Aug 15 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 August 15, 2025. This week, big new hypertension guidelines, ultrarocessed foods, coronary sinus reduction and evidence-based medicine, and more good news on PFA for AF ablation. The hypertension guidelines, there are new AHA guidelines out yesterday. The

0:49 PDF is more than 100 pages. There's no way to hit every highlight. I'm going to write a column on what I like and don't like for next week on Medscape. Here are some nuggets from the massive document that's only been out for a day. The writers start with a top take-home messages section. This actually I do not like for the same reasons that I don't like summary figures or infographics or threeinut recap videos, no matter how funny the narrator may be. Medicine is about details. Evidence-based medicine is about details and these efforts to reduce a 100page PDF into take-home messages is in my opinion a bad idea. Now, I do like the early and welldetailed emphasis on taking blood

1:36 pressure properly. You know, feet on the floor, armrested, not talking, all that stuff. This is not done this way in many offices, which boggles my mind. The committee is strongly against cuffless blood pressure devices and I actually did not know that that was such a prohibition but it's good to know. There's also a nice section on secondary hypertension. The two most common causes are primary aldsteroneism and obstructive sleep apnea both of which should be referred to specialty physicians. Other important causes of hypertension of is alcohol or certain drugs like non-steroidal drugs. Much less common is renovascular disease. The authors write now the prevalence of primary eldestoneism is

2:22 approximately 5 to 10% among individuals with stage 1 hypertension and 11 to 22% among individuals with stage 2 hypertension which varies depending on the modality of testing and testing thresholds used to diagnose the primary aldsteroneism. The authors do not give short shrift to prevention or hypertension via lifestyle either. Now, I have little to say about it because a it's so obvious that diet, exercise, moderation of alcohol, proper sleep is foundational for having good health and good blood pressure. One large change in this document is the treatment threshold using cardiovascular disease risk estimation. Now, not with the PCE, but the prevent score, which is

3:09 new from AHA, and I've covered the prevent score on previous podcasts. It's pretty controversial because it is felt to be more accurate risk estimator but and this is a huge but the prevent score results in fewer people reaching the statin starting threshold but prevent features prominently in these hypertension guidelines and first is the choice to start therapy. So if blood pressure is 140 over 90, that's one criteria. The authors just say start therapy regardless of comorbid conditions. But for the greater than 130 over 80 patients, initiation turns on the presence of cardiovascular disease, diabetes, CKD, or a prevent score greater than 7.5%

3:56 for 10 years. Now prevent also features in treatment goals and the aim is usually to get below 130 over 80 and to push towards less than 120 systolic when prevent is greater than 7.5%. So I've heard from some colleagues a concern that since prevent is better calibrated than the PCE pulled cohort equation, it might result in fewer people being started on treatment than the PCE. The risk of that seems lower though in hypertension than in statin initiation. And here's why. Because with statins, the decision is largely a riskbased decision. You put the numbers in, you calculate it above 7.5%, you start uh statin therapy. Whereas in

4:42 hypertension, there is also the marker of that single 140 over 90 or you might reach criteria because you have cardiovascular disease, CKD, diabetes. And remember that cardiovascular disease is being diagnosed much more easily in the modern era. For instance, there are some people who believe that coronary calcium is a diagnosis of cardiovascular disease. I don't know about that, but the days of having to be diagnosed with cardiovascular disease by a cardiac cathization are certainly gone. Now, the authors don't say this, but I'm going to repeat myself. The main purpose and largest value of hypertension treatment comes in treating younger people early in life so that they avoid

5:28 stroke, kidney and heart disease and live to old age. When they reach old age, they have won. Prevention now must be balanced against harm. The authors do spend many words and they write very academically on the treatment in the elderly. I would summarize it more simply as just use common sense. An oxygenarian is winning the game of life. Our job is not to mess things up with hypotension induced broken hips or subdural hematis. Now nothing new comes in the choice of medications. It's dioide type diuretics, long acting dihydropirines, calcium channel blockers, ACE inhibitors, ARBs are all recommended as firstline therapy. Note however the absence of

