Current Cardiology Reports最新文献

Purpose of review: Patients living with cancer are at risk for significant potential cardiovascular complications as a direct result of cancer treatment or due to underlying comorbid cardiovascular disease. This article reviews the methods of risk stratification as well as pharmacologic and nonpharmacologic approaches to cardioprotection in cardio-oncology.

Recent findings: Several cancer-specific risk stratification tools have incorporated variables such as age, sex, cancer subtype, traditional cardiovascular risk factors and cancer treatment-related parameters to assess cardiovascular specific risk prior to cancer therapy. Cardioprotective strategies, namely neurohormonal blockade and statins, have yielded mixed results in patients with cancer. Non-pharmacologic strategies, including exercise and dietary interventions, have shown potentially promising results in observational and randomized studies. Ultimately, the optimal cardioprotective strategy should be personalized based on each patient's unique risk profile and clinical context. Further research is needed to better define the role of cardioprotection across different cancer subtypes and cardiovascular risk groups, with an emphasis on refining individualized prevention and treatment strategies.

Purpose of review: VO₂ max is a fundamental marker of cardiorespiratory fitness with substantial prognostic and diagnostic value within the field of cardiology. This review analyzes current and emerging evidence regarding its clinical uses, highlights key evidence gaps, and explores emerging developments poised to broaden its clinical application.

Recent findings: Evidence supports VO2 max as a powerful independent predictor for heart failure, coronary artery disease, hypertrophic cardiomyopathy, and cardiac amyloidosis, supporting it use in identifying high-risk patients for advanced interventions. Recent developments including the integration of machine learning and wearable devices can facilitate accurate VO2 estimation in routine clinical practice without the necessity of specialized diagnostic tools. Despite its robust diagnostic and prognostic value, VO₂ max assessment remains underutilized in routine cardiovascular care, primarily due to the need for specialized equipment and personnel. Future research should explore emerging technological innovations for VO2 max estimation and the development of evidence-based protocols to support its broader clinical implementation for improved cardiovascular outcomes.

Purpose of review: Metabolic changes can play a critical role in the structural and functional decline of the aging cardiovascular system. In this review, we examine how key metabolic pathways and regulatory mechanisms influence cardiovascular aging, highlighting recent studies into metabolic flexibility, mitochondrial function, nutrient sensing, and energy utilization in the aging heart. Potential metabolic-based interventions to mitigate cardiac aging are also discussed.

Recent findings: Various metabolic changes have been observed in the aging heart. Impaired metabolic flexibility, as seen by reduced fatty acid oxidation with an increased reliance on glucose, is observed. Mitochondrial dysfunction and increased oxidative stress in aged cardiomyocytes may lead to energy deficits, contributing to myocardial fibrosis and diastolic dysfunction. Accelerated cardiovascular aging is also connected to the dysregulation of nutrient-sensing pathways- such as AMP-activated protein kinase (AMPK), sirtuins, and the mechanistic target of rapamycin (mTOR). Enhancing the age-dependent decline in autophagy and mitophagy, which clears damaged organelles, appears to preserve cardiac function in aging. Recent studies have shown that interventions such as caloric restriction, exercise, and metformin can favorably remodel cardiac metabolism and delay age-related cardiac deterioration. Metabolic changes, including energy substrate shifts, mitochondrial oxidative stress, and impaired nutrient signaling, play a direct role in cardiovascular aging. Targeting these metabolic factors and pathways holds promise for alleviating age-associated cardiac dysfunction. Recent studies focusing on lifestyle or pharmacologic means of metabolic modulation provide and outline for the promotion of healthy cardiovascular aging, thereby reducing the burden of cardiovascular disease in the growing aging population.

Purpose of review: To highlight important recent findings demonstrating the interconnectedness of planetary and human health with a focus on cardiovascular disease.

Recent findings: Data continue to demonstrate a clear interconnectedness between the health of the planet and human health, with cardiovascular disease as an important outcome. The central roles of air pollution, non-optimal temperatures, water/waste management, and food/biodiversity are highlighted. We also highlight the clear opportunity for healthcare organizations to facilitate change that will yield positive environmental and patient outcomes. The undeniable interconnectedness of the health of the planet and human health serves as a call to action for physicians, scientists, and policy makers to implement change that will lead to sustainability, a reduction in pollution, and a step into a better future.

Purpose of review: To provide a comprehensive review of cardiovascular risks associated with premature menopause.

Recent findings: Premature menopause, defined as permanent cessation of menstruation before the age of 40, is associated with an increased risk of developing cardiovascular disease. A variety of disease states and treatment exposures can lead to premature menopause resulting in a growing population of women at risk for the development of cardiovascular disease. This review summarizes current data substantiating the adverse cardiovascular outcomes seen in premature ovarian insufficiency, surgical menopause, polycystic ovarian syndrome, and cancer treatment-induced menopause. Premature menopause significantly increases the risk of long-term cardiovascular events. Multidisciplinary healthcare models that emphasize screening women with premature menopause for cardiovascular risk factors are essential to improving the cardiovascular health and longevity of this vulnerable population.

Purpose of review: This review aims to analyze the current state of transcatheter edge-to-edge repair (T-TEER) for tricuspid regurgitation, emphasizing patient phenotypes enrolled in major trials and registries, and discussing potential pharmacological treatment strategies for this complex pathology.

