Cardiology

FAME 2: 11-year data support FFR-guided PCI for stable CAD with significant lesions

At 11.2 years’ median follow-up, FFR-guided PCI plus medical therapy reduced the composite of death, MI, or urgent revascularization versus medical therapy alone. The primary endpoint occurred in 33.6% with PCI and 41.3% with medical therapy, corresponding to a win ratio of 1.25 in favor of PCI. Benefit was driven mainly by fewer urgent revascularizations, with a win ratio of 4.57, while all-cause mortality showed no significant difference. The number needed to treat to prevent one composite event was 17, supporting FFR-guided PCI for hemodynamically significant stable CAD. 1

2025 ASE diastolic criteria substantially underdiagnose HFpEF, including invasively proven cases

In ambulatory, invasively confirmed HFpEF, the 2025 ASE diastolic algorithm classified about two-thirds as normal or Grade 1 dysfunction. More than 60% of patients labeled normal or Grade 1 had resting pulmonary artery wedge pressure ≥15 mm Hg on catheterization. In decompensated HFpEF, 25% were still labeled normal or Grade 1, rising to 51.1% after recompensation, indicating persistent undergrading. In Grade 1 HFpEF undergoing stress testing, ASE-recommended criteria detected only 9.5% of cases, yielding a 90.5% false-negative rate. 2

Stopping OAC after AF ablation: low-risk patients only, higher-risk patients require continuation

This meta-analysis of 32 studies (271,808 AF patients) compared oral anticoagulation discontinuation versus continuation after catheter ablation. Overall, stopping anticoagulation did not significantly change thromboembolic or mortality risk but significantly reduced major bleeding events. In patients with CHA2DS2-VASc scores >2, discontinuation significantly increased thromboembolic risk, supporting ongoing anticoagulation for this group. For CHA2DS2-VASc 0–2 and patients maintaining sinus rhythm, thromboembolic and mortality risks were similar whether anticoagulation was continued or stopped. 3

Prediabetes plus subclinical myocardial injury or stress markedly increases HF risk in hypertension

Among 8,234 hypertensive SPRINT participants without diabetes or prior HF, prediabetes and elevated hs-cTnI or NT-proBNP were frequent. Compared with normoglycemia and no myocardial injury, combined prediabetes and elevated hs-cTnI conferred the highest HF risk (HR 4.20). Prediabetes plus elevated NT-proBNP similarly yielded markedly increased HF risk (HR 5.20) versus normoglycemic, biomarker-negative peers. A ≥25% increase in hs-cTnI or NT-proBNP over 12 months in prediabetes further heightened HF risk, emphasizing dynamic biomarker monitoring. 4