6:13 beta blockers are not recommended for first line. Now, one twist on initiation comes in section five where the authors recommend starting medical therapy for patients with stage 2 hypertension that's greater than 140 over 90 with two firstline meds of different classes in a single pill combination and they recommend this for adherence's sake. I used to be against combination pills but I've changed because anything that decreases the work of being a patient I am for. What's more, there is strong empirical evidence that combination pills increase medication adherence. Now, treatment goals follow the trials, namely the sprint trial, which found advantages to the goal of 120 over 80 in

7:00 patients with high cardiovascular risk. And this is fine, but again, I think more beneficial in 50 and 60 year olds so that they get to age 90 without a stroke or MI. Now recall that the Accord trial in patients with diabetes did not find benefit for this lower target. So the question arises, do aggressive blood pressure targets not work for patients with diabetes? I would cite two lines of evidence suggesting that we should also consider lower targets in patients with diabetes. And one is the recently published BP road trial which was published in New England Journal of Medicine and it found that in sprint-like patients there were benefits for the 120 versus 140 targets. This was

7:45 12,000 patients uh randomized in China. I also love a paper by Luke Laughaflin where he and colleague Francis Allenot created a sprint trial score based not on inclusion criteria of sprint but on the actual clinical characteristics from table one in the sprint trial and then they applied it to patients in accord and lo and behold the sprint trial score was able to discriminate a subop of patients with diabetes who were actually in sprint datari zone and they responded to intensive blood pressure control in the same way as they did in the sprint trial even though in accord blood pressure trial on the whole was a negative trial. Now there are large

8:31 sections in the document on managing blood pressure in stroke and intraanial hemorrhage as well as in pregnancy and since these are often a subsp specialty field that I'm not involved in I won't say much about those. One section that I do want to comment on is the section on resistant hypertension and renal denervation. I think the authors are quite sober about renal denervation. I really like their section 5.6 on resistant hypertension. They urge us first to of course confirm resistant hypertension. Look closely at drug adherence. And I can't emphasize this enough because throughout my years, I've stopped counting how many times a patient with resistant hypertension becomes hypotensive in the hospital when put back on blood pressure meds.

9:17 Another nugget, use mineraloid receptor antagonist for resistant hypertension and when they are poorly tolerated, try auroride. This is a trick that my nephrology friends taught me. Now the putitive wonder drug finerone is mentioned only once in the document in the references but I do have to wonder if there may be a role once bernolactone and eperinone are poorly tolerated in these patients with resistant hypertension. As for renal denervation the authors are cautious and I highlight this passage. Quote, "While some trials showed a small but significant reduction in 24-hour ambulatory systolic blood pressure by 3 to 5 millimeters of mercury over the sham arm, others failed to reach their primary end point. Although broader

10:05 indications are approved for the renode deninovation devices by the FDA, given the relatively short duration of follow-up in clinical trials with modest blood pressure lowering effects and the absence of cardiovascular disease outcome trials, renal dinovation should not be considered as curative therapy for hypertension or full replacement for anti-hypertensive drugs. I think that's a good statement. I would have been stronger, but it's pretty strong. And then in the colored box where they give the recommendations a 2B level and they write that renal denervation may be reasonable if meds are not effective or intolerable. Now of course I really worry about this intolerable label for medicines. While there are surely some patients who tolerate medicines poorly,

10:53 I worry that if Reno Dinovation earns reimbursement status from payers, there will be an epidemic of patients who cannot tolerate blood pressure medicines. I can even imagine direct to consumer ads creating a disease category of not being able to tolerate blood pressure medicines. This could morph into the left atrial appendage occlusion situation where there's posters in lobbies of hospitals encouraging patients to consider a non-medical option for their stroke prevention. And I cannot be more clear. These sorts of things are a blemish on our profession. We shred our status as respected professionals when we promote procedures like left atrial appendage occlusion and renal denervation. Renal denovation trials were either negative or they found minimal

