American heart journal最新文献

Background: Cardiovascular disease and cancer have numerous shared risk factors. Our objective is to determine whether American Heart Association (AHA) cardiovascular health (CVH) metrics are associated with cancer outcomes.

Methods: We searched PubMed and Scopus (inception to July 15, 2025). We included cohort studies examining the association of AHA CVH metrics with cancer risk and cancer mortality. We conducted meta-analyses to generate summary risk ratios (RRs) and standard errors for outcomes with at least three contributing studies reporting associations with low (worse), moderate, and high (best) CVH score groups. We utilized meta regression to examine dose-response relationships of CVH score groups.

Results: Our systematic review included 26 studies. Moderate (RR, 0.85; 95% CI, 0.79-0.91, p<0.001) and high (RR, 0.72; 95% CI, 0.64-0.81, p<0.001) CVH scores were associated with decreased overall cancer risk with evidence of a dose-response effect for more favorable groups (coefficient, -0.09; standard error [SE], 0.02; p<0.001). High CVH scores were associated with statistically significantly decreased risk of breast (RR, 0.72; 95% CI 0.58-0.90), colorectal (RR, 0.65, 95% CI 0.57-0.74), and lung cancer (RR, 0.34; 95% CI 0.16-0.70). We found evidence for lower cancer mortality in the moderate (RR, 0.64; 95% CI, 0.61-0.68, p<0.001) and high (RR, 0.47; 95% CI, 0.41-0.53, p<0.001) CVH score groups. Meta regression demonstrated a dose-response effect on all cancer mortality (coefficient, -0.33; SE 0.05; p<0.001).

Conclusions: We provide evidence for a dose response association of better CVH scores with decreased cancer incidence and cancer mortality. Optimizing CVH may improve cancer outcomes.

This letter evaluates whether overestimation of control event rates and the use of absolute noninferiority margins influenced conclusions of randomized trials comparing transcatheter and surgical aortic valve replacement. By reanalyzing published noninferiority trials using observed event rates and corresponding relative margins, we assessed the robustness of trial conclusions to alternative margin specifications. Our findings inform interpretation of noninferiority evidence underlying contemporary clinical decision-making in aortic valve replacement.

Background: Transcatheter aortic valve replacement (TAVR) is a key treatment for severe aortic stenosis (AS). Several studies have consistently shown discrepancies between transvalvular gradients measured by transthoracic echocardiography (TTE) and those obtained invasively. The aim of this study was to evaluate this discrepancy in a large patient cohort and determine whether it is associated with clinical outcomes.

Methods: This study included patients with severe AS who underwent TAVR using either balloon-expandable (BEVs) or self-expanding valves (SEVs). The primary endpoint was the magnitude of discrepancy between peak transvalvular gradients measured by TTE and invasive hemodynamic assessment. Secondary endpoints included the association of this gradient difference with in-hospital, 30-day, and 1-year mortality. In addition, multivariable linear regression analysis was performed to identify independent predictors of gradient discrepancy.

Results: A total of 1,798 TAVR patients were included: 799 received BEVs and 999 received SEVs. Post-procedural mean peak gradients by echocardiography were significantly higher in the BEV group (20 ± 8 mmHg) than in the SEV group (15 ± 7 mmHg; p < 0.001). Invasive mean peak gradients were lower overall, at 5.9 ± 4 mmHg for BEVs and 5.3 ± 3.8 mmHg for SEVs (p = 0.001). The mean difference between echocardiographic and invasive measurements was significantly greater in the BEV group (14 ± 8 mmHg) compared to the SEV group (10 ± 7 mmHg; p < 0.001). There were no statistically significant differences in mortality between the BEV and SEV groups. Additionally, female sex, hypertension, preserved left ventricular function, small valve size, and small aortic annulus were all linked to greater differences between echocardiographic and invasive gradients.

Conclusion: echocardiographic gradients after TAVR consistently overestimate invasive values, especially with balloon-expandable valves, but without impacting short or mid-term mortality.