Recent findings: Recent studies have highlighted the significant impact of tricuspid regurgitation on morbidity and mortality in patients with valvular heart disease, heart failure, and pulmonary hypertension. Advances in multimodality imaging have improved phenotyping of TR, while T-TEER trials and registries have demonstrated improvements in TR severity and quality of life. However, mortality outcomes remain neutral. Novel therapies such as SGLT2 inhibitors show promise, particularly in patients with concomitant HFpEF and HFrEF, and ongoing trials are broadening the inclusion criteria to better represent real-world populations. T-TEER represents a promising interventional strategy for managing tricuspid regurgitation, yet challenges persist due to the heterogeneous nature of the disease and differences between trial and real-world populations. Optimizing patient selection and integrating advanced imaging and novel pharmacotherapies may further enhance clinical outcomes and reduce hospitalizations, paving the way for more personalized treatment approaches.

Purpose of review: Due to differences in cardiac structure and function, it has become increasingly clear that many aspects of cardiovascular anatomy, physiology, biochemistry, and disease are not well modeled in mice. This has spurred a search for new model organisms with the practical advantages of mice but that more closely mimic human biology and disease.

Recent findings: Until recently, little was known of lemur cardiovascular physiology, cell types, or pathology. In a recent trinity of papers, we established the mouse lemur (Microcebus spp.) - the world's smallest, most prolific, and among the most abundant non-human primates - and the cheapest and easiest to maintain, as a new tractable genetic model organism. In one of these studies, we conducted the first systematic phenotypic screen and classical genetic mapping in a non-human primate, leading to the identification and characterization of human-like cardiac arrhythmias. We successfully genetically mapped one familial lemur arrhythmia to a novel disease gene. In the other two studies, we built and applied a transcriptomic cell atlas for the mouse lemur, profiling 226,000 cells across 27 organs. This included the transcriptomic profiles of over 4000 cardiac cells, identifying 15 heart cell types that included several rare heart cell types. We documented the first null mutations in lemur, including nonsense mutations in three primate genes absent in mice, and exploited the atlas to reveal their transcriptional phenotypes, demonstrating the potential of the model organism along with synergy with the atlas. To propel these advances, we recently generated a new near telomere-to-telomere (T2T), phased diploid genome assembly for the mouse lemur, using a combination of short-, long-, and ultralong-read sequencing technologies - providing a foundational genomic resource to enhance gene and mutation discovery, functional genomics, and the applicability of cell atlas data in this new primate model. This review examines the mouse lemur (Microcebus species) as a new tractable genetic model organism for investigating primate-specific cardiovascular function and disease. Recent studies from our lab have laid a robust cellular, molecular, and genomic foundation for this model, including the first systematic phenotypic screens and classical genetic mapping in a non-human primate, showing that both forward and reverse genetic approaches are now feasible in lemurs. Collectively, these advances present a compelling case for the mouse lemur as a valuable and practical model organism for primate biomedical research.

Purpose of review: To evaluate the efficacy of bariatric surgery in the management of hypertension by answering: How does surgical weight loss compare with non-surgical methods in short-, medium-, and long-term blood pressure control? Which procedure types and patient factors predict sustained hypertension remission? What underlying mechanisms drive blood pressure improvements after surgery?

Recent findings: Multiple trials and cohort studies confirm that bariatric procedures yield greater short- to medium-term reductions in systolic and diastolic blood pressure, and higher remission rates, than diet, medication, or lifestyle interventions. Long-term follow-up reveals variable durability: a substantial subset of patients experience hypertension relapse beyond 3-5 years, underscoring the importance of continued monitoring. Meta-analyses show gastric bypass confers superior long-term remission compared with sleeve gastrectomy. Key predictors of sustained remission include shorter preoperative hypertension duration, fewer baseline antihypertensive agents, greater postsurgical weight loss, and younger age at surgery. Emerging mechanistic studies highlight improved insulin sensitivity, reduced systemic inflammation, favorable endothelial remodeling, and altered gut hormone profiles as drivers of blood pressure reduction. Bariatric surgery offers marked advantages over non-surgical treatments for hypertension control in the short and medium term, with gastric bypass generally outperforming sleeve gastrectomy in the long run. Predictive factors (e.g., hypertension chronicity, medication burden, weight-loss magnitude, patient age) can guide candidate selection and personalized follow-up. Although metabolic and vascular improvements explain much of the benefit, the pathways underlying remission of non-metabolic hypertension remain incompletely understood. Future research should focus on clarifying these mechanisms and developing targeted postoperative strategies to minimize relapse and optimize cardiovascular outcomes.

Purpose of review: Overview the current landscape of pharmacoequity in cardiovascular-kidney-metabolic (CKM) syndrome.

Recent findings: CKM syndrome is a key driver of the significant morbidity and mortality associated with cardiovascular disease, and poses a significant threat to public health. Despite a growing armamentarium of evidence-based therapies for the prevention and management of CKM syndrome, access to these treatments remains unequal. For instance, gender, race, and ethnicity-based disparities have been noted in use of first-line, guideline-directed, disease-modifying drugs. Barriers to pharmacoequity in CKM including multimorbidity/polypharmacy, low awareness, clinical inertia, cost, pharmacy inaccessibility, unequal socio-contextual factors, and fragmented care require urgent attention including equity-promoting policy.​​ Individual- and system-level barriers to pharmacoequity in CKM syndrome impede optimal CKM management, particularly among minoritized populations. We describe how a multifaceted, multi-level approach to CKM equity including interdisciplinary care and clinical decision support tools designed from an implementation science lens may help combat these inequities.