11:40 differences in systolic blood pressure over no more than a few months and do not be fooled by any of the extension studies with render denervation because the nancond that a render denervation trial unblinds the patients the results are basically worthless. And I would site simplicity one and two trials for that. I'll write up my thoughts on this hypertension guideline document coming next week and stay tuned for that. Now the second topic is ultrarocessed foods. The AHA was been busy this week. There's also in circulation a very long scientific statement on ultrarocessed foods and their association with cardioabolic health. I am not a nutrition expert. Perhaps you

12:26 are not either, but we all know some basic facts. Fact number one is that cardiomabolic health in the US is a public health crisis of massive proportions. The saddest part of this crisis is how it has decimated the health of children, especially children in lower socioeconomic levels. Fact number two, snack foods taste good, are easy to obtain, less expensive, but have extremely poor nutritional quality. For instance, when there is junk food in break rooms in the hospital, it just disappears. Donuts gone. Fact number three, many of these snack foods are ultrarocessed and filled with artificial dyes. And fact number four,

13:11 my grandkids go to public schools that do not have gym class every day. Let me repeat that. They don't have gym class every day. How can kids concentrate on learning without exercise? I cannot do it. While I am not sure how to untangle the ultrarocessing and chemical components from the fact that most of the foods are full of empty calories, I think the medical profession we must try to help sort out this public health crisis of terrible cardtabolic health. And I think there's lowhanging fruit. Excess calories in the form of car carbohydrates is surely one of them. Not having enough focus on exercise is another. I'm not sure food processing and artificial dye is the best initial

13:58 target. Now, I may be wrong or just naive, but it strikes me how different other countries handle this problem. When you go to ESC and it's in Amsterdam, you look out the window of that convention center and you see packs packs of lean Dutch kids riding their bikes to school. Now, in my country, in United States, you see lines of running cars at schools waiting to drive their kids home or drop them off. And therein lies a clue, I think. All right. Next topic is refractory anga and the coronary sinus reducer, a lesson in evidence-based medicine, especially for tricuspid valve colleagues. Now the coronary sinus reducer is a balloon expandable hourglass shaped

14:44 stent that when deployed causes narrowing of the coronary sinus. It increases coronary sinus pressure which is believed to redistribute blood flow from non-eskeemic into eskeemic myioardium. This device is not used or approved in the US. So my colleagues here may not know about it but a recently published metaanalysis injack interventions is still worth your time. And I would say this from an EBM perspective, evidence-based medicine perspective. It's from the group led by Rasha Alami at Imperial College in London. They metaanalyzed the data for coronary sinus reduction to treat refractory anga. It stems from single arm unblinded studies and three sham control trials. Now that recall that coronary sinus

15:31 reduction can relieve anga by two mechanisms. One is the physical effects of directing blood flow to underperfused areas. But the second way and the authors of the meta analysis call this contextual effects or non-treatment related phenomenon. This includes the placebo effect, the Hawthorne effect, the care setting effect as well as things like confounding bias and simply natural history. These nontreatment related phenomenon is the reason you always tell patients who you just put in a stent or pacemaker that they will be hard to contain after the procedure. Now the RCTs are a bit divergent. In general they find reduction of angula symptoms but mostly do not show any

16:18 objective differences in profusion. The most recent and largest CSR trial, also from the Imperial College group, called the Orba Cosmic Trial, 50 patients, half got CSR, half got a sham CSR, and found no significant differences in stress myioardial blood flow, but they did observe significant reductions in daily anga episodes. So the main findings of this meta analysis was that the single arm studies the non-controlled studies showed much larger effects on the reduction of angula than the poolled estimate from the three sham control trials. For instance, 81% of patients in the non-blinded studies improved one functional class with CSR versus only 26% in the sham control arm.

