Dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) increases the risk of upper gastrointestinal bleeding (UGIB). Proton pump inhibitors (PPIs) are widely used for gastroprotection but have limitations including delayed onset of action and potential interactions with clopidogrel. Potassium-competitive acid blockers (P-CABs) might provide an alternative with more rapid and consistent acid suppression. This systematic review and meta-analysis of observational studies compared P-CABs versus PPIs for the prevention of UGIB in patients receiving DAPT after PCI. Major literature databases were searched for articles published until March 2026. Risk of bias was assessed with ROBINS-I, and pooled odds ratios (ORs) were estimated with random-effects models. Six cohort studies in 42,304 patients were analyzed. No significant difference in UGIB was observed between P-CABs and PPIs (OR 1.03, 95% CI 0.77–1.37; I 2 = 4%). Sensitivity analysis excluding studies with high risk of bias yielded consistent results (OR 0.96, 95% CI 0.70–1.30). No significant differences were observed in major adverse cardiovascular events or all-cause mortality. The certainty of evidence was very low because of confounding and imprecision. P-CABs appeared comparable to PPIs in preventing UGIB in this population; however, randomized trials are needed.
Low consumption of fruits and vegetables (FV) is a major preventable contributor to cardiovascular disease (CVD). Insufficient FV intake has been estimated to account for nearly 3 million CVD deaths and more than 70 million disability-adjusted life years worldwide. This review examines global patterns of FV intake; evidence linking FV consumption to cardiovascular outcomes; underlying biological mechanisms determined through in vitro and in vivo studies; serving size frameworks; current global recommendations; barriers to FV intake; and practical advice to increase FV intake. Although global FV intake has modestly increased in recent decades, consumption remains substantially below recommended levels in all regions, and marked disparities exist among countries. Evidence from meta-analyses of randomized controlled trials and intervention studies of individual fruits and vegetables has shown that FV intake improves cardiometabolic risk factors, and large prospective cohort studies have consistently demonstrated inverse associations between FV intake and CVD incidence and mortality. Experimental mechanistic studies have further supported these findings by identifying shared cardioprotective mechanisms mediated by FV-derived bioactive compounds. However, several practical and theoretical constraints limit the recommendation of adequate FV intake. This review proposes a practical serving-size framework based on macronutrient content, wherein one serving of fruit provides approximately 15 g carbohydrates (~60 kcal), and one serving of vegetables provides approximately 5 g carbohydrates (~25 kcal). By addressing key barriers and presenting practical dietary strategies, this review highlights the importance of promoting FV consumption at both the individual and population levels to decrease CVD risk and improve cardiovascular health outcomes.
The global burden, secular trends, and future projections of ischemic cardio-cerebrovascular disease (ICCVD), a composite indicator of ischemic heart disease (IHD) and ischemic stroke (IS), have not been specifically described in women. This study was aimed at estimating the global ICCVD burden from 1990 to 2021, and the projected burden from 2022 to 2050, in women. Age-standardized incidence, prevalence, mortality, and disability-adjusted life years (DALYs) with 95% uncertainty intervals (UI), and corresponding average annual percentage change (AAPC) with 95% confidence intervals (CI) and associated P-values, were calculated for women at global, regional, and national levels according to data from Global Burden of Disease 2021. Age-specific patterns, DALYs attributable to risk factors, and DALY projections to 2050 were also examined. In women, the global age-standardized prevalence of ICCVD increased from 3063 (95% UI: 2786 to 3339) per 100,000 population in 1990 to 3127 (2778 to 3476) per 100,000 population in 2021, and the AAPC was 0.03% (95% CI: 0.02% to 0.05%), whereas the incidence, mortality, and DALYs decreased (all P < 0.001). Notably, the age-standardized ICCVD incidence among women resurged in the past decade (0.29%), following a decline from 1990 to 2011 (−0.66%), whereas men experienced a consistent decline between 1990 and 2021. Low-middle Sociodemographic Index (SDI) countries consistently exhibited the highest age-standardized ICCVD incidence among women from 1990 to 2021, whereas only middle SDI countries demonstrated an increasing trend in age-standardized incidence over this period. Age-specific incidence rates increased among people younger than 60 years (0.14%) but decreased among people older than 60 years (−0.55%). High systolic blood pressure remained the leading risk factor for ICCVD in women, whereas high temperatures exhibited the most rapid relative increase in associated DALYs. DALYs for ICCVD in women are projected to continue declining through 2050, but the fatal burden will remain substantial, accounting for 87.4% of the total burden in 2050. ICCVD has posed a severe burden on women, largely driven by a notable resurgence in its incidence and prevalence over the past decade, alongside a pronounced increase in early-onset cases. Despite the projected decreasing trend in DALYs by 2050, the fatal burden is expected to remain the leading health threat. Our findings highlight the urgent need for public health strategies focusing on risk factor management and effective treatment to mitigate the ICCVD burden among women.
