and reading more about this. My one

4:39 comment and this is not at all a criticism of the paper or papers but as a clinician as a doctor I struggle with these risk thresholds say in hypertrophic cardiammyopathy what if the five-year risk is 5% not 6%. or in the case of cardiac sarcoid the LG LG mass is 7% not 9.9%. The dichotomization of ICD or no ICD based on continuous variables makes me nervous. It makes me nervous because we have a prevention of sudden cardiac death and that's the ICD. But of course I realize it would be unwise to place ICD in all patients including these low-risk people because of ICD harm. But

5:25 not having an ICD and needing it is also a serious risk. I don't have the answer and perhaps there never will be an answer to finding the ideal patient for an ICD. But hypertrophic cardopathy and cardiac sarcoid are clearly different from the RCTbased heart failure ICD criteria. In heart failure we have entry criteria from trials albeit old trials and it's sort of right. We used to be able to say that if you were like a made it to patient, you would have a 30% lower mortality with an ICD compared to no ICD. That's from a trial. The modern problem of course is that medical therapy is a lot better. And that 30%

6:10 benefit may be a lot less. And by the way, that is why that if you practice in Europe, you should be participating in the profit trial of ICD versus no ICD in patients with es schemic cardiammyopathy. One practical comment from my experience is that if a patient with cardiac soyid has heart block and you're implanting hardware, it seems wise to strongly considering an ICD if the LG is even close to any threshold that you're worried about. Once again, thanks for the listener feedback. I learned a ton from it. All right, next topic is news in out of hospital cardiac arrest. The AA sent me two emails yesterday regarding their efforts to increase awareness of bystander CPR. One was an

6:56 NFL player named Justin Reed who is leading an effort. The other email said the Atlanta Falcons are teaming up with the AHA to equip players and coaches with the life-saving CPR skills during National CPR and AED week. The second note is that CIRC outcomes published a paper recently from a group at Mid America Heart finding that resuscitation practices for out of hospital cardiac arrest differ by geographies. Namely, compared to white catchment areas, communities serving black and Hispanics areas have lower rates of out of hospital cardiac arrest survival. Now, of course, the causes of this could be a lot of things, but the research team noted that in black and Hispanic areas, first responders were less likely

7:43 to recognize cardiac arrest, police were less likely to respond to a cardiac arrest, and patients were less likely to be defibrillated. Basically, community level out of hospital cardiac arrest care was less than what it is in white catchment areas. And this may explain the difference in survival. uh perhaps I think it explains some of the differences but out of hospital cardiac arrest survival rates are complicated and differences could also be due to the severity of the disease. My point in highlighting out of hospital cardiac care is that it's one of the highest value interventions in all of medicine. I spend many hours on this podcast discussing new treatments with marginal benefits. bystander CPR and

8:30 adequate EMS system is hugely valuable. Why? Because only 10% of patients with out of hospital cardiac arrest in the US survive. Ventricular fibrillation without CPR or an AED occurring out of the hospital is nearly 100% deadly. A patient with VF depends on the knowledge and availability of his or her neighbors. Since survival is so bad, any tick up is likely highly cost effective. Plus, bystander CPR and public AEDs are nearly free of risk. It's all benefit. And look, I realize that cardiac arrest care isn't as exciting as the newest ablation catheter or stent or drug, but it's surely a lot higher in value than either of these things. A new tricuspid

9:18 valve clip or more AEDs in your city. I'd go with the ladder every time. So, good on the AHA and the NFL. The other thing I love about promoting out of hospital cardiac arrest care is that it brings communities together for an obviously great and totally uncontroversial cause. All right, third topic today is post stent antiplatlet therapy. And I hesitate to even delve into this topic because it is perhaps the most confusing in all of cardiology. But I will because yet another study finds that less is more. Now this seems too simple to state but the idea is that having a metal cage propping open a coronary lesion is

10:04 neither a fix nor is it free. Metal in the coronary attracts platelets and then clots can form. Stent thrombosis is a medicalized jargon word, but it's a terrible outcome because you go from a 0% blockage to a 100% blockage. The good news is that the body eventually and usually forms a layer around the stent protecting it from circulating platelets. This we call and jargon wise it is a whopper endothelialization. The problem of course is that antiplatlet drugs which prevent stent thrombosis are also not free. Blocking platelets increases the risk of major bleeding in the gut, kidneys and brain. So the quest and it is surely a quest is