Rationale: Older patients hospitalized for acute decompensated heart failure (ADHF) with preserved ejection fraction (HFpEF) experience persistently poor outcomes, including physical disability, cognitive impairment, depression, impaired health-related quality of life (HRQOL), rehospitalizations, loss of independence, and mortality. In our previous phase 2 REHAB-HF trial, an innovative physical rehabilitation intervention, delivered across three phases-inpatient, 12-week outpatient, and 3-month home-based maintenance-produced large improvements in physical function and HRQOL, with signals of reduced clinical events among patients with acute HFpEF. These findings provide a compelling rationale for a definitive, event-powered trial to evaluate clinical outcomes.

Hypothesis: Targeting physical frailty and multisystem functional impairments using the REHAB-HF intervention-a transitional, tailored, structured, and progressive multidomain rehabilitation program focused on balance, mobility, strength, and endurance-will reduce clinical events in older, predominantly frail patients hospitalized for acute HFpEF.

Design: REHAB-HFpEF is a multicenter, randomized, single-blind, attention-controlled phase 3 trial across 22 U.S. health system centers, enrolling 880 patients aged ≥60 years hospitalized for acute HFpEF. The primary endpoint is combined all-cause rehospitalizations and mortality at 6 months. Key secondary endpoints include major mobility disability (defined as inability to walk ≥160 meters on the 6-minute walk test) and HRQOL measured by the Kansas City Cardiomyopathy Questionnaire. Healthcare costs will also be assessed.

Conclusions: REHAB-HFpEF is designed to address care gaps for frail older adults with acute HFpEF, who currently lack an evidence-based rehabilitation pathway. If successful in meeting endpoints, this trial could establish a scalable rehabilitation intervention that improves recovery, reduces adverse events, and lowers healthcare costs. Findings may shift HF management paradigms, inform guidelines, and influence national coverage policy for this growing, high-risk population.

Current status: Enrollment ongoing, 478 of 880 (66%) as of 24Feb2027 TRIAL REGISTRATION: Clinicaltrials.gov ID NCT05525663, https://clinicaltrials.gov/study/NCT05525663?term=NCT05525663&rank=1.

Background: Longer total stent length (TSL) increases the risk of target lesion failure (TLF) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) with second-generation drug-eluting stents (DES). We aimed to assess the long-term impact of TSL on patient- and stent-related outcomes in STEMI patients treated with different newer-generation DES designs.

Methods: We performed a post hoc subgroup analysis of the BIOSTEMI Extended Survival randomized trial (NCT05484310). Patients undergoing primary PCI for STEMI were randomized to ultrathin-strut biodegradable-polymer sirolimus-eluting stents (BP-SES) or thin-strut durable-polymer everolimus-eluting stents (DP-EES) and categorized according to TSL implanted at the culprit site (≤40 mm vs. >40 mm). The device-oriented composite endpoint (TLF) was the composite of cardiac death, target-vessel (TV) myocardial reinfarction, or clinically indicated target lesion revascularization (TLR), and the patient-oriented composite endpoint (POCE) was the composite of all-cause death, any myocardial reinfarction, any revascularization, or any stroke, at 5 years.

Results: A total of 1,686 STEMI patients were included (mean age, 62.4 years; female, 23%; mean TSL, 33.8 mm), of whom 423 (25%) were treated with TSL >40 mm. At 5 years, TSL >40 mm was associated with a significantly higher risk of POCE compared with TSL ≤40 mm [31.7% vs. 27.4%; hazard ratio (HR), 1.30; 95% confidence interval (CI), 1.03-1.64; p=0.029], whereas no difference was observed in TLF. However, there was a significant interaction between DES type and TSL for TLF at 5 years. Among patients with TSL >40 mm, BP-SES were associated with a lower risk of TLF compared with DP-EES (7.3% vs. 17.1%; HR, 0.39; 95% CI, 0.21-0.74; p=0.004; p for interaction=0.032), a difference primarily driven by a lower rate of target vessel myocardial reinfarction. No significant differences between BP-SES and DP-EES were observed in patients with TSL ≤40 mm. After adjustment for multivessel treatment, increasing TSL with DP-EES, but not BP-SES, was independently associated with a higher risk of TLF (adjusted HR per 5-mm increase, 1.07; 95% CI, 1.02-1.11; p=0.003).

