Journal of the American College of Cardiology最新文献

Heart failure (HF) is a public health challenge with high morbidity and mortality risk, and societal economic costs. The lifetime risk of developing HF stands at 1 in 4. A significant portion of the population already is in precursor stages, with roughly two-thirds of adults in the United States classified as either stage A (at risk) or stage B (pre-HF). Despite advances in drugs and device-based therapies, once HF develops, these patients remain at an unacceptably high risk for mortality, morbidity, and adverse health status, underscoring the need for focus on primary prevention of HF. The prevention of atherosclerotic cardiovascular disease is supported by established guidelines with clear targets and pharmacotherapies with specific labels for prevention. However, prevention of HF remains less well established. No therapeutic agent is approved yet specifically for the primary prevention of HF. Defining and adjudicating incident HF is challenging. Most trials report initial HF hospitalizations only. The conventional hospitalization-based definition of incident HF does not take into account outpatient settings where most HF is diagnosed. A fundamental reevaluation of preventive strategies for HF is required, moving incrementally from coronary disease-based approaches to more global populations, because many HF cases arise from nonatherosclerotic causes, such as obesity, hypertension, cancer therapies, and the cardio-kidney-metabolic syndrome. This review addresses practical challenges in defining incident HF, trial duration, and regulatory pathways, while summarizing the landscape of current and ongoing prevention trials, identifying evidence gaps, and highlighting future priorities.

Background: The optimal approach for the early diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) remains uncertain, because no large trials have been performed. Accordingly, guideline recommendations differ and do not overall give a clear answer.

Objectives: The authors aimed to directly compare the European Society of Cardiology 0/1-hour algorithm (ESC 0/1h-algorithm) and the high-sensitivity troponin in the evaluation of patients with acute coronary syndrome 0/2-hour or 0/3-hour pathway (High-STEACS 0/2h-0/3h-pathway) in patients presenting with acute chest discomfort.

Methods: This prospective, international, multicenter, diagnostic study enrolled patients presenting to the emergency department with acute chest discomfort. Final diagnoses were centrally adjudicated by 2 independent cardiologists. The primary diagnostic endpoint was NSTEMI type 1. Both algorithms were applied in parallel using 3 high-sensitivity cardiac troponin (hs-cTn) assays: hs-cTnI-Architect, hs-cTnI-Centaur/Atellica, and hs-cTnT-Elecsys. The findings were externally validated in an independent prospective diagnostic study.

Results: Among 4,663 eligible patients (median age: 61 years; 32% women), 663 (14.2%) had NSTEMI type 1. The ESC 0/1h-algorithm had higher sensitivity when using hs-cTnI-Architect (100% [95% CI: 99.4-100]) compared with the High-STEACS 0/2h-pathway (98.1% [95% CI: 96.7-99], P < 0.001), but the proportion of patients assigned to the rule-out group was lower (52% vs 72.5%, P < 0.001). Differences were similar but were less pronounced for hs-cTnI-Centaur/Atellica and absent for hs-cTnT-Elecsys. Specificity was consistently higher for the ESC 0/1h-algorithms vs the High-STEACS 0/2h-0/3h-pathways for all hs-cTnT/I-assays. These findings were confirmed when using High-STEACS 0/3h-pathways and in the external validation cohort (n = 2,485; median age: 64 years; 37% women).

Conclusions: Overall, both algorithms exhibited comparable and excellent performance. When using hs-cTnI, the ESC-0/1h-algorithms showed higher sensitivity, whereas the High-STEACS 0/2h-0/3h-pathways demonstrated higher efficacy. Consistently, the ESC 0/1h-algorithms showed higher specificity for NSTEMI. These findings provide direct, validated evidence to guide hospitals in selecting an hs-cTn pathway aligned with their clinical and operational priorities. (Advantageous Predictors of Acute Coronary Syndromes Evaluation [APACE] Study [APACE], NCT00470587; Biomarkers in Acute Cardiac Care [BACC], NCT02355457).

Background: Stabilizers/silencers limit new transthyretin amyloid formation, whereas emerging agents aim to clear existing deposits. Cardiovascular magnetic resonance (CMR) extracellular volume (ECV) reflects myocardial amyloid and may provide a quantitative framework for therapeutic planning OBJECTIVES: The aim was to define calibrated ECV thresholds, evaluate their diagnostic and prognostic value, and explore how CMR-ECV could provide a quantitative framework for disease staging and therapeutic planning.

Methods: We studied 1,541 subjects undergoing CMR for transthyretin amyloidosis (ATTR) classified as TTR-variant carriers (n = 123), extracardiac ATTR (n = 41), early-stage ATTR-CM (n = 70), or overt ATTR-CM (n = 1,308). The endpoint was all-cause mortality.

Results: ECV was similar in carriers and extracardiac ATTR but rose from early-stage to ATTR-cardiomyopathy (CM). Associations with biomarkers, National Amyloidosis Centre (NAC) stage, Perugini grade, and echocardiographic measures were modest, with wide overlap. Diagnostic performance was excellent: ECV <30% excluded and ≥40% confirmed cardiac involvement, whereas 30% to 39% indicated early infiltration. Over a median follow-up of 2.8 years (IQR: 1.4-4.3 years), 612 patients (40%) died. Prognostically, ECV independently predicted mortality (HR: 1.22 per 10% increase; 95% CI: 1.10-1.34 per 10% increase; P < 0.001) after multivariable analysist. Stratifying patients by ECV categories (degree of infiltration: none <30%; mild = 30%-39%; moderate = 40%-49%; moderate-to-severe = 50%-59%; severe ≥60%) showed monotonic risk increase across categories. ECV retained prognostic value across hs-troponin and N-terminal pro-B-type natriuretic peptide (NT-proBNP) strata, Perugini grades 1 to 3, and left ventricular mass index (LVMI) tertiles, with steeper gradients in low-biomarker/low-LVMI strata.

Conclusions: ECV directly quantifies myocardial amyloid load and, for the first time, defines reproducible thresholds that stratify burden and refine risk prediction beyond stage, biomarkers, and imaging, providing a quantitative framework for staging and therapeutic planning in ATTR amyloidosis.