10:51 to find the Goldilocks recipe for preventing thrombotic or clotting events after a stent such as MI with the lowest rate of bleeding. Now the usual regimen is to use two antiplatlet drugs like aspirin and either clitigil or tyagular or proagril for a period before switching to a single antiplatlet. Now perhaps you can see the complexity already right so there's four antiplatlet drugs of varying intensity and there are near infinite ways to break up the time after the stand. 1 month 2 months 3 months 6 months 12 months. There's different types of patients. There's ACS versus stable CAD patients. And then there's high bleeding risk and not high bleeding risk

11:37 patients. And then there are different stances. And you start multiplying all these and you can get about a quadrillion different ways to do antiplatlet drugs after stances. Today I'll tell you about one trial, but know that there are many. The South Korean trial recently reported was called the 4D ACS trial and it was a pretty clean trial. It's a comparison of two procural based strategies in about 650 patients who had PCI instead during an acute coronary syndrome. One group gets one month of dual antipllet therapy with aspirin 100 and procural 10 except the procil dose is adjusted to five milligrams for older patients or one or patients less than 60 kg versus the

12:23 control arm which was 12 months of DAP with aspirin 100 and procural 5. The primary endpoint is called NACE, not MACE, but NACE with an N or net adverse clinical events. That's death, MI, stroke, eskeemia driven revascularization, and bleeding. Bleeding also has five different grades. The trial measures types two and five. So, the most minor bleeding was not included. And what they found was that short duration dual antipllet therapy is better. NACE occurred in 4.9% of the 1-month DAP group versus 8.8% of the 12-month DAP group. Now, the trial was a non-inferiority comparison, which is a good use of non-inferiority because the

13:09 short duration is very much less intense than the standard 12-month stat. If it was just as good, it would be a win. And indeed, 4.9 versus 8.8% easily made non-inferiority. In fact, the hazard ratio was 0.51. And that also made superiority. Now why was this so? The driver of the lower NACE was a 77% lower rate of bleeding in the short duration DAP arm 1.2 versus 5.5%. There were almost no differences in thrombotic events such as MI stroke and eskeemia driven revascularization. I cover this study because it is such a clear result. If you're using parasogil, a one-mon dap regimen seems surely better than the 12-month DAP. So, you would think it's

13:56 clear now, but it's not clear. First of all, all these patients were Korean and and Asian patients may respond differently to anti-platelets than other groups. Second, the study used a type of stent that is not used in the US. Third, what about one month's DAP versus three months of DAP? What about combos of different antiplatlets like culpitigril tyagul? In general, I can say that the trend of late is for shorter courses of DAP. But my solution in real life is to use one of the most important tools in all of medicine and that is phone a friend. So I spend a lot of time calling my interventional cardiology colleagues and asking what they think. They've done the stent and a bifurcation stent in a prox is probably going to be different than a mid circumflex lesion. And

14:43 perhaps I can make five general statements about this. Right? So ACS patients generally require longer DAP due to higher thrombotic risk. NonACS patients most likely can safely use shorter DAP durations. High bleeding risk risk patients may benefit from abbreviated DAP regardless of their presentation. and P2Y12 monotherapy after initial DAP shows some promise for reducing bleeding while maintaining efficacy. And of course, an individual risk assessment may may prove helpful in guiding duration intensity of DAB. Finally, my friends, I've said this a million times, but if you're having a STEMI, you want a stent done fast. If

15:31 you have chronic coronary disease, medical therapy first avoids the entire issue of deciding on the combination of antiplatlets. Sadly, this doesn't happen enough in many places in the US. All right, next topic. Let's talk about lipoprotein little a and the new prevent equation for predicting cardiac events. Jamama Cardiology has published an interesting study looking at the value or lack of value in adding lipoprotein little a into the new prevent equation. Now the first thing to say is that I covered the AHA's prevent equation in August of last year. The proponents of the prevent equation say it's better than the standard pulled cohort equation which of course both these output tenure

