Coronary computed tomography angiography (CCTA) following PCI for unprotected left main disease did not reduce the composite primary endpoint of all-cause death, spontaneous myocardial infarction (MI), unstable angina or definite or probable stent thrombosis at 18 months, based on findings from the PULSE trial presented at ESC Congress 2025 and simultaneously published in JACC. However, researchers said CCTA was associated with fewer spontaneous MIs and more imaging-triggered revascularizations.

An analysis of the STRONG-HF trial from Rahul Aggarwal, MD, et al., found that an algorithm-driven high-intensity titration of beta-blockers, ACEI/ARB/ARNIs and mineralocorticoid receptor agonists within two weeks of heart failure (HF) hospitalization reduced rates of 180-day all-cause death and HF readmissions compared with usual care regardless of ischemic or nonischemic etiology, although ischemic patients had higher rates of readmission.

A single center study conducted in Madrid, Spain, by Nerea Mora-Ayestarán, MD, et al., found that among consecutive patients with hereditary transthyretin amyloidosis (ATTRv) systematic cascade genetic screening identifies a median of two genetic carriers per proband in families with ATTRv. Of more than 700 at-risk relatives in 86 families, 62% underwent genetic testing, with a median of five relatives per family screened. Affected relatives were diagnosed at a younger age than their probands (53 years vs. 66 years; p<0.001) and started disease-modifying therapies sooner (57 years vs. 66 years; p<0.001). Older age in proband, living in a different province or country from the proband, male sex and distance relationship with proband were independent predictors of no genetic screening. Nearly one-third of relatives did not undergo genetic testing.

Taking low-dose colchicine daily may slow the progression of clonal hematopoiesis (CH), based on a subanalysis of the LoDoCo2 trial presented at ESC Congress 2025 and simultaneously published in JACC.

Heart failure with preserved ejection fraction (HFpEF) appears to arise "primarily from the expansion and dysfunctional transformation of visceral adipose tissue, leading to the secretion of an altered suite of signaling molecules (adipokines), which causes systemic inflammation, plasma volume expansion, and cardiac hypertrophy and fibrosis," according to the Adipokine Hypothesis authored by Milton Packer, MD, FACC, and published as a State-of-the-Art Review in JACC.

Click here to read JACC's Focus Issue: Adipokine Hypothesis Spotlight.