Background: Cardiovascular disease (CVD) is a leading cause of mortality among cancer survivors, yet the contributions of socioeconomic, lifestyle, and clinical factors to CVD remain unexplored. Objective: This study was aimed at examining associations between these factors and prevalent CVD in adults with prior cancer and comparing them with those in a matched non-cancer cohort. Methods: We analyzed 97,648 adults from the National Health and Nutrition Examination Survey. Associations of socioeconomic, lifestyle, and clinical factors with a composite endpoint of five self-reported cardiovascular events were assessed with multivariable logistic regression. Interaction analyses assessed differences by cancer status, and sensitivity analyses examined individual cardiovascular outcomes. Results: We included 5584 cancer survivors and 9933 matched participants without cancer. Age, sex, unemployment, low income, current smoking, obesity, diabetes, hypertension, and hypercholesterolemia were associated with elevated odds of CVD prevalence in both groups. Among only cancer survivors, an absence of private insurance, or the presence of food insecurity or low educational attainment, was also independently associated with CVD prevalence. Sensitivity analyses indicated broadly consistent results across individual outcomes. Conclusions: Socioeconomic, lifestyle, and clinical factors were associated with prevalent CVD among cancer survivors, with socioeconomic disadvantage contributing to disparities in CVD burden. Because the outcomes were self-reported, and the study was cross-sectional, the findings should be interpreted as associative rather than causal or predictive.
Cardiovascular disease develops through gradual accumulation of risk factors and progressive vascular damage. Longitudinal studies are well suited to determine when and how these changes occur, but they introduce several analytic challenges, including repeated measurements on the same individuals, irregular or sparse follow-up schedules, missing data, and non-linear trajectories. We conducted a narrative, application-focused review categorizing methods into five major classes: traditional or marginal models, mixed-effect models, joint models, trajectory and mixture models, and functional or machine-learning approaches. For each class, we provide intuitive descriptions, typical cardiovascular applications, and a balanced discussion of assumptions, strengths, limitations, and recommended sensitivity analyses. We emphasize practical guidance for method selection, model validation, and transparent reporting. In summary, no single method addresses every research goal. The analytic strategy should fit both the clinical question and data characteristics, with clear definition of objectives, careful assessment of assumptions, appropriate handling of missing data, and validation on independent samples whenever possible. Future methodological development should focus on making hybrid models more accessible, improving integration of sparse and dense data sources, and advancing reporting standards for longitudinal cardiovascular research.
The long-term effects of sustained weight gain and loss on atrial fibrillation (AF) risk remain unclear. Herein, we examined associations between long-term weight change and incident AF. We analyzed 64,119 AF-free participants from the Kailuan cohort whose height and weight were measured in 2006–2007 and 2010–2011. Weight change was assessed as changes in body mass index (BMI), body weight, and percentage weight changes. Incident AF was ascertained according to International Classification of Diseases codes and biennial electrocardiograms. Multivariable Cox models estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Over a median 10.0 years’ follow-up, 583 participants developed AF. Compared with stable BMI (−3 to 3 kg/m 2 ), BMI loss ≥3 kg/m 2 was associated with diminished AF risk (HR 0.61, 95% CI 0.41–0.91), whereas BMI gain ≥3 kg/m 2 was associated with elevated risk (HR 1.41, 95% CI 1.01–1.97). Similarly, weight loss ≥10 kg was associated with diminished AF risk (HR 0.54, 95% CI 0.31–0.92), whereas weight gain ≥10 kg was associated with elevated AF risk (HR 1.66, 95% CI 1.12–2.36). The findings were consistent across percentage-change definitions. Long-term weight gain was associated with elevated incident AF risk, whereas sustained weight loss was associated with diminished risk, thus supporting the importance of long-term weight management for AF prevention.
Acute coronary syndrome (ACS), a primary manifestation of coronary artery disease (CAD), remains a leading cause of global mortality, particularly in low- and middle-income countries. Despite advances in diagnostics and therapy, accurate early risk stratification of ACS remains challenging. Traditional biomarkers such as cardiac troponins and CK-MB are essential for diagnosis but do not capture the full complexity of disease severity, particularly in cases involving inflammation, endothelial dysfunction and plaque instability. This review highlights emerging evidence regarding the roles of inflammatory cytokines and novel biomarkers in ACS pathophysiology, diagnosis and prognostication. Pro-inflammatory cytokines such as IL-6, IL-18 and TNF-α play key roles in atherogenesis and plaque destabilization, whereas anti-inflammatory mediators such as IL-10 and TGF-β decrease vascular injury. Novel biomarkers including Copeptin, GDF-15, microRNAs, sST2, Galectin-3, Endocan and MMP-9 offer enhanced prognostic capabilities and, in contrast to traditional biomarkers, often provide additional prognostic information in specific scenarios. Integrating these biomarkers with advanced risk models such as the GRACE score and digital health technologies, including AI, is transforming ACS management. However, challenges persist in standardization, cost-effectiveness, real-time implementation and interpretation in comorbid populations. This review emphasizes the potential of these biomarkers in improving personalized care and treatment for patients with ACS, while addressing evidence levels, clinical bottlenecks and integration strategies.
In normal cardiac energy metabolism, 95% of the heart’s energy is provided by mitochondria, and preferences for energy-providing substrates vary at different times (Nguyen BY, Ruiz-Velasco A, Bui T, Collins L, Wang X, Liu W. Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials. Br J Pharmacol 2019;176(22):4302–4318). However, prolonged metabolic alterations impair cardiac function (Hu L, Tang D, Qi B, Guo D, Wang Y, Geng J, et al. Mfn2/Hsc70 complex mediates the formation of mitochondria-lipid droplets membrane contact and regulates myocardial lipid metabolism. Adv Sci (Weinh) 2024;11(14):e2307749). Therefore, this study primarily focuses on the relationship between amino acid metabolism and diabetic cardiomyopathy and atherosclerosis. Changes in metabolic processes also promote the development and worsening of these two diseases. Lipid and glucose metabolism in such diseases have been extensively studied, and emerging evidence suggests that amino