Aug 15 2025 This Week in Cardiology

Medscape

20 hours ago

Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast
For the week ending August 15, 2025, John Mandrola, MD, comments on the following topics: Big, new hypertension guidelines, ultraprocessed foods, coronary sinus reduction and evidence-based medicine, and more news on pulsed field ablation for atrial fibrillation.
BP Meds Should Begin Promptly, New ACC/AHA Guidelines Say
There are new AHA-led guidelines on hypertension out yesterday. The PDF is more than 100 pages. There's no way to hit every highlight; I will write a column on what I like and don't like next week.
Here are some nuggets from the massive document that's only been out for a day.
The writers provide a 'Top Take-Home messages' section. This I do not like, for the same reasons I don't like summary figures or infographics or 3-minute recap videos, no matter how funny the narrator may be. Medicine is about details, and these efforts to reduce a 100-page PDF into take-home messages is a bad idea.
I do like the early and well-detailed emphasis on taking blood pressure (BP) properly. You know, feet on the floor, arm rested, not talking, etc. This is not done in many offices—which boggles my mind. The committee is strongly against cuffless BP devices. I did not know that — and it's good to know.
There is a nice section on secondary hypertension; the two most common causes are primary aldosteronism and obstructive sleep apnea, both of which should be referred to specialty physicians. Other important causes of hypertension are alcohol or certain drugs, like NSAIDs. Much less common is renovascular disease, the authors write.
The prevalence of primary aldosteronism is 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 primary aldosteronism.
The authors do not give short shrift to prevention or hypertension via lifestyle. I have little to say about it because a) it is obvious that diet, exercise, moderation of alcohol, and proper sleep is foundational for having good health — and good BP.
One large change in this document is the treatment threshold using cardiovascular disease (CVD) risk estimation with the PREVENT score, which is new from AHA. I've covered PREVENT on previous podcasts. It's pretty controversial because it is felt to be a more accurate risk estimator, but — and this is a huge but — the PREVENT score results in fewer people reaching statin-starting threshold.
But PREVENT features prominently in these hypertension guidelines, and the first is the choice to start therapy. BP > 140/90 is one criteria, regardless of comorbid conditions, but for BP >130/80 patients, initiation turns on the presence of CVD, diabetes, CKD, or PREVENT > 7.5%.
PREVENT also features in goals. The aim is usually below 130/80 and push toward < 120 systolic when PREVENT is > 7.5%.
So, there is a concern that since PREVENT is better calibrated than the pooled cohort equations (PCE), it might result in fewer people being started on treatment than the PCE. The risk of that seems lower, though, in hypertension than in statins, because with statins it is largely a risk-based decision, whereas in hypertension, there is also the marker of 140/90 or 130/80 with CVD, chronic kidney disease (CKD), and diabetes.
The authors don't say this, but I will repeat myself: the main purpose and largest value of hypertension treatment comes in treating younger people early in life, so that they avoid stroke, kidney disease 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 spend many words and academic-speak on treatment in the elderly. I would summarize it this way: Use Common Sense . An octogenarian is winning the game of life. Our job is to not mess things up with hypotension-induced broken hip or subdural hematoma.
Nothing new comes in the choice of medication. It's thiazide-type diuretics, long-acting dihydropyridines, calcium channel blockers, and ACE inhibitor or angiotensin receptor blockers — all recommended as first-line therapy to prevent CVD. Note, no beta-blockers are listed as first line.
One twist on imitation comes in section 5, where the authors recommend starting medical therapy for patients with stage 2 hypertension (>140/90) with two first-line meds of different classes in a single-pill combination — for adherence's sake. I used to be against this. I've changed. Because anything the decreases the work of being a patient, I am for. What's more, there is strong empirical evidence that combination pills increase adherence.
Treatment goals follow the trials — namely SPRINT, which found advantages to BP 120/80 in patients with high CV risk. This is fine, again, more beneficial in 50- and 60-year-olds, so that they get to 90 without a stroke or myocardial infarction (MI). Recall that the ACCORD trial in patients with diabetes did not find benefit for the lower target. So, do aggressive targets not work for patients with diabetes? I would cite two lines of evidence suggesting that we also consider lower targets in patients with diabetes: one is that the recently published BPROAD trial found SPRINT-like benefits for 120 vs 140 target in 12,000 patients from China.