Conclusion: In STEMI patients treated with contemporary DES, TSL >40 mm was associated with an increased risk of patient-oriented, but not device-related, adverse outcomes at 5 years. Among patients requiring TSL >40 mm, ultrathin-strut BP-SES significantly reduced the risk of TLF compared with DP-EES, whereas no between-DES differences were observed in patients treated with TSL ≤40 mm.

Background: Higher maximal oxygen consumption (VO₂ max) is associated with lower risk of developing heart failure (HF). Empagliflozin improves VO₂ max in HF with reduced ejection fraction (HFrEF), but the effect on VO₂ max in individuals at risk of HF remain unknown.

Objective: This study aimed to evaluate the effect of 180 days treatment with empagliflozin compared to placebo on VO₂ max, daily physical activity level and quality of life (QoL) in individuals with overweight or obesity and risk of HF.

Method: This investigator-initiated, double-blinded, randomized, placebo-controlled, multicenter trial included elderly individuals with body mass index (BMI) >28 kg/m² and at least one additional risk factor for HF, including hypertension, ischemic heart disease, stroke, or chronic kidney disease. Individuals with HF or T2D were excluded. The primary endpoint was the mean difference in change of VO₂ max. The secondary outcome was objectively measured physical activity level. QoL was an explorative outcome.

Results: Among 191 randomized individuals (94 empagliflozin, 97 placebo), 89% had hypertension and 66% ischemic heart disease. At baseline, 69% were male, median age was 68 years, median BMI 31.9 kg/m², mean left ventricular ejection fraction 65±9%, and mean VO₂ max 18.1±4.3 ml/min/kg. Empagliflozin did not change VO₂ max with an estimated treatment difference of -0.2 ml/min/kg (97.5% CI -1.2 to 0.8), adjusted P=1.00. No significant treatment differences were observed for neither daily physical activity nor QoL.

Conclusion: Empagliflozin did not affect VO₂ max, physical activity level or QoL in elderly individuals with overweight or obesity and risk of HF.

Background and aims: Conventional biomarkers such as Low-density Lipoprotein (LDL), and High-density Lipoprotein (HDL) may fail to identify patients' risk for significant coronary artery disease (CAD). This study evaluates the associations between multiple biomarkers and different CAD phenotypes exploring a machine-learning biomarker-based patient clustering.

Methods and results: We included 787 patients on primary prevention from the prospective ACTION registry (January 2024-June 2025). All patients underwent coronary CTA and simultaneous biomarker testing including LDL, HDL, Triglyceride, Apolipoprotein A-1(ApoA-1), Apolipoprotein B (ApoB), Lipoprotein(a) [Lp(a)], glycated hemoglobin (HbA1c), and high-sensitivity C reactive protein (hs-CRP). Of 382 patients (48.5%) with CAC=0, 42 (11%) had coronary plaque. These patients showed higher Lp(a) vs. those without plaque (16.5 vs. 11.5, p=0.030), despite comparable SCORE2 risk (3.5% vs. 3.0%, p=0.284). Three biomarker-defined groups were identified after a machine learning unsupervised clustering: Cluster 1 had a favorable lipid profile with the lowest prevalence of CAD-RADS≥3 (9.9%). Cluster 2 and 3, despite their significant inter-cluster differences in terms of Lp(a), LDL and HbA1c levels both showed a significantly higher prevalence of CAD-RADS≥3 compared to cluster 1 (respectively 21.8% and 17.9%; vs. cluster 1 p=0.001). High risk biomarker signatures were significantly associated to the prevalence of CAD-RADs≥3, independently from the baseline SCORE2 (adjusted OR 2.25; 95%CI 1.32-3.82).

Conclusions: Distinct biomarker signatures associate with distinct CAD prevalence and severity that conventional lipid markers fail to distinguish. Lp(a) appears relevant for early plaque detection in CAC=0 patients. A comprehensive biomarker evaluation may help identifying high-risk subgroups overlooked by a conventional assessment.

