This Week in Cardiology — Jun 6, 2026

Welcome to This Week in Cardiology. This week we're covering 10 notable papers spanning the optimization of medical therapy for atherosclerotic disease, the expanding role of finerenone in chronic kidney disease, new insights from advanced imaging and structural intervention, and a look at the basic science shaping future treatments. Let's dive in.

We begin with three papers from the European Heart Journal that refine our approach to secondary prevention in patients with established atherosclerotic disease. First, a meta-analysis addresses the optimal duration of dual antiplatelet therapy, or DAPT, after percutaneous coronary intervention [1]. This analysis of eleven randomized trials with over 37,000 patients confirms that switching to P2Y12 inhibitor monotherapy by discontinuing aspirin is a viable strategy. Compared to continuing DAPT for 12 months, stopping aspirin at either one month or three months showed no significant difference in the risk of major adverse cardiovascular events. The major benefit was in bleeding, which was significantly reduced with earlier aspirin cessation. Stopping aspirin at or before one month cut the risk of major bleeding by more than half, and this bleeding benefit was more pronounced than stopping at three months. However, there's a critical nuance. In a subgroup analysis of acute coronary syndrome patients, very early aspirin discontinuation, meaning less than one month, was associated with a nearly doubled risk of stent thrombosis. The clinical takeaway here is that for many patients, especially those with stable disease undergoing PCI, dropping aspirin after one month appears to be a safer strategy regarding bleeding, without an ischemic penalty. But for higher-risk ACS patients, we should be more cautious about discontinuing aspirin so early. Still in the realm of secondary prevention, another study from the European Heart Journal, a sub-study of the FOURIER trial, investigated the safety of very low Lipoprotein(a), or Lp(a), levels [9]. With potent Lp(a)-lowering therapies on the horizon, this is a crucial question. The analysis of over 25,000 patients with ASCVD found no association between low Lp(a) levels and adverse events like hemorrhagic stroke, serious bleeding, or cancer. This is reassuring. However, the study did confirm an inverse relationship with diabetes: for every 50 nmol/L *lower* the baseline Lp(a) was, there was a 5% higher risk of developing diabetes during follow-up. Importantly, for patients on the PCSK9 inhibitor evolocumab, the drug did not increase the risk of new-onset diabetes, even in those who had the largest drops in their Lp(a). This suggests the link is likely genetic or biological, rather than a direct effect of the drug itself. The bottom line is that low Lp(a) appears safe from most standpoints, but the intriguing link to diabetes risk warrants continued observation as we enter an era of targeted Lp(a) reduction. Finally, to help contextualize these long-term prevention strategies for our patients, a third paper in the European Heart Journal introduces the updated SMART-REACH2 model [3]. This tool is designed to estimate the lifetime risk of recurrent cardiovascular events and, crucially, the potential benefits of preventive treatment in patients with established ASCVD. Validated in a massive cohort of over two million patients from 54 countries, the model accounts for geographic and sex-specific variations. It moves the conversation beyond just relative risk reduction to tangible gains. For example, the model estimates that for a hypothetical 50-year-old patient, intensifying treatment to achieve a 15 mmHg drop in systolic blood pressure and a 1.0 mmol/L reduction in LDL-cholesterol could add between 2 and 4.4 years of cardiovascular disease-free life, depending on their baseline regional risk. This is a powerful tool for shared decision-making, helping to motivate patients by illustrating the long-term, personal benefits of adhering to therapy.

Next, we turn to chronic kidney disease, with two papers exploring the role of the nonsteroidal mineralocorticoid receptor antagonist finerenone in patients *without* diabetes. The landmark FIND-CKD trial, published in The New England Journal of Medicine, randomized nearly 1,600 adults with albuminuric CKD but no diabetes to either finerenone or placebo [4]. The primary outcome was the rate of eGFR decline. Over 32 months, patients on finerenone had a significantly slower decline in kidney function compared to placebo, with a difference of 0.7 mL per minute per 1.73 m² per year. While this may seem small, it represents a meaningful preservation of kidney function over time. Furthermore, finerenone was associated with a lower risk of the composite outcome of major kidney or cardiovascular events, with a hazard ratio of 0.77. As expected, hyperkalemia was more common with finerenone, occurring in 17% of patients versus 13% with placebo, but it led to permanent drug discontinuation in only 1.5% of participants. This trial effectively extends the proven cardiorenal benefits of finerenone to a large new population of patients with CKD. Complementing this, a prespecified exploratory analysis of the same trial, published in JAMA, focused specifically on the 903 participants who had glomerular diseases like IgA nephropathy or focal segmental glomerulosclerosis [5]. The results were consistent and compelling. In this challenging-to-treat subgroup, finerenone again slowed the annual rate of eGFR decline, reduced albuminuria at 12 months by a substantial 42%, and lowered the risk of a hard kidney outcome—defined as kidney failure or a sustained 40% or more drop in eGFR. Together, these two papers provide strong evidence to support the use of finerenone to preserve kidney function in patients with albuminuric CKD, regardless of whether they have diabetes or what the underlying glomerular cause may be.