16:18 risks of atheroscerotic events based on clinical criteria. Now, of course, the proponents of prevent don't just say it's better. It has been validated in observational data sets. Prevent differs from the pulled cohort equation because it incorporates kidney function, statin use, social determinance of health, and it removes the race category. It also starts at a younger age. Here's the most provocative aspect of prevent and I I I find this interesting. It simultaneously is felt to be more accurate. So that's good. But it lowers estimates of CV risk and lowers the number of statin eligible people. Oh, I say gulp, double gulp. Anyways, the question of the jamoc

17:04 cardiology study was whether the prevent equation can be made better by adding lipoprotein little a which as you probably know is mostly genetically determined and when elevated is strongly associated with a higher risk of CV vents. This is a reasonable question because since race is removed from prevent and race can bear on the likelihood of having elevated lipoprotein little A, adding it could be important. So here's what the group did. It's a complicated study. There's two databases, the UK Bioank and Mesa. This is of course a very big big data paper. Both databases have long-term follow-up and lots of clinical uh characteristics. Individuals in the database were put into four categories. Low risk, that's 5% or less 10 years.

17:51 Borderline risk of 5 to 7.5% risk. Intermediate, which is a large category from 7.5 to 20% risk, and high risk greater than 20%. Then they measure tenure event rates and they correlate it with with lipoprotein levels overall and by risk category. And of course, they do adjustments by age and sex. Their main end point is the net re reclassification improvement or NRI which is a complicated endpoint. Let me try to explain. The NRI measures how well a new risk prediction model reclassifies people compared to an old model. But it does this by tracking movements in both directions and then netting them out. The NRI splits re reclassification into

18:39 events, people who actually had the outcome and non-events, people who didn't. And for each group, it calculates the proportion who moved up in risk categories minus the proportion who moved down. This gives you a net movement figure for each group. Now, the problem with NRI comes in relative versus absolute differences. You you've seen this in the NRI studies of CAC for instance where when you consider the absolute numbers vastly more people don't have events and are actually misclassified using the NRI. Now I asked Claude about this because Claude helps and Claude came up with a conceptual trap that I think it's worth talking about. Claude says that

19:24 people often interpret NRI as a 20% improvement in classification when it's really a 20% net improvement after accounting for movements in both directions. The absolute amount of reclassification which tells you how much the models actually disagree gets hidden in this netting process. So in this study they measured NRI both categorically that is how many moved into a different risk category based on lipoprotein little a for example going from a borderline risk to an intermediate risk and they also measured the NRI category free which is simply whether the patient moved up or down in risk at all and these differed a lot in the category free net reclassification

20:12 improvement for athoscerotic events using lipoprotein little a was about 06 or 6%. Now the categorical NRI was 10 times lower at 6%. Now the way I would trans translate this is to say that adding lipoprotein little a reclassifies about 6% of people on net for CV risk but it is far less valuable for moving people between low borderline intermediate and high-risisk categories. Here it was well less than 1%. Now the study did something else that is perhaps somewhat useful. They looked at subgroups of people who get who may get more reclassification from lipoprotein little a. They found that

20:59 adding the the lipoprotein little a measure resulted in slightly more reclassification for borderline risk and lowrisk people. And that might be important because borderline risk people are trying to decide about statins. And there may be low-risk people who have an elevated lipoprotein A that might benefit from statins. But I have to say when I looked at these absolute differences, they're modest. For instance, the NRI for lowrisk coronary prediction was 10% versus 7.5% for intermediate risk. 10 versus 7.5%. Doesn't seem like a big difference. So overall my comments, I feel like this is a nice paper. It's a nice effort. Adding lipo lipoprotein

21:45 little a helps a little with prediction. A low-risk person, for instance, who has an elevated lipoprotein little A may want to take statins. A borderline person with a super low lipoprotein little A may want to pass. But here's the thing, and I feel it's the same with CAC. I've seen patients in clinic for nearly 30 years in the middle of America and the vast majority of patients that I see perhaps 90% or more have no idea how to conceptualize the difference between a 7% and 9% and 13% risk of 10-year events. I've had lipids done recently and I'm borderline risk and I can't really conceptualize a 10-year risk of a non-fatal event. Now, maybe you can, but