Rationale: Abbreviated dual antiplatelet therapy (DAPT) strategies effective in percutaneous coronary intervention among patients with high bleeding risk (HBR) may not be applicable to carotid artery stenting (CAS) owing to anatomical and procedural differences.

Primary hypothesis: Among patients with HBR undergoing CAS, abbreviated DAPT followed by SAPT will reduce clinically significant bleeding compared to prolonged DAPT, while maintaining non-inferiority in net clinical outcomes including ischemic and major bleeding events.

Design: CHET trial is a multicenter, randomized, open-label, superiority trial in HBR patients undergoing CAS. Assuming a 38% relative reduction in bleeding (10.4% to 6.45%), 1,524 participants (762 per group) provide 80% power with a two-sided alpha of 0.05; the final target is 1,556 (778 per group) allowing 2% dropout. Key HBR criteria include age ≥ 75 years, ischemic stroke within 6 months, renal insufficiency, anemia, and thrombocytopenia. All patients will receive aspirin and clopidogrel for 30 days after CAS (enrichment period). Event-free patients on day 30 were randomized 1:1 to receive SAPT (aspirin 100 mg daily or clopidogrel 75 mg daily, at the treating physician's discretion) or continued DAPT for 11 months. The primary safety endpoint is clinically significant bleeding (BARC 2, 3, or 5) from day 30 to 12 months post-CAS. The secondary efficacy endpoint is a composite of non-fatal stroke, non-fatal myocardial infarction, cardiovascular death, and major bleeding (BARC 3 or 5).

Enrollment dates and current status: CHET began enrollment on July 15, 2024. As of February 5, 2026, the trial is currently enrolling, with 328 participants enrolled. Enrollment is expected to be completed by November 2029, and follow-up by December 2030.

Conclusions: CHET trial is the first randomized controlled trial to define optimal DAPT duration in HBR patients after CAS.

Trial registration: www.

Clinicaltrials: gov (NCT06276374).

Background: Results of observational studies assessing clinical benefits of guideline directed medical therapy (GDMT) for heart failure (HF) in adults with congenital heart disease (CHD) are conflicting. This is because these studies were based on a heterogenous population and lacked standardized criteria for assessing adequacy of HF therapy across studies. The current study addressed these limitations by studying the effect of GDMT (using a standardized GDMT score) in adults with repaired systemic biventricular CHD, systemic left ventricle and HF with reduced ejection fraction (HFrEF).

Method: HFrEF was defined as stage B/C HF and systemic left ventricular EF<50%. GDMT score was assessed at baseline encounter (baseline GDMT score) and 1-year follow-up. GDMT uptitration was calculated as defined as ∆GDMT (∆=delta or change in) score from baseline. Cox regression was used to assess the relationship between HF therapy (baseline and ∆GDMT score) and outcomes (HF hospitalization and mortality).

Results: Of 778 patients, baseline and ∆GDMT scores were 2 (1,3) and 0.56 (0.49,0.62), respectively. Of 778, only 258 (33%) had GDMT uptitration (∆GDMT score >0). Higher use of GDMT at baseline (adjusted HR per 1 point increase in GDMT score 0.83, 95%CI 0.74, 0.92, p<0.001), and increased use of GDMT over time (adjusted HR for 1 point increase in ∆GDMT score HR 0.71, 95%CI 0.62, 0.82, p<0.001) were associated with lower risk of HF hospitalization. Higher baseline GDMT score (adjusted HR 0.87, 95%CI 0.76, 0.98, p=0.01), and ∆ GDMT score (adjusted HR 0.84, 95%CI 0.72, 0.86, p=0.002) were also associated with lower mortality.

Conclusions: GDMT use at baseline and GDMT uptitration were associated with improved outcomes and suggest a dose-dependent relationship between use of GDMT and risk of adverse outcomes. Furthermore, 67% of patients did not receive GDMT uptitration, suggesting suboptimal therapy, and opportunities for improvement.