Cardiology in Review最新文献

Epicardial adipose tissue (EAT) is located between the heart muscle and visceral pericardium, where it has direct contact with coronary blood vessels. Elevated thickness of this tissue can induce local inflammation affecting the myocardium and the underlying coronary arteries, contributing to various cardiovascular diseases such as coronary artery disease, atrial fibrillation, or heart failure with preserved ejection fraction. Recent studies have identified EAT thickness as a simple and reliable biomarker for certain cardiovascular outcomes. Examples include the presence of atherosclerosis, incident cardiovascular disease (CVD) in individuals with type 2 diabetes mellitus (T2DM), and the prevalence of atrial fibrillation. Furthermore, EAT measurements can help to identify patients with a higher risk of developing metabolic syndrome. Since the EAT thickness can be easily measured using echocardiography, such examinations could serve as a useful and cost-effective preventive tool for assessing cardiovascular health. This review also summarizes therapeutical interventions aimed at reducing EAT. Reducing EAT thickness has been shown to be possible through pharmacological, surgical, or lifestyle-change interventions. Pharmaceutical therapies, including thiazolidinediones, glucagon-like peptide 1-receptor agonists, sodium-glucose cotransporter 2 inhibitors, dipeptidyl peptidase-4 inhibitors, and statins, have been shown to influence EAT thickness. Additionally, EAT thickness can also be managed more invasively through bariatric surgery, or noninvasively through lifestyle changes to diet and exercise routines.

Cerebral embolic protection devices (CEPD) during transcatheter aortic valve replacement (TAVR) have been shown to lower the risk of stroke during the procedure. However, their long-term and clinical effects on neuro-cognition are unknown. Therefore, we hypothesized the benefit of CEPD in TAVR patients with a prior history of stroke or transient ischemic attack (TIA). National Inpatient Sample (2019) and International Classification of Diseases, 10th Revision codes were used to identify patients undergoing TAVR with prior stroke or TIA. Propensity-matched analysis was performed to adjust for baseline characteristics and comorbidities. Primary outcome measures were postoperative stroke and all-cause mortality. Length of stay and hospital cost were secondary outcomes. Of 8450 unmatched TAVR patients with prior stroke or TIA in 2019, 1095 (13%) utilized CEPD. After propensity matching previous myocardial infarction (MI), coronary artery bypass grafting, and drug abuse were higher in the TAVR-only cohort. Postoperative stroke rate (1.4% vs 2.2%; P = 0.081) and odds [adjusted odds ratio (aOR), 0.48; 95% confidence interval (CI), 0.11-2.17; P = 0.341] were lower in the CEPD group. There was no difference in all-cause in-hospital mortality between the 2 groups (0.9% vs 1.0%). Length of stay (3 vs 2 days, P <0.001) and hospital expenditure ($172,711 vs $162,284; P = 0.002) were higher for the TAVR-only cohort. CEPD in TAVR patients with prior stroke or TIA did not show statistically significant postoperative stroke benefits. However, further larger-scale prospective studies are needed to evaluate the long-term neurocognitive benefits of CEPD in these patients. As the use of TAVR continues to expand, optimizing peri-procedural strategies such as the use of CEPD remains a critical area of research to improve patient outcomes.

Pulmonary hypertension (PH) may be the result of many different pathological processes. PH is a rare but recognized vascular complication following major lung resection. We describe the diagnosis and management of moderate PH resulting more than 50 years in a patient who underwent a total unilateral pneumonectomy in infancy. Unfortunately, patients who undergo pneumonectomy will likely go on to develop PH and their functional status will be greatly impacted. In the case presented, we report on a patient whose PH and symptoms improved following off-label WHO group 1 treatment.

Statins, originally developed as lipid-lowering agents, have effects that extend well beyond cholesterol. By altering inflammatory signaling, vascular tone, fibrogenesis, and immune regulation, they engage pathways that shape a wide range of gastrointestinal diseases. Human data now suggest that these biological actions carry clinical weight. In metabolic dysfunction-associated steatotic liver disease and its progressive form, metabolic dysfunction-associated steatohepatitis, alcohol-associated liver disease, and chronic viral hepatitis (HBV and HCV), statin exposure is safe and associated with slower disease progression, fewer episodes of decompensation, and lower incidence of hepatocellular carcinoma. Randomized studies in cirrhosis show reductions in portal pressure, with cohort data linking use to fewer variceal bleeds, ascites, and hepatic encephalopathy. In inflammatory bowel disease, large registries and pilot trials indicate reduced flares, lower corticosteroid requirements, and decreased need for surgery, with early biomarker evidence supporting an anti-inflammatory effect. Smaller studies hint at benefits in other gastrointestinal contexts, though the evidence remains fragmented. Across these populations, true hepatotoxicity is rare; risk of myopathy is modest and largely confined to advanced cirrhosis or drug-drug interactions. Collectively, these findings support cautious repurposing of statins in gastroenterology and underline the need for definitive randomized trials to resolve class effects, optimize dose and duration, and identify reliable biomarkers of response.