22:33 I can't. There's two reasons I struggle with this. One is philosophically. I'm almost convinced that much of disease and health is just good and bad luck, as in stuff happens. The second reason I struggle with a 10-year risk prediction is relative to Ukraine attacking Russia's planes and the threat of World War II. How much should I worry uh whether my non-fatal risk of a CV event is 7% without lipoprotein little A or 9% with lipoprotein little A. I come back to my bottom line when it comes to prevention. There are maximizers and for these patients they want to do everything. For them you don't need lipoprotein little A. It seems useless because they're

23:19 already going to take maximal statin and lipid lowering therapy. And then there are minimizers who aren't taking pills no matter what. And for these patients, lipoprotein little A is useless. So for the few in the middle who sweat the details, fine. You might benefit a little from adding lipoprotein A to the mix. All right. Final topic today sort of quickly is atrial fib and heping in Europace. A group of prominent researchers, EP researchers, reanalyzed the TopCat America's trial, looking at the role of AIB in predicting bad outcomes in patients with hepath. It's always worthwhile looking at TOPCAT. It's one of the most important trials in cardiology. Sadly, it was marred by data

24:05 irregularities from Russia and Georgia. Topcat was spirolactone versus placebo and heepath and the hazard ratio of the overall trial was 0.89 for the compositive death, cardiac arrest or heart failure, hospitalization. This 11% reduction did not reach statistical significance. But all cause death was 22% in the Americas and only 8% in Russia and Georgia. And the drug had little effect in that region. And further metabolic studies found that a third of patients supposedly randomized to spiralactone had undetectable metabolites. So excluding Russia and Georgia, Topcat ended up being a positive trial with a hazard ratio of82 and conference interval

24:51 0.69 to 0.98. And I think this is a really important point because now with fenerinone um we we have spironolactone and if you consider just the Americas part of top spirolactone is a effective heft pep drug. So the europace authors made two groups. They were interested in aphib study patients who had aphib before or at study entry. This was called the any aphib group. And then they looked at study patients with ongoing AIB who had it at entry. Then they propensity matched patients with no AIB and looked at future outcomes in the trial. Now I know it's pretty easy to predict what will happen. Before I tell you the results, I

25:37 hope you are thinking small hyperdamic non-compliant left ventricles are not going to do well losing the atrial kick when aphib occurs. So the primary outcome of this study was was really comparisons in CV mortality. They had about 580 patients in TOPCAT who had any AIB, 400 who had ongoing AIB. And they found that any AIB was associated with a statistically higher level of CV hospitalization, heart failure, hospitalization, and progression of heart failure. Any AIB, however, was not associated with an increased risk of sudden death. ongoing AIB similarly was associated significantly with cardiovascular death,

26:23 pump failure death, CV hospitalizations and heart failure hospitalizations. And it was interesting to me, I think this is the most interesting finding from this paper that neither any AIB or ongoing AIB was not not strongly associated with sudden death. AIB seemed to associate mostly with progression of heart failure or palm failure. Now this paper has a lot of complicated comparisons but I think it can be summarized as AIB is a bad thing to have if you have underlying heft. The question of course the clinical question is how to modify this problem with therapy. So my first recommendation when you have this is to phone a friend your EP colleague. I can't give you a generic right answer

27:10 because there isn't one in these patients. half patients often have serious co-orbidities that have to be considered. Things like polyfarm pharmacy and CKD and valvular heart disease and frailty. So maybe antirethmic drugs are the right answer. Maybe catheter ablation. And I think underused in many places is the pace and ablate strategy. We're going to see a lot more hep these days because people live longer with more chronic illnesses. And when Aphib occurs in these patients, it's serious. Take Mr. Rogers advice and and realize that we all need helpers in our lives. And please call your EP friends. So that's it for this week in cardiology. As always, I'm grateful that

27:57 you listen. Uh thank you. Next week on Friday, I'm going to be speaking at the London Arhythmia Summit, and I'm excited to be there. If you're there, please come up and say hello. And remember, if you like this podcast, please take the time, write us a review or give us a rating. If you don't agree with anything I said, please email me or make a comment on the website. I learn a lot from this feedback. Until next week, this is John Mandola from the heart.org Medscape Cardiology. You're listening to this week in cardiology from the heart.org Medscape Cardiology. This podcast is intended for health care professionals only. Any views expressed are the presenter's own and do not necessarily reflect the views of WebMD or Medscape.