Cardiology in Review最新文献

Glucagon-like peptide-1 receptor agonists and glucose-dependent insulinotropic polypeptide coagonists have revolutionized the treatment of type 2 diabetes and obesity. They demonstrate significant cardiovascular benefits, including a reduction in major adverse cardiovascular events and heart failure hospitalizations. However, these medications are associated with substantial lean body mass loss, comprising 15-45% of total weight reduction. This review examines the pathophysiological mechanisms underlying muscle loss with incretin-based therapies, analyzes clinical trial data on body composition changes, explores the bidirectional relationship between sarcopenia and cardiovascular disease, and evaluates emerging pharmacological and lifestyle interventions to preserve muscle mass. Understanding and mitigating muscle loss is critical for optimizing cardiovascular outcomes, particularly in older adults and those with established heart disease, where sarcopenia is associated with increased mortality and functional decline.

Acute coronary syndromes most commonly arise from rupture of biologically vulnerable, rather than hemodynamically severe, coronary plaques. Advances in intravascular and noninvasive imaging techniques, including intravascular ultrasound, optical coherence tomography, near-infrared spectroscopy, and coronary computed tomography angiography, have enabled precise identification of high-risk plaque features such as thin fibrous caps, large lipid cores, and high plaque burden. While intensive lipid-lowering therapy favorably modifies plaque composition and reduces cardiovascular risk, interventional strategies are needed to directly stabilize nonflow-limiting but biologically vulnerable plaques. Intracoronary cryotherapy has emerged as a novel, investigational approach aimed at modifying plaque biology through controlled thermal modulation without permanent intracoronary implantation. Preclinical studies demonstrate increased fibrous cap thickness and collagen content following cryotherapy, consistent with plaque stabilization. Early first-in-human experience suggests technical feasibility and short-term safety. This review summarizes contemporary approaches to vulnerable plaque identification, existing pharmacologic and interventional strategies, and the evolving role of intracoronary cryotherapy as a potential plaque-directed therapy.

The Utstein Formula for Survival, the ethos of the American Heart Association's 2025 guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, is a conceptual model for survival of out-of-hospital cardiac arrest that equally weighs medical science, educational efficiency, and local implementation. With this formula in mind, the American Heart Association has put forth new guidelines that emphasize not only high-quality chest compressions and early defibrillation but also robust systems of care, equitable access, advanced resuscitation techniques, and postcardiac arrest recovery. The 2025 updates carry significant weight for health policy, clinical practice, education, and ethical discussions. In this review, we highlight the major changes, discuss their implications, and propose directions for future research and implementation.

Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) form an endocrine axis with broad cardiovascular relevance because their receptors in cardiomyocytes and vascular cells link hormonal signaling to myocardial growth and performance, vascular tone, endothelial nitric oxide biology, and cardiometabolic risk. This review synthesizes mechanistic, clinical, and epidemiologic evidence to clarify cardiovascular effects across GH/IGF-1 deficiency and excess, and to highlight implications for therapeutic decision making. Key themes include receptor-driven pathways, imaging, and functional phenotyping that distinguishes a "small-heart" pattern with microvascular and endothelial dysfunction in adult GH deficiency from concentric remodeling, diastolic impairment, arrhythmias, and a stiffness/volume-expanded hemodynamic profile in acromegaly, and evidence that timely endocrine control or replacement can yield partial reverse remodeling while residual abnormalities may persist with longer disease duration. Clinically, the review emphasizes that cardiometabolic tradeoffs differ across GH-directed therapies, so biochemical control alone may not capture risk. Major gaps include heterogeneous cohorts, confounding by comorbidities and concurrent hormone replacement, variable endpoints, and limited event-driven prospective data, motivating standardized phenotyping, hard-outcome studies, and validation of IGF-system biomarkers for risk stratification and treatment selection.

Cardiovascular disease remains the leading cause of morbidity and mortality worldwide. Given the global burden, the potential role of micronutrients-particularly vitamins-in modifying cardiovascular risk has been a topic of intense investigation. This review synthesizes current evidence on the associations between various vitamins and cardiovascular health. It explores biological mechanisms, including antioxidant activity, endothelial function, lipid modulation, homocysteine metabolism, and vascular calcification. Vitamins D, C, E, K, and several B-complex vitamins are highlighted for their relevance. While observational data often support associations between deficiencies and adverse cardiovascular outcomes, large-scale randomized controlled trials have yielded mixed or null results, particularly regarding supplementation efficacy in primary or secondary prevention. Despite a high prevalence of supplement use in the United States, with over half of adults reporting intake, robust evidence supporting cardiovascular benefit remains limited. In some subgroups-such as individuals with hypertension, heart failure, or vitamin deficiencies-certain vitamins may offer modest benefits. However, indiscriminate supplementation has generally not been proven effective and, in some cases, may carry risks. The review emphasizes the need for targeted interventions, individualized assessment, and further high-quality research to clarify the role of vitamins in cardiovascular prevention and treatment.