Our next theme covers insights from advanced cardiac imaging and structural intervention. A study in Circulation explored the prognostic value of subendocardial myocardial flow reserve, a more granular metric than the standard transmural flow reserve measured by PET scans [7]. Researchers analyzed over 6,600 patients who had normal perfusion on their PET scans. They stratified patients into three groups: those with normal transmural and normal subendocardial flow, those with abnormal transmural flow, and a 'discordant' group with normal transmural flow but impaired subendocardial flow. Over a median follow-up of nearly 5 years, this discordant group had a significantly higher risk of major adverse cardiovascular events and all-cause mortality compared to those with completely normal flow studies. Their risk was intermediate, sitting squarely between the low-risk normal group and the high-risk group with abnormal transmural flow. This tells us that subendocardial flow reserve can unmask clinically meaningful risk from microvascular dysfunction that is missed by conventional metrics. It helps refine risk stratification in a large population of patients who might otherwise be falsely reassured by a 'normal' PET scan. Shifting to structural heart disease, a paper in the Journal of the American College of Cardiology addressed a key question about the COAPT trial: do its findings on mitral transcatheter edge-to-edge repair, or MTEER, apply to real-world patients [10]? The COAPT trial's positive results have been debated, especially in light of other neutral trials. Using data from the TVT Registry in the United States, investigators found that patients undergoing MTEER in contemporary practice are indeed different from the trial population—for instance, they are less likely to have ischemic cardiomyopathy and more likely to have more severe mitral regurgitation. Using a statistical technique called transportability analysis, the researchers estimated what the treatment effect would have been if these real-world patients had been enrolled in COAPT. The result? The estimated absolute risk reductions for two-year heart failure hospitalizations and all-cause death were similar to those seen in the original trial. This analysis provides welcome reassurance that the significant benefits of MTEER for secondary MR demonstrated in COAPT are likely generalizable to the broader, more diverse patient population being treated today.

Finally, we briefly touch on three papers that provide a deeper look at the mechanisms of vascular disease and cardiac metabolism. A report in the European Heart Journal highlights distinct lipid metabolic profiles in atherosclerosis versus abdominal aortic aneurysm [2]. Using multi-omics and machine learning, researchers found that atherosclerosis is characterized by an enrichment of neutral lipids like triglycerides, whereas AAA is dominated by phosphoglycerides. Restoring a specific fatty acid oxidation pathway inhibited atherosclerosis but had little effect on AAA, suggesting these two common vascular diseases may one day have distinct, targeted metabolic treatments. From Circulation Research, a second study identifies a mitochondrial protein called ATAD3A as a key protector against aortic dissection in mouse models [8]. ATAD3A appears to work by regulating contacts between mitochondria and lysosomes and by restraining a form of copper-dependent cell death called cuproptosis in vascular smooth muscle cells. This work uncovers a novel pathway that could become a future therapeutic target for this catastrophic condition. Lastly, a comprehensive review, also in Circulation Research, covers the complex world of cardiac lipid metabolism [6]. It details the delicate balance the heart must maintain—avoiding both the lipotoxicity of too much fat and the energy depletion of too little—and how this is regulated by diet, fasting, and our own circadian clocks, offering a roadmap for future research into metabolic therapies for heart failure.

If you only have time for one paper this week, make it the FIND-CKD trial in The New England Journal of Medicine [4]. This study provides clear, high-quality evidence that finerenone slows kidney function decline in patients with chronic kidney disease *without* diabetes, significantly expanding the therapeutic options for this large and growing patient population.

Here are the key takeaways from this week in Cardiology. First, in patients with albuminuric chronic kidney disease without diabetes, finerenone slows eGFR decline and reduces cardiorenal events, establishing it as a new therapeutic option for this group. Second, after PCI, dropping aspirin after 1 to 3 months and continuing a P2Y12 inhibitor is a sound strategy to cut bleeding risk without increasing MACE, but very early discontinuation in ACS patients requires caution due to a potential signal for stent thrombosis. Third, the benefits of transcatheter edge-to-edge repair for secondary mitral regurgitation seen in the COAPT trial appear to be applicable to the broader patient population treated in contemporary United States practice. Fourth, new tools are refining risk stratification; the SMART-REACH2 model helps quantify the lifetime benefits of prevention to aid shared decision-making, while subendocardial flow reserve on PET can identify residual risk in patients with otherwise normal perfusion. And finally, while very low Lp(a) levels are not linked to major safety events, they are associated with a slightly higher risk of developing diabetes, a finding to keep in mind as potent Lp(a)-lowering drugs approach the clinic.

That's your roundup for This Week in Cardiology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

This is an automated summary generated by artificial intelligence, which can make mistakes. Always review the original source materials.