Cardiology in Review最新文献

Hypertensive disease remains one of the leading contributors to cardiovascular morbidity and mortality worldwide, with hyperlipidemia as a major metabolic comorbidity. There is a relative absence of long-term mortality trends that directly assess the co-occurrence of hypertension and hyperlipidemia. We analyzed mortality data from the CDC WONDER platform (1999-2023), including adults aged ≥65 years with hypertensive disorders I10-I15 and hyperlipidemia E78 (E78.0-78.5, E78.8, E78.9) as multiple causes of death. Age-adjusted mortality rates (AAMRs) and average annual percentage changes were calculated using Joinpoint regression, stratified by sex, race/ethnicity, urbanization, region, and age. A total of 960,024 deaths in the United States from 1999 to 2023 were identified. The AAMR per 100,000 ranged from 6.56 [95% confidence interval (CI), 6.29-6.83] in 1999 to 163 (95% CI, 162-164) in 2023. The highest AAMR was reported in 2021, at 164 (95% CI, 163-166). AAMRs were highest among non-Hispanic Black or African American patients. Overall, the mortality rates for both women and men increased steadily over the study period, with men consistently showing higher mortality rates than women. Mortality rates for both women and men increased steadily over the study period, with men showing higher mortality rates than women. Mortality rates from hypertension and hyperlipidemia together have escalated in the United States over the past 25 years. However, the death trends were unequal across demographics, which underscores the necessity for equitable access to medical services and integrated risk reduction to improve cardiometabolic outcomes.

Accurate assessment of volume status and venous congestion is essential in the management of congestive heart failure (CHF), particularly in patients with cardiorenal syndrome (CRS). Traditional approaches, including physical examination, laboratory biomarkers, and noninvasive hemodynamic monitoring, have notable limitations in reliably detecting venous congestion. The Venous Excess Ultrasound (VExUS) score, introduced in 2020, offers a noninvasive and widely available method to evaluate systemic congestion by integrating Doppler assessment of the inferior vena cava, hepatic, portal, and intrarenal veins. This narrative review summarizes the current evidence supporting the utility of VExUS in CHF and CRS, highlighting its diagnostic performance, advantages, and challenges. Studies demonstrate that VExUS correlates strongly with right atrium pressure and outperforms individual ultrasound or biochemical markers in predicting elevated filling pressures and acute kidney injury. Its application may help detect subclinical renal congestion and guide diuretic therapy before irreversible renal injury occurs. Despite these strengths, the technique has limitations, including technical complexity, operator dependence, and potential inaccuracy in the presence of liver disease or significant tricuspid regurgitation. Overall, VExUS represents a promising and widely accessible tool that enhances risk stratification and treatment optimization in CHF and CRS. Further prospective studies are needed to standardize image acquisition, validate its prognostic value across diverse populations, and define its role within heart failure management algorithms and diuretic-guided therapy protocols.

Globally, cardiovascular disease is the most prevalent cause of death, and there are other risk factors involved that are not captured through traditional means. We present a review of the literature on microplastic exposure and discuss the clinical implications of microplastics for cardiovascular disease. Experimental studies show that micro- and nanoplastics induce oxidative stress, mitochondrial dysfunction, endothelial dysfunction, inflammation, thrombosis, dyslipidemia, and direct cardiotoxicity. These microplastics and nanoplastics have been identified in coronary plaque. Emerging clinical data have recently reported evidence in patients having microplastics in carotid plaques that are at a 4.5-fold increased risk of myocardial infarction, stroke, or death, in a cohort from the New England Journal of Medicine in 2024. Microplastics remain a potential modifiable risk for cardiovascular disease.

Coenzyme Q10 (CoQ10), or ubiquinone, is a lipid-soluble antioxidant essential for mitochondrial adenosine triphosphate production and cellular energy metabolism. Its therapeutic potential has been investigated in conditions marked by mitochondrial dysfunction, particularly chronic heart failure and statin-associated muscle symptoms. Robust evidence, including data from the Q-SYMBIO trial, demonstrates that CoQ10 supplementation can improve functional capacity, ejection fraction, and reduce major cardiovascular events in heart failure with reduced ejection fraction. However, studies on its efficacy for statin myopathy have yielded inconsistent results, with some reporting symptom relief and others showing no significant benefit. CoQ10 is generally safe, well-tolerated, and affordable, and emerging research supports its classification as a conditionally essential nutrient in heart failure. While routine supplementation for all statin users is not currently recommended, targeted use in advanced heart failure with reduced ejection fraction or in patients with high mitochondrial demand may be justified. As further evidence and cost-effectiveness data become available, formal guideline recommendations for CoQ10 may follow.

Air pollution is a significant environmental determinant of cardiovascular diseases, yet evidence from India remains limited. This systematic review aimed to synthesize studies assessing the associations between ambient and household air pollution and cardiovascular morbidity, including hypertension, ischemic heart disease, stroke, and vascular alterations. A comprehensive search of PubMed/MEDLINE was conducted up to August 2025 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines (International Prospective Register of Systematic Reviews: CRD420251131056). Observational and cohort studies were included, and the risk of bias was evaluated using the Joanna Briggs Institute tools. Eighteen studies met the inclusion criteria. Exposure to fine particulate matter (PM2.5) was found to increase systolic blood pressure by 1.4-3.3 mmHg and the odds of hypertension by 4-5% for every 1-10 µg/m3 increment. Household biomass fuel exposure was associated with elevated blood pressure, tachycardia, and early atherosclerotic changes, particularly among women. Long-term exposure to pollutants such as sulfur dioxide, nitrogen dioxide, and PM2.5 showed potential links with ischemic heart disease and stroke. Overall, the findings suggest that both ambient and household air pollution significantly contribute to cardiovascular morbidity in the Indian population. The limited availability of longitudinal and mechanistic data highlights the urgent need for high-quality, region-specific studies to better understand exposure-response relationships and guide public health interventions.