Remote ischemic conditioning (RIC) is a simple, noninvasive intervention hypothesized to reduce ischemia-reperfusion injury in acute ischemic stroke (AIS). Its role as an adjunct to intravenous thrombolysis (IVT) remains unclear. We conducted a systematic review and meta-analysis of randomized controlled trials assessing RIC in AIS patients treated exclusively with IVT. Major databases were searched through February 2025 (PROSPERO: CRD420251144277). The risk of bias was evaluated using the Cochrane tool, and evidence certainty was assessed with Grading of Recommendations Assessment, Development, and Evaluation. Trial sequential analysis was also performed. Six randomized controlled trials (n = 955; RIC = 502, control = 453) met eligibility. Safety outcomes were comparable between groups, with no significant differences in stroke recurrence [risk ratio (RR) = 0.97; 95% confidence interval (CI), 0.63-1.48], hemorrhagic transformation (RR = 1.24; 95% CI, 0.67-2.31), or 90-day mortality (RR = 1.19; 95% CI, 0.46-3.07). RIC did not significantly improve excellent functional outcome (modified Rankin Scale 0-1 at 90 days: RR = 1.07; 95% CI, 0.95-1.20) or functional independence (modified Rankin Scale 0-2: RR = 1.03; 95% CI, 0.89-1.03). Barthel Index scores showed a nonsignificant trend toward benefit (mean difference = 2.77; 95% CI, -1.51-7.06), and National Institutes of Health Stroke scores at 24 hours, 7 days, 30 days, and follow-up were unchanged. Trial sequential analysis showed the required information size was not reached, and the Grading of Recommendations Assessment, Development, and Evaluation certainty was low to very low. RIC is safe but has not yet been shown to significantly improve functional or neurological outcomes in AIS patients treated with IVT. Future trials should assess RIC in patients receiving different types of thrombolysis (alteplase vs tenecteplase).

Right ventricular (RV) hypertrophy is the principal adaptive response to increased afterload. This response can be appropriate, preserving RV systolic function and RV-pulmonary artery coupling, or maladaptive, leading to RV dilatation and failure. While pure pressure overload typically induces adaptive hypertrophy, concomitant myocardial injury and ischemia often drive maladaptive changes. Multimodality imaging plays a crucial role in distinguishing these states by characterizing the relationship between RV mass, volume, and function. Cardiac magnetic resonance imaging, in particular, provides the reference standard for quantifying these parameters and offers unique insights through myocardial tissue characterization. This narrative review outlines the pathophysiology of RV hypertrophy and the application of cardiovascular imaging for its clinical assessment. We conclude by highlighting the critical clinical utility of evaluating RV hypertrophy for screening for pulmonary hypertension, risk stratification, and as a potential therapeutic target.

Pediatric heart failure is a heterogeneous, high-risk clinical syndrome that differs fundamentally from adult heart failure in its etiologies, pathophysiology, and therapeutic responses. Although its absolute prevalence is lower, children experience disproportionate morbidity and mortality, with up to 40% of patients with symptomatic cardiomyopathy progressing to death or transplantation within 2 years of diagnosis. Congenital heart disease, cardiomyopathies, and genetic or metabolic disorders dominate the etiologic spectrum, while developmental differences in myocardial signaling, neurohormonal activation, and ventricular remodeling limit direct extrapolation of adult guideline-directed medical therapy. Evidence supporting pharmacologic treatment remains limited, and most therapies are symptom-modifying rather than outcome-modifying, particularly in single-ventricle physiology. Advances in mechanical circulatory support and heart transplantation have substantially improved survival, yet pose unique anatomic, physiological, and ethical challenges in children. This review synthesizes contemporary evidence across medical, device-based, and transplant therapies, highlights lesion- and age-specific considerations, and identifies critical research gaps needed to advance outcomes in pediatric heart failure.

Coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD) exhibit a significant bidirectional relationship, whereby the presence of 1 condition significantly increases the risk of developing the other, resulting in their frequent co-occurrence. We seek to assess demographic and geographic disparities and examine mortality trends from CAD and COPD in the United States from 1999 to 2023. We retrieved mortality data for patients with CAD and COPD from the Centres for Disease Control and Prevention, Wide-Ranging Online Data for Epidemiologic Research Multiple Cause of Death database from 1999 to 2023. Age-adjusted mortality rates (AAMRs) per 100,000 population were calculated, and trends were analyzed using the Joinpoint regression model to estimate the annual percent change (APC) in AAMR. Mortality data were stratified by age, sex, race/ethnicity, urbanization, and Census regions. A total of 1,471,054 mortalities showed the existence of CAD and COPD on death certification. The AAMR decreased from 61.1 to 41.8 from 1999 to 2023. The AAMR declined sharply until 2018 (APC -1.9), followed by a significant incline till 2021 (APC 4), after which it continued to decrease significantly until 2023 (APC -6.12). AAMR was twofold greater in males (71.7) than in females (34.3). Among races/ethnicities, non-Hispanic Whites (52.7) had the top AAMR. Mortality rates were 13 times greater among older adults than among middle-aged adults. From geographics, nonmetropolitan areas (63.3) and the Midwest region (55.2) had the highest AAMRs. These disparities across demographic and geographical variables necessitate appropriate resource allocation and targeted interventions to reduce the CAD-COPD mortality burden.

Guidelines and much of the literature favor bioprosthetic heart valves in women with pregnancy desire, yet most evidence is restricted to pregnancy and the first decade after surgery, a period when bioprostheses are usually functionally intact, and late structural valve degeneration and reintervention are underrepresented. This review synthesizes data across the life course and examines how time-window bias may magnify early advantages of bioprostheses while obscuring long-term tradeoffs. Evidence suggests that bioprostheses often yield better fetal outcomes and fewer anticoagulation-related complications around pregnancy, whereas beyond 10-15 years, cumulative risks of degeneration, valve-in-valve limitations, and prosthesis-patient mismatch may erode these early benefits. In carefully selected patients, particularly in higher-risk positions such as the mitral valve, mechanical valves can provide superior long-term durability when high-quality anticoagulation and multidisciplinary pregnancy planning are feasible. Individualized decision-making should integrate valve position, anticoagulation capacity, pregnancy timing, patient preferences, and health system resources. Future studies should extend follow-up beyond 15 years, apply standardized definitions of structural degeneration, use competing-risk and modern causal methods, and incorporate decision-analytic modeling to quantify lifetime tradeoffs and support shared decisions.

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.