This Week in Cardiology — Sep 14, 2026

Welcome to This Week in Cardiology. This week we're covering 10 notable papers spanning acute coronary care and mechanical support, the diagnosis and treatment of heart failure with preserved ejection fraction, and a cluster of studies on cardiovascular risk prediction and novel risk factors. Let's dive in.

We'll start with ischaemic heart disease, where Circulation has published a state-of-the-art review of the contemporary clinical management of myocardial infarction from Landi and colleagues [1]. It's worth reading as a consolidation piece: it walks through the atherothrombotic mechanism of plaque rupture and erosion, the diagnostic and risk-stratification framework, the evidence on revascularisation strategy including the timing and guidance of complete revascularisation, and emerging pharmacological options for secondary prevention, with particular attention to myocardial infarction without obstructive coronary disease. The framing matters. Despite systems of care built around primary percutaneous coronary intervention within 120 minutes, coronary disease and infarction still account for more than 370,000 deaths a year in the United States, and a meaningful proportion of patients have recurrent events even when conventional risk factors are well controlled. The authors are explicit about where the remaining gaps sit: better prediction of occlusive infarction, shorter delays to reperfusion, cardiogenic shock mortality, and actually implementing the secondary prevention we already know works.

That last point about shock leads naturally into the most directly practice-relevant interventional paper of the week, a network meta-analysis in the Journal of the American Heart Association from Bujak and colleagues on mechanical circulatory support during complex high-risk indicated percutaneous coronary intervention [2]. This pooled eight randomised trials, just over 1,850 patients undergoing non-emergent high-risk procedures, and compared percutaneous left ventricular assist devices, intra-aortic balloon pump, veno-arterial extracorporeal membrane oxygenation, and standard care. The headline is negative. No support strategy reduced major adverse cardiovascular events at 30 days, and none reduced them over a weighted mean follow-up of about eleven months. There was no signal of benefit for death, infarction, stroke, or repeat revascularisation with any device. What the devices did do was reduce periprocedural major adverse events — roughly a seventy percent relative reduction with both percutaneous left ventricular assist devices and the balloon pump — but that periprocedural advantage did not translate into any durable clinical gain. The authors' conclusion is one I'd take to the cath lab: these data do not support routine prophylactic support, and mechanical circulatory support should be reserved for selected patients. Given the cost and the vascular and bleeding burden of these devices, that is a meaningful brake on a practice that has been expanding faster than its evidence base.

Staying with the coronary tree but moving into cardio-oncology, JAMA Cardiology reports a prospective mechanistic cohort from Rankin and colleagues asking whether immune checkpoint inhibitors accelerate atherothrombosis by inflaming plaque [7]. Fifty-five patients with cancer in the West of Scotland network underwent fluorodeoxyglucose PET-CT and blood sampling before treatment and again at 24 weeks, receiving checkpoint inhibitor monotherapy, vascular endothelial growth factor inhibitor monotherapy, or the combination. Arterial fluorodeoxyglucose uptake did not rise above baseline in any group, and that held across artery type, calcification status, prior atherosclerotic disease, and steroid exposure. Systemic inflammatory markers moved only modestly, though the two adhesion molecules, intracellular and vascular cell adhesion molecule-1, did increase with checkpoint inhibitor exposure, and checkpoint inhibitors selectively altered circulating T-cell subsets in a way that was attenuated by concurrent vascular endothelial growth factor inhibition. The interpretation is that macrophage-driven plaque activation is probably not the main mechanism behind checkpoint-inhibitor-associated infarction and stroke, and that endothelial and thrombotic pathways deserve the attention instead. It's a small cohort and a surrogate endpoint, so treat it as mechanism, not reassurance about clinical risk.

The heart failure theme this week is dominated by preserved and mildly reduced ejection fraction, and it gives us one negative trial and one genuinely useful diagnostic advance. In Nature Medicine, Lund and colleagues report a phase 2b trial of the myeloperoxidase inhibitor mitiperstat in 711 patients with heart failure and an ejection fraction above 40 percent [3]. The rationale was attractive — myeloperoxidase-derived oxidants reduce nitric oxide availability and drive microvascular dysfunction, cardiomyocyte stiffening and fibrosis — but the result was flatly null. Against placebo, mitiperstat at either 2.5 or 5 milligrams did not improve the Kansas City Cardiomyopathy Questionnaire total symptom score or six-minute walk distance at 16 weeks, and no secondary endpoint moved, including natriuretic peptides, inflammatory markers, and echocardiographic parameters. Safety was reassuring apart from maculopapular rash, which occurred in about one in thirty patients on drug versus almost none on placebo. Another plausible anti-inflammatory mechanism fails to convert into symptom benefit in this phenotype.

