Obtaining informed consent for clinical trial participation in acute myocardial infarction presents unique ethical and logistical challenges because of the patient distress, sedation, and the urgency of treatment. Traditional consent procedures often conflict with the narrow enrollment windows, prompting the use of legally authorized representatives and short- and long-form consent models. Although these approaches enable faster trial enrollment, they may compromise patient autonomy, introduce selection bias, or create postenrollment ethical dilemmas. This review explores the complexities of informed consent in acute myocardial infarction research, evaluating the advantages and limitations of existing strategies, including legally authorized representative consent, 2-step consent processes, and alternatives such as deferred and verbal consent. It also examines international variations in regulatory oversight and presents emerging solutions, such as preemptive consent, opt-out models, electronic platforms, and registry-based trials, to streamline the enrollment without delaying care. Ultimately, consent regulations should be re-evaluated and potentially relaxed to better support timely research. A thoughtful reassessment of consent frameworks is essential to ethically and effectively advance acute myocardial infarction research in time-sensitive settings.

There is heterogeneity in coronary artery disease (CAD) severity among individuals with severe aortic stenosis (AS), but whether this differentially influences prognosis is unknown.

Sinoatrial node (SAN) dysfunction is commonly associated with atrial dysrhythmia (tachy-brady syndrome) and is a particularly important feature of inherited atrial cardiomyopathies leading to artificial pacemaker implantation. Essential MYL4 (myosin light chain-4) is an atrial-selective protein that associates with the myosin light chain and participates importantly in cardiacmuscle contraction. MYL4 gene variants encoding dysfunctional versions of MYL4 cause familial atrial cardiomyopathy with a high incidence of early SAN dysfunction (SND) and pacemaker requirement. In this study, we used a rat line, genetically modified to express an E11K gene mutation responsible for familial atrial cardiomyopathy, to address the mechanisms underlying SND.

Dilated cardiomyopathy (DCM) is substantially influenced by genetic factors. Sarcomere function is intricately associated with other organelles, particularly the reciprocal regulation between sarcomeres and mitochondria. Mitochondrial stress dysregulation is linked to DCM progression, yet mechanisms remain unclear. In this study, we investigated the effects of cTnT (cardiac troponin T) dysregulation on sarcomere-mitochondrial communication in DCM.

Most polygenic risk scores (PRS) have been developed in European populations, frequently leading to limited transferability across diverse ancestry populations. This study aimed to develop and evaluate PRS for blood pressure (BP) traits in continental African populations and investigate how African genetic diversity influences PRS performance.

Identifying causal variants among tens or hundreds of associated variants at each locus in genome-wide association studies is challenging. As the vast majority of genome-wide association studies variants are noncoding, sequence variation at cis-regulatory elements (CREs) affecting transcriptional expression of specific genes is a widely accepted molecular hypothesis. Following this hypothesis, combined with the observation that open chromatin is a universal hallmark of all types of CREs, we aimed to identify candidate causal cis-regulatory variants underlying QT interval genome-wide association studies loci.

Desmosomal gene variants (DGVs) have been associated with a diverse spectrum of phenotypic manifestations within arrhythmogenic cardiomyopathy, but data on genotype-specific outcomes are lacking. We investigated genotype-specific arrhythmic and heart failure (HF) outcomes in DGV carriers.

Acute decompensated aortic stenosis is an increasingly common condition associated with a high rate of morbidity, mortality, and health care resource utilization. Among patients with acute decompensated aortic stenosis, this study aimed to assess the impact of time to transcatheter aortic valve implantation (TAVI) on outcomes, hypothesizing that longer durations are associated with worse outcomes.

Heterozygous pathogenic variants in the central region (exon 23-34) of FBN2 cause a hereditary connective tissue disorder named congenital contractural arachnodactyly, which presents with obligatory skeletal features but rarely with vascular manifestations. Scarce data exist on the association between FBN2 variants and aortic disease. This study aimed to investigate whether the location of FBN2 variants correlates with distinct clinical features, including aortic disease.

Recent findings emphasize the potential role of invasive hemodynamic assessment in guiding transcatheter mitral and tricuspid valve percutaneous interventions. Right heart catheterization-derived parameters offer insights into hemodynamic changes associated with valvular heart diseases, pulmonary hypertension phenotyping, and right ventricular to pulmonary artery coupling. This might improve prognostic stratification for candidates to transcatheter therapies. This review provides a clinical overview of available data regarding the utility of preoperative right heart catheterization-derived parameters in patients undergoing mitral and tricuspid percutaneous repair or replacement.

Proteomic signatures might improve disease prediction and enable targeted disease prevention and management. We explored whether a protein risk score derived from large-scale proteomics data improves risk prediction of atrial fibrillation (AF).

Physiology assessment of coronary lesion prepercutaneous coronary intervention (PCI) using hyperemic and nonhyperemic pressure ratios is useful to determine if a lesion requires treatment. Whether the physiology after PCI is superior to angiography guidance only is unknown. The study sought to investigate whether post-PCI physiology improves clinical outcomes compared with standard angiographic guidance.

Myocardial ischemia/reperfusion (I/R) injury is a substantial challenge to the management of ischemic heart disease, the leading cause of mortality worldwide. Arachidonic acid (AA) is a prominent polyunsaturated fatty acid in the human body and plays an important role in various physiological and pathological conditions. AA metabolic enzymes determine AA levels; however, currently there is no comprehensive analysis of AA enzymes in cardiac I/R injury.

Although pretranscatheter aortic valve replacement-computed tomography angiography (TAVR-CTA) has shown a good correlation with invasive coronary angiography (ICA) for ruling out obstructive coronary artery disease (CAD), its clinical effectiveness and safety as a gatekeeper for ICA pre-transcatheter aortic valve replacement (pre-TAVR) remain unclear. This study aims to determine whether routine TAVR-CTA, without premedication, could safely defer and guide the need for ICA pre-TAVR.