Heart failure (HF) remains a prevalent global health challenge and burden, prompting researchers to seek further therapies that provide morbidity and mortality benefits in this patient population. In recent years, the development of proven pharmacotherapeutics has stalled partly due to the continued poor understanding of the various underlying mechanisms of HF. However, a potential therapeutic target has emerged after recent evidence identified the role of inflammation in the pathogenesis of HF. Systemic and myocardial inflammation caused by activation of specific inflammasomes and the subsequent production of downstream cytokines, including interleukins and tumor necrosis factor, contribute to cardiomyocyte dysfunction, fibroblast activation, and extracellular matrix deposition and fibrosis. A key driver, the inflammasome is activated in cases of myocardial infarction, pressure overload, and sympathetic overactivation, subsequently leading to cardiac hypertrophy, fibrosis, and pyroptosis. Additionally, chronic inflammation driven by factors such as oxidative stress, metabolic disturbances, and neurohormonal activation leads to adverse cardiac remodeling and impaired myocardial function, with the inflammatory processes likely representing a common final pathway in the pathophysiology of HF. To target these pathways, numerous anti-inflammatory therapies, originally approved for other conditions, have been investigated for a potential benefit in HF. While previous small studies of these anti-inflammatory therapies in HF showed limited potential benefit, many of these trials were ultimately inconclusive. Therefore, multiple larger trials have subsequently investigated these anti-inflammatory therapies, including a novel agent targeting a critical inflammasome, to better elucidate the role, if any, of these medications in the treatment of HF.

Ischemic heart disease and sepsis remain a significant public health challenge with a large number of mortalities. Our study examined mortality trends due to ischemic heart disease and sepsis in the United States from 1999 to 2023. We conducted a retrospective analysis using the Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research from 1999 to 2023 per 100,000 population. Join-point regression determined annual percentage change (APC) and average annual percentage change with 95% confidence intervals. From 1999 to 2023 the overall age-adjusted mortality rate (AAMR) decreased with a notable change from 2005 to 2009 (APC: -3.98%). However, rates significantly increased from 2018 to 2021 (APC: 5.78%) before experiencing a steep decline from 2021 to 2023 (APC: -7.72%). Men consistently had a higher overall AAMR (12.04) than women (7.11). Among races, the non-Hispanic Black or African American population had the highest overall AAMR (12.53). Geographic trends indicated the highest mortalities in the Northeast region (7.98) and metropolitan areas (9.53). Age group trends revealed older adults having the highest AAMR, which declined from 1999 to 2023 (40.32). Although there was an overall decline from 1999 to 2023, a significant increase was observed from 2018 to 2021, followed by a rapid decline. Disparities persist with men, Black, older adults, and individuals in the Northeast and metropolitan areas experiencing higher death rates. These findings highlight the need for targeted intervention to reduce the burden of conditions, particularly in high-risk groups.

Atrial fibrillation (AF) and heart failure (HF) often coexist, worsening outcomes through a bidirectional interaction. Catheter ablation has become a cornerstone therapy, improving function, symptoms, and survival. However, recurrence of AF postablation remains a challenge, particularly in HF patients. This review synthesizes findings from 14 clinical studies (2015-2025) examining predictors of recurrence after ablation in HF with preserved ejection fraction and HF with reduced ejection fraction. Key predictors include persistent or long-standing AF, enlarged left atrial diameter, elevated inflammatory biomarkers (high-sensitivity C-reactive protein, N-terminal proBNP), red blood cell distribution width, and early arrhythmia recurrence. Comorbidities such as diabetes, thyroid dysfunction, and malnutrition (controlling nutritional status score) also contributed to recurrence risk. Procedural factors such as pulmonary vein reconnection and timing of ablation influenced outcomes. Protective factors included SGLT2 inhibitors and high-dose statins. These findings emphasize the multifactorial nature of AF recurrence in HF patients and highlight the need for individualized risk stratification. Integration of clinical, imaging, biomarker, and procedural factors may optimize patient selection and improve long-term rhythm control.

Sedation is essential for modern intensive care management, yet its effects on autonomic regulation, circadian biology, and cardiac electrophysiology remain incompletely understood. This review synthesizes current evidence on how commonly used sedative agents influence autonomic tone, sleep architecture, and electrophysiologic stability in critically ill patients. Mechanistic data indicate that propofol, dexmedetomidine, benzodiazepines, and ketamine exert distinct autonomic signatures that alter heart rate variability, baroreflex sensitivity, and ventricular repolarization. Clinical studies show that deeper or prolonged sedation is associated with increased incidences of atrial fibrillation, bradyarrhythmias, ventricular ectopy, and QT interval abnormalities, particularly in the context of sepsis, hypoxia, or metabolic derangements. Sleep disruption and circadian misalignment further diminish nocturnal vagal dominance, heighten sympathetic activation, and contribute to arrhythmogenic vulnerability. Advances in physiologic monitoring, including heart rate variability metrics, QT variability, T-wave alternans, and electroencephalogram-electrocardiogram coupling, offer emerging tools to detect early neuro-cardiac instability and guide individualized sedation strategies. Collectively, current evidence supports viewing sedation as a modifiable determinant of neuro-cardiac homeostasis. Optimizing sedation depth, preserving circadian cues, and integrating multimodal physiologic monitoring may reduce arrhythmia risk and improve outcomes in the intensive care unit, although further research is required to address substantial gaps in physiologic characterization and high-risk populations.