Diagnosis, though, moves forward. In the European Heart Journal, Harada and colleagues took 482 patients with unexplained dyspnoea through invasive haemodynamic exercise testing with simultaneous echocardiography, with heart failure with preserved ejection fraction confirmed in 386 of them [4]. The sobering finding is that current algorithms — the H2FPEF, HFA-PEFF and HFpEF-ABA scores — combined with guideline-recommended exercise echocardiography detected only about 55 to 60 percent of true cases, with overall accuracy in the low-to-mid sixties. Adding resting left atrial compliance, defined as reservoir strain divided by E over e-prime, pushed sensitivity into the mid-eighties but at the cost of a substantial false-positive rate. The elegant part is what they did next: separate rule-in and rule-out thresholds. An exercise E over e-prime of 13.8 or higher, or a resting left atrial compliance of 1.6 percent or less, rules the diagnosis in; an exercise E over e-prime below 7.2 together with compliance above 4.4 percent rules it out; everyone in between is indeterminate and still needs invasive testing. Among definitively classified patients sensitivity reached 95 percent or better, and the proportion of patients requiring invasive exercise haemodynamics fell from roughly sixty percent to roughly thirty percent, with replication in an international validation cohort. The honest message is that exercise echocardiography cannot replace invasive testing — but adding left atrial strain to your protocol can halve how often you need the cath lab.

Rounding out heart failure, the European Journal of Heart Failure carries a patient-level pooled analysis of 13 randomised trials from Chimura and colleagues, more than 61,000 patients, examining pulse pressure across phenotypes [5]. The direction of risk inverts with ejection fraction. In reduced ejection fraction, low pulse pressure marks danger, with the highest event rates in patients below 40 millimetres of mercury. In preserved and mildly reduced ejection fraction the relationship is J-shaped and the risk sits at the top end, above about 66 millimetres of mercury. Mildly reduced ejection fraction behaved essentially like preserved. Pulse pressure added information beyond systolic pressure, but the gain in discrimination was small, so read this as a physiological insight that sharpens bedside gestalt rather than a new score.

Finally, three papers on prediction and risk. In the BMJ, Liang and colleagues derived parallel five-year cardiovascular risk equations in equivalent primary-prevention diabetes cohorts in New Zealand and China, each with roughly 47,000 participants [9]. Most of the 16 predictors behaved similarly across countries, but the effect of age did not: per decade, age carried substantially more weight in the Chinese cohort. Simply recalibrating the New Zealand equations in the Chinese population failed to fix calibration, whereas swapping in locally derived age coefficients brought expected and observed events almost exactly into line. For anyone importing a high-income-country risk score into a different population, recalibration alone is not enough — key coefficients, age above all, need updating. Complementing that, the European Heart Journal reports on nighttime light exposure and the heart, from Dai and colleagues, using wrist accelerometry with an integrated light sensor in more than 11,000 UK Biobank participants who later had cardiac magnetic resonance [10]. High nighttime light exposure above three lux was associated with concentric left ventricular hypertrophy, lower myocardial contraction fraction, and impaired strain in all three directions, plus larger right ventricular volumes and a larger, weaker left atrium, with linear dose-response and roughly a quarter to half of each association statistically mediated by shorter sleep. In the larger outcome cohort of over 73,000 people, high exposure carried about a 29 percent higher risk of heart failure, about a quarter higher risk of myocardial infarction, a third higher risk of stroke, and about a quarter higher cardiovascular mortality. Observational, but a cheap and plausible lifestyle target: dark bedrooms and adequate sleep. And in JAMA Cardiology, Chiu and colleagues offer a special communication on how to design cardiovascular outcomes trials in clonal haematopoiesis of indeterminate potential [6], laying out why a one-size-fits-all trial will fail — driver mutations differ mechanistically, risk scales with clone size, sequencing thresholds are not comparable across platforms, and screening asymptomatic elderly carriers raises real ethical problems. Their pragmatic suggestion is to embed clonal haematopoiesis analyses into ongoing cardiovascular trials rather than wait for dedicated ones.

One aortic paper deserves a mention: in Heart, Ahn and colleagues pooled individual data on 485 patients with type A intramural haematoma from eight Asian and Western centres [8]. Caucasian patients presented sicker — more shock, more visceral and limb ischaemia, thicker haematoma, larger ascending aortas — and were far more likely to go to urgent surgery, while Asian patients were mostly managed medically. After adjustment, race was not associated with long-term mortality over a median of nearly seven years. What predicted death was age, ascending aortic diameter, and being managed medically because surgery was prohibitively risky, which roughly tripled mortality. Presentation and anatomy, not ethnicity, should drive the decision.

If you only have time for one paper this week, make it the network meta-analysis of mechanical circulatory support in complex high-risk percutaneous coronary intervention [2]. It is randomised-trial evidence against a costly, invasive practice that has grown largely on registry data and enthusiasm, and it should change how your lab selects patients for prophylactic support tomorrow.

Here are the key takeaways from this week in Cardiology. Prophylactic mechanical circulatory support in elective high-risk percutaneous coronary intervention reduces periprocedural events but does not improve clinical outcomes at 30 days or at a year, so reserve it for selected patients. In suspected heart failure with preserved ejection fraction, current scores plus standard exercise echocardiography miss close to half of true cases; adding resting left atrial compliance with separate rule-in and rule-out thresholds can halve referrals for invasive exercise testing but cannot eliminate them. Myeloperoxidase inhibition with mitiperstat was safe but did not improve symptoms or exercise capacity in preserved or mildly reduced ejection fraction. Pulse pressure carries opposite prognostic meaning by phenotype: low is bad in reduced ejection fraction, high is bad in preserved and mildly reduced. And when using risk equations across populations, recalibration alone may be insufficient — particularly for the effect of age — while nighttime light exposure emerges as a modifiable correlate of adverse cardiac remodelling and incident events.

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.

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