Daily Cardiology Research Analysis

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).

IMPORTANCE: Androgen deprivation therapy (ADT) for men with prostate cancer (PCa) is associated with cardiovascular (CV) morbidity, yet the biological basis remains unclear. Recent studies have yielded conflicting results regarding the CV safety of gonadotropin-releasing hormone (GnRH) agonists vs antagonists. OBJECTIVE: To test the hypothesis that ADT is associated with accelerated coronary atherosclerosis and is more prominent with a GnRH agonist compared with a GnRH antagonist. DESIGN, SETTING, AND PARTICIPANTS: This open-label randomized clinical trial was conducted at 4 centers affiliated with a single academic institution in Atlanta, Georgia. Participants were men with nonmetastatic PCa without prior ADT exposure receiving pelvic radiotherapy with ADT of 6 months duration or longer. Patients were randomly assigned 1:1 to either the GnRH agonist leuprolide or the GnRH antagonist relugolix. Trial enrollment was completed between June 16, 2022, and March 6, 2024. Data analysis was completed between March 31, 2025, and June 23, 2025. INTERVENTION: Pelvic radiotherapy plus either GnRH agonist leuprolide or GnRH antagonist relugolix. MAIN OUTCOMES AND MEASURES: The primary end point was change in coronary artery total plaque volume (TPV), measured by coronary computed tomographic angiography completed at baseline and 12 months after ADT initiation. The secondary end point was change in coronary artery noncalcified plaque volume (NCPV). Other outcome measures included change in calcified plaque volume (CPV) and low-attenuation plaque volume (LAPV). RESULTS: Of 65 men enrolled, 62 (31 in each arm) completed all study procedures for analysis. Mean (SD) age was 68.5 (8.5) years, and 35 of 62 participants (56%) were taking statins. Compared with relugolix, leuprolide was associated with a significantly greater 12-month increase in TPV (estimated difference, +68.9 mm3; 95% CI, 23.2-114.5 mm3; P = .02) and NCPV (+64.5 mm3; 95% CI, 31.6-97.3 mm3; P = .004) after adjustment for baseline plaque volume, age, and statin use. There was no significant difference in 12-month change in CPV or LAPV between patients treated with leuprolide vs relugolix. CONCLUSIONS AND RELEVANCE: In this randomized clinical trial in men with localized PCa treated with radiation plus ADT, the GnRH agonist leuprolide was associated with greater coronary plaque progression within 12 months compared with the GnRH antagonist relugolix. This change was driven by an increase in noncalcified plaque volume and may be mediating ADT-associated CV risk. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT05320406.

BACKGROUND: Long-term mortality rates among postdischarge acute coronary syndrome (ACS) patients remain substantial. The temporal evolution and cause-specific drivers of this residual risk remain incomplete. OBJECTIVES: This study aimed to comprehensively investigate the cumulative incidence of cardiovascular (CV) and non-CV mortality after ACS discharge using a competing-risks framework. METHODS: In this multicenter cohort study, we analyzed data from the China Cardiovascular Association Database-Chest Pain Center. Mortality outcomes were ascertained through linkage with the Chinese Center for Disease Control and Prevention Cause of Death Reporting System via national mortality surveillance. Eligible patients were aged 18 years or older with a discharge diagnosis of ACS between January 2018 and December 2021. The primary outcome was all-cause mortality. Causes of death were categorized as CV or non-CV, which were analyzed as competing events. Cumulative incidence and landmark analysis at 12 months were conducted to evaluate temporal mortality patterns. Multivariate competing risks regression (Fine and Gray model) was used to identify predictors associated with the cause-specific mortality. Subgroup analyses were conducted across age, sex, and ACS subtypes. RESULTS: Of 1,562,956 eligible patients, 1,074,289 (68.7%) were men, and the mean age was 63.8 ± 12.3 years. The competing risks analysis revealed that CV death was the primary driver of mortality at 1-month discharge (1.24% vs 0.26% for non-CV); yet, non-CV mortality showed a higher relative growth than CV mortality after 12-month discharge. Ischemic heart disease (68.5%) was the predominant CV death, whereas non-CV death was dominated by malignancy (38.3%) and chronic pulmonary disease (15.8%). Age ≥65 years (subdistribution HR [sHR]: 3.78; 95% CI: 3.72-3.849), chronic kidney disease (sHR: 2.07; 95% CI: 2.03-2.11), and chronic heart failure (sHR: 1.99; 95% CI: 1.96-2.02) were leading predictors of death. Lipid-lowering therapy was associated with lower risks of all-cause, CV, and non-CV death. CONCLUSIONS: This national study demonstrates a transition in post-ACS mortality from CV to non-CV causes over time, with malignancy emerging as the leading cause of late-term death. These findings necessitate moving beyond traditional secondary prevention toward integrated survivorship care that addresses the full spectrum of competing risks.