Multiple academic sites have reported that social isolation can pose a public health hazard, specifically premature cardiovascular disease and cerebrovascular disease. This article reports on cardiovascular complications discovered by clinicians and public health researchers. In addition, there are reports that social isolation is associated with pulmonary disease, cancer, autoimmune disease, and even adverse outcomes during pregnancy. Social isolation has been a known factor for serious adverse outcomes in psychiatric circles since the time of Emil Kraepelin, Paul Eugen Bleuler, and Emile Durkheim before the 20th century. In the past, there have also been sporadic case reports from biologically oriented psychiatrists reporting severe medical conditions in these patients, mostly regarded as due to poor access to medical assessments of patients with social isolation. While still a valid pathway for the explanation of some findings, recently, there has been a great deal of interest in the discovery of pathophysiological mechanisms as causative of deadly outcomes in victims of social isolation. This is based on the robust association between social isolation and the development of premature cardiovascular disease. Using Scopus, PubMed, and the Bernard Becker Medical Library at Washington University, the authors reviewed articles from Europe, England, North America, and East Asia published within the past 2 years. Descriptions of pathophysiological mechanisms published in the past 20 years are included in this paper.

Hypoglycemia is defined as low blood glucose levels. While it is uncommon in healthy adults, diabetics and other vulnerable patient populations remain at increased risk. The neuroglycopenic symptoms of hypoglycemia, such as dizziness, lethargy, loss of consciousness, etc., are well known. However, hypoglycemia has significant cardiovascular manifestations. During an acute hypoglycemic episode, sympathoadrenal activation causes increased epinephrine release. Epinephrine directly increases myocardial workload via stimulating β1 adrenoreceptors; in vulnerable populations, increased cardiac stress may provoke ischemia and infarction. Additionally, epinephrine may induce hypokalemia via stimulating β2 adrenoreceptors on various cells; electrolyte disturbances induce electrocardiogram changes, increasing the risk of cardiac arrhythmias. Endothelial dysfunction may also arise due to epinephrine-mediated adrenergic activation. This article reviews the current literature addressing pathogenesis, diagnostic criteria, and cardiovascular complications of hypoglycemia.

Cancer-associated venous thromboembolism (CA-VTE) is a leading, severe, and potentially life-threatening complication in patients with malignancy. Low-molecular-weight heparin has historically been the standard of care; however, direct oral anticoagulants, particularly direct factor Xa inhibitors, have emerged as effective alternatives. These agents offer the convenience of oral administration, predictable pharmacokinetics, elimination of routine laboratory monitoring, and improved adherence. Despite the expanding role of direct oral anticoagulants in CA-VTE management, concerns regarding bleeding risk-particularly in patients with gastrointestinal and genitourinary malignancies-remain central to clinical decision-making. In this narrative review, we evaluate the efficacy, safety, and clinical applicability of apixaban for the treatment and prophylaxis of CA-VTE. Current evidence from randomized controlled trials, including CARAVAGGIO and AMPLIFY, demonstrates that apixaban has noninferior efficacy compared with low-molecular-weight heparin and conventional anticoagulation strategies, with comparable or lower rates of recurrent venous thromboembolism. In addition, apixaban appears to have a favorable safety profile, with no statistically significant increase in major bleeding in selected cancer populations, including those without active gastrointestinal lesions. Apixaban's pharmacokinetic properties, including limited renal clearance and stable drug exposure, further enhance its clinical utility in oncologic populations. However, evidence supporting apixaban use across all cancer subtypes remains limited and heterogeneous, highlighting the need for additional comparative and real-world studies.

Obesity and hypertension are interdependent chronic conditions that substantially elevate global cardiovascular risk. Rising obesity prevalence has led to a parallel increase in hypertension, driven by complex physiological disturbances that extend beyond excess body weight alone. This review synthesizes current evidence on the mechanisms linking adiposity to blood pressure elevation, emphasizing the roles of sympathetic nervous system overactivity, insulin resistance, renal sodium retention, and adipose-derived hormonal and inflammatory dysregulation. Particular attention is given to visceral adiposity, which exerts adverse vascular, renal, and metabolic effects that accelerate development of hypertension-mediated organ damage, including left ventricular hypertrophy, arterial stiffness, and early renal injury. The manuscript also evaluates therapeutic strategies for obesity-related hypertension. Lifestyle interventions-caloric restriction, structured physical activity, and behavioral therapy-remain the cornerstone of management, producing clinically meaningful reductions in body weight and blood pressure. However, sustained weight loss is difficult for many individuals, necessitating adjunctive approaches. Contemporary pharmacotherapies, particularly glucagon-like peptide-1 receptor agonists such as semaglutide, have demonstrated substantial benefits in both weight reduction and blood pressure control. For patients with severe obesity or inadequate response to medical therapy, metabolic and bariatric procedures offer the most durable outcomes, improving cardiometabolic profiles and reducing antihypertensive medication burden.