I also love a paper by Luke Lafflin where he and Francis Alenghat created a SPRINT Trial score based not on inclusion criteria but actual clinical characteristics from Table 1 . And then applied it to patients in ACCORD... Boom: the SPRINT Trial Score was able to discriminate a subpopulation of patients with diabetes who were in SPRINT's data-rich zone and responded to intensive blood pressure control in the same way as SPRINT even though ACCORD-BP, on the whole, was a 'negative' trial.
There are large sections on managing BP in stroke and intracranial hemorrhage as well as pregnancy, and since these are so often a subspecialty field that I am not involved in, I have won't say much about those.
One section that I do want to comment on is Resistant Hypertension and Renal Denervation (RDN). I think the authors are quite sober about RDN. First, section 5.6 on resistant hypertension is very good. Confirm it. Look closely at adherence. I can't emphasize this enough, because throughout my years, I stopped counting how many times a patient with resistant hypertension becomes hypotensive in the hospital when put back on meds.
Another nugget: use mineralocorticoid receptor antagonists (MRAs) for resistant hypertension, and when they are poorly tolerated, use amiloride. This is a trick my nephrology friends taught me. The putative wonder drug finerenone is mentioned only once in the document, in the references, but I do have to wonder if there may be a role when spironolactone and eplerenone are poorly tolerated.
As for RDN, the authors are cautious, and I highlight this passage: 'While some trials showed a small but significant reduction in 24-hour ambulatory systolic blood pressure by SBP by 3 to 5 mm Hg over the sham arm, others failed to reach their primary endpoint. Although broader indications are approved for the renal denervation devices by the FDA, given the relatively short duration of follow-up in clinical trials with modest BP-lowering effects and the absence of CVD outcome trials, renal denervation should not be considered as a curative therapy for hypertension or full replacement for antihypertensive drugs.'
I think this is a good statement. I would have been stronger, but this is pretty strong. In the colored box where they give the recommendations a 2b level, they write that RDN may be reasonable if meds are not effective or intolerable. I really worry about the intolerable label. While there are some patients who poorly tolerate meds, I worry that if RDN earns reimbursement status from payers, there will be an epidemic of patients who cannot tolerate BP meds. I can even imagine direct-to-consumer ads creating a disease category of not tolerating BP meds. This could morph into the left atrial appendage occlusion (LAAO) situation where there are posters in lobbies of hospitals encourage patients to consider a nonmedical option for stroke prevention.
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 LAAO and RDN. RDN trials were either negative, or found minimal differences in systolic blood pressure, over no more than a few months. Do not be fooled by any of the extension studies with RDN, because the nanosecond that a RDN trial unblinds patients, results are worthless — see the SYMPLICITY 1 and 2 trials.
I will write these thoughts up in a formal column next week. Stay tuned for that.
The American Heart Association has been busy. Also in Circulation is a long scientific statement on ultraprocessed foods and their association with cardiometabolic health.
I am no nutrition expert. Perhaps you are not either. But we all know a few facts:
Fact 1: Cardiometabolic health in the US is public health crisis of massive proportions. The saddest part is how it is has decimated the health of children—especially children in lower socioeconomic levels.
Fact 2: Snack foods taste good, are easy to obtain, less expensive but have extremely poor nutritional quality. When there is junk food in break rooms in hospitals, it disappears. Donuts — gone!
Fact 3: Many of these snack foods are ultraprocessed and filled with artificial dyes.
Fact 4: 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 of his how to untangle the ultraprocessing and chemical components from the fact that most of the foods are full of empty calories, I think the medical profession must try to help sort out this public health crisis of terrible cardiometabolic health. There is low-hanging fruit. Excess calories in the form of carbohydrates is one of them. Not having enough focus on exercise is another. I am not sure food processing and artificial dye is the best initial target.
I may be wrong, or just naive, but it strikes me how different other countries handle this problem. When you go to the European Society of Cardiology (ESC) meeting in Amsterdam, for instance, you look out the window of the conference center and see packs of lean Dutch kids riding their bikes to school. In the 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.
Coronary Sinus Reducer Shows Promise, With Caveats
The coronary sinus reducer (CSR) is a balloon-expandable hourglass-shaped stent that when deployed causes narrowing of the coronary sinus. It increases coronary sinus pressure, which is believed to redistribute blood flow from nonischemic into ischemic myocardium.
The device is not used or approved in the United States, so my colleagues here may not know about it. But a recently published meta-analysis in JACC: Cardiovascular Interventions is still worth your time, from an evidence-based medicine (EBM) perspective.
