Trends in Cardiovascular Medicine最新文献

As cannabis use accelerates globally with expanding legalization and availability of high-potency formulations, concerns regarding its cardiovascular safety have grown. However, the evidence remains unclear and often inconsistent. This narrative review aimed to summarize the current evidence on the cardiovascular effects of cannabis. We performed a narrative review of peer-reviewed studies on cannabis and cardiovascular outcomes, searching PubMed and Google Scholar for relevant human research published 2014-August 2025. Included evidence encompassed observational cohorts, randomized trials, meta-analyses, Mendelian randomization studies, and mechanistic investigations, supplemented by reference screening. Observational studies reveal mixed associations between THC use and myocardial infarction, stroke, and MACE, with many findings attenuated after adjustment for confounders. A stronger and more consistent association exists for atrial arrhythmias. Evidence for venous thromboembolism remains inconsistent. Interpretation of the available evidence is also hindered by exposure misclassification (e.g., dose, route, frequency), reliance on administrative coding, insufficient differentiation between medical and recreational use, residual confounding (e.g., tobacco, other substances), and limited translational data. Cannabis use is rising, and while mechanistic data suggest THC-related autonomic, endothelial, and platelet effects, overall cardiovascular evidence remains mixed with the most consistent signal seen for atrial arrhythmias. Risk appears influenced by dose, route, and co-use of substances, and current studies are limited by heterogeneity and exposure misclassification. Until higher-quality data emerge, clinicians should adopt a precautionary, harm-reduction approach, especially in patients with cardiovascular comorbidities.

Cardiovascular disease remains the leading cause of death worldwide, with many events occurring in individuals classified as having intermediate or even low risk according to traditional prediction models. Although contemporary risk calculators for coronary artery disease have offered modest improvements, their ability to provide individualized risk assessment remains limited. Noninvasive imaging techniques have gained growing recognition for their ability to detect evidence of subclinical atherosclerosis, refine risk stratification beyond conventional clinical parameters, and guide targeted preventive therapies. This review outlines the current evidence, clinical utility, and future potential of imaging-based strategies in enhancing primary prevention of coronary artery disease.

Inherited cardiac conditions (ICCs) such as hypertrophic cardiomyopathy and Marfan syndrome pose significant global health challenges, often rooted in complex genetic mutations. Recent advances in gene editing, particularly the CRISPR/Cas9 system, have opened new avenues for precise, personalized interventions. This review examines the current landscape of gene editing in cardiology, with emphasis on its scientific promise, integration with epigenetics, gene therapy, and artificial intelligence, and its potential to transform clinical outcomes. Key gene editing strategies are analyzed for their efficacy and translational potential. The review also explores ongoing clinical trials and emerging research, offering practical insights for future studies. Ethical implications are critically evaluated, with proposed frameworks to address concerns around safety, equity, and long-term consequences. By synthesizing these developments, this review underscores the urgent need for continued interdisciplinary research in the quest to mitigate inherited cardiac diseases.

Sodium-glucose co-transporter-2 (SGLT2) inhibitors have become a cornerstone of heart-failure (HF) therapy, lowering hospitalization and cardiovascular mortality in patients with and without diabetes across the spectrum of ejection-fraction phenotypes. Their cardioprotective effects extend beyond glycemic control and are best explained by a hierarchy of mechanisms initiated in the kidney. Early tubular inhibition restores tubuloglomerular feedback, producing osmotic diuresis, natriuresis, and modest reductions in plasma volume and blood pressure that together relieve ventricular preload and afterload. These renal and hemodynamic actions are followed by sustained adaptations involving neurohormonal modulation, erythropoiesis, improved cortical oxygenation, and progressive anti-inflammatory, antifibrotic, and mitochondrial effects. Through these interrelated pathways, SGLT2 inhibition preserves kidney function, limits congestion, and promotes cardiac reverse remodeling. Recognizing that these mechanisms act sequentially and in parallel clarifies how SGLT2 inhibitors complement standard therapies and guides ongoing mechanistic studies to refine their role in HF management.

Inherited cardiomyopathies are a diverse group of diseases with overlapping clinical features and genetic basis. Once thought to be primarily monogenic diseases, it is now known that disease severity and penetrance can be impacted by both genetic and non-genetic factors, such as comorbidities. Inherited cardiomyopathies include hypertrophic (HCM), dilated (DCM), arrhythmogenic (ACM) and restrictive cardiomyopathies (RCM). Although many causative genes have been identified for these conditions, a monogenic cause cannot be discovered in many cases, and other factors play a role. Moreover, the clinical heterogeneity observed cannot be explained by a single variant, even when one has been identified. Here we review non-genetic factors, including presence of concomitant conditions such as obesity, hypertension, sleep apnea, diabetes and pregnancy, in addition to the impact of lifestyle behaviours such as physical activity and drug taking. Further, we summarise the role of common variants in tipping the balance on disease penetrance and/or severity. Clinical considerations and opportunities to improve outcomes in inherited cardiomyopathies will be examined, with a particular focus on the potential to reduce disease severity or even prevent disease onset, through lifestyle modification and recognition of non-genetic contributing factors.