17:06 And for the Seattle ANGA questionnaire domain measures of ANGA, the RCTs actually found no statistically significant differences whereas all the domains were positive in the uncontrolled settings. I highlight this study and Medscape Cardiology wisely has a news story on it because it so beautifully reveals the need for proper placeboc control trials in the procedural interventional field. And I don't know what the resistance is. If all we used were non-controlled studies, we'd think that CSR was an amazing anti-angal device. Yet, it seems too obvious to say this that doing procedures comes with the physiologic effect of the procedure plus all the other things like expectation and changes in natural history and Hawthorne

17:51 effect. I mean, who I ask has not had a post AF ablation patient sing your praises because you did such a skillful procedure. You improved their quality of life. They're so happy they're giving you five stars on Google and they're in atrial fibrillation during that visit. Now, in the matter of the coronary sinus reducer, the Imperial College team are actually in the midst of doing another larger RCT called Corsera 2, which will hopefully further sort out the true placebesistant effect size of this procedure. And it's an important thing to know because the implant procedure can have serious albeit low incidence complication. It also boggles my mind that medical scientists felt that we could measure quality of life benefit in patients with

18:37 tricuspid valve interventions without a proper placebo control. This this metaanalysis is clear evidence that you need placeos every bit as much for procedures as you do for tablets. And placebo controls are not only for subjective endpoints. Remember that the Simplicity 3 hypertension trial found that the excitement of blood pressure reductions from renderovation were much more modest when compared against the sham control. All right, another topic is PFA and it's still looking strong. I'm going to report on another positive albeit preliminary study on PFA for AF ablation. Now you know that I am a slow adopting medically conservative doctor. New things worry me. But it's been about

19:24 a year with PFA during AF ablation. I have not once gone back to thermal ablation since adopting PFA and RCTs of PFA versus thermal ablation have shown similar efficacy and safety. You still can get tampenod and stroke with PFA. But the dreaded complications of death from AE fistula have not occurred with PFA because it is cardio selective at least purportedly. Now, at my center, my partner and I have done at least 300 cases of PFA ablation, and we feel that the efficacy is better. I emphasize feel. We seem to do fewer repeat procedures, but patients clearly have less post-procedural symptoms of inflammation like less chest pain and less heart failure episodes.

20:10 This month, a group led by professor Andrea Natali have published an interesting observational prospective non-random comparison of anti-coagulation after thermal and PFA ablation. And I emphasize it's a non-random study and we must be careful. But here's what they did and found. They had about 400 patients who had RF, 400 patients who had PFA at multiple institutions. They then did propensity matching to attempt to balance the characteristics. Now the good news is that colleagues of Dr. Nutelli tend to do AF ablation in the same way. PVI and posterior wall isolation with both RF and now PFA. So at least there's not much procedural variation.

20:56 Half of each group 200 patients thereabout each stopped the oral anti-coagulation after one month. The other 200 stopped after two months. So they had four subgroups. There was no protocol. Stopping oral anti-coagulation was done for different reasons. The groups that stopped oral anti-coagulation after only one month, they called group one. The groups that continued oral anti-coagulation for more than two months were called group two. And the findings were dramatic, very dramatic. In fact, in the groups one stopping anti-coagulation after 1 month, there were zero strokes in the PFA group and 16 in the RF group. In the groups two, those who continued oral anti-coagulation for more than 2 months,

21:43 there were two stroke events in the PFA group versus seven in the RF group. And what's more, AF recurrences occurred in 18% of the PFA group versus 27% in the RF group. a statistically significant difference which of course could have been the driver of these major differences in stroke events and so my comments this paper was published in heart rhythm it's observational surely confounded because the doctor chose to do PFA versus RF but it is prospective data that finds that in at least 200 patients who stopped anticoagulation one month after PFA there were zero stroke events whereas that whereas there were a lot of stroke events after stopping oral anti-coagulation after RF.

22:28 It suggest suggests that perhaps there is less inflammation and/or endothelial disruption with PFA than with RF. And if this is confirmed in other studies, it would be yet another huge advantage to be able to stop oral anti-coagulation that quickly after AF ablation. I I reiterate though that this observation needs further confirmation. So that's it for this week in cardiology. As always, if you like this podcast, please take the time, give us a rating, write me a review. If you don't agree with anything, by all means, let me know. We'll do it as listener feedback. Until next week, this is John Mandola from theheart.org Medscape Cardiology.

23:14 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.