It's from the group led by Rasha Al-Lamee at Imperial College in London. They meta-analyzed the data for CSR to treat refractory angina. It stems from single-arm, unblinded studies and three sham-controlled trials.
Recall that the CSR can relieve angina by two mechanisms: one is by the physical effects of directing blood flow to under perfused areas. 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 natural history. These nontreatment related phenomena are the reason you tell patients who you just put in a stent or pacemaker that they will be hard to contain.
The randomized controlled trials (RCTs) are a bit divergent: in general, they find reductions of angina symptoms but mostly do not show any objective differences in perfusion. The most recent and largest trial, also from the Imperial College group, the ORBITA-COSMIC trial of 50 patients (50% got CSR and 50% got a sham CSR) found no significant difference in stress myocardial blood flow, but they did find significant reduction in daily angina episodes.
The main finding of the meta-analysis was that the single-arm studies showed much larger effects on reduction of angina than the pooled estimate from the 3 sham-controlled RCTs. For instance, 81% of patients in the non-blinded studies improve 1 functional class with CSR vs only 26% in the sham-controlled arm. And for the Seattle Angina Questionnaire domain measures of angina, 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 placebo-controlled trials in the procedural interventional field. If all we used were noncontrolled studies, we'd think the CSR was an amazing anti-anginal 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 effect. Who, I ask, has not had post-AF ablation patient sing your praises for improving their quality of life after ablation only to be in AF during the visit?
In the matter of the CSR, the Imperial College team are doing a larger RCT called COSIRA-II, which will hopefully further sort out the true placebo-resistant effect size of this procedure. It's an important thing to know because the implant procedure can have serious, albeit low incident, complications.
It boggles my mind that medical scientists felt that we could measure quality-of-life (QoL) benefits in patients with tricuspid valve interventions without a proper placebo control. This is clear evidence that you need placebos every bit as much for procedures as you do for tablets.
And placebo controls are not only for subjective endpoints. Recall that the SYMPLICITY III hypertension trial found that the excitement of blood pressure reductions from renal denervation were much more modest when compared against a sham control.
I am going to report on another positive, albeit preliminary, study on pulsed field ablation (PFA) for atrial fibrillation (AF) ablation. You know that I am a slow-adopting medically conservative doctor. New things worry me. But it's been about a year with PFA during AF ablation. I have not once gone back to thermal ablation since adopting PFA.
RCTs have shown similar efficacy and safety. You still can get tamponade and stroke. But the dreaded complications of death from atrioesophageal fistula have not occurred in PFA, because it is cardioselective.
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 do far fewer repeat procedures. Patients also have less post-procedure symptoms of inflammation. Less chest pain. Less heart failure episodes.
This month, the group led by Professor Andrea Natale have published an interesting observational non-random comparison of anticoagulation after thermal and PFA ablation. It's nonrandom and we must be careful, but here is what they did, and found:
About 400 patients had radiofrequency ablation (RFA) and 400 had PFA at multiple institutions. The authors did propensity matching to attempt to balance the characteristics. The good news is that the colleagues of Dr Natale tend to do AF ablation in the same way. Pulmonary vein isolation (PVI) and posterior wall isolation, with both RFA, and now PFA. So at least there is not much procedural variation.
Half of each group (n= 200) each stopped the oral anticoagulant (OAC) after 1 month; the other 200 stopped after 2 months. So, they had four subgroups. There was no protocol. Stopping OAC was done for different reasons. The groups that stopped OAC after only 1 month were called Group 1. The groups that continued OAC for more than 2 months were called Group 2.
The findings were dramatic, very dramatic in fact: in the Groups 1, stopping after one month, there were 0 strokes in the PFA group and 16 in the RFA group . In the Groups 2, those who continued OAC for more than 2 months, there were 2 stroke events in the PFA group vs 7 in the RFA group.
What's more, AF recurrence occurred in 18% of the PFA group vs 27% in the RFA group. A statistically significant difference, which could have been a driver of differences in stroke events.
While this is observational, and surely confounded, but it is prospective data finding that in at least 200 patients who stopped OAC 1 month after PFA, there were 0 strokes—whereas there were a lot of stroke events after stopping OAC after RFA.
It suggests that perhaps there is less inflammation and/or endothelial disruption with PFA than with RFA. And, if this is confirmed in other studies, it would be yet another huge advantage to be able to stop OAC that quickly after AF ablation. I reiterate, though, that this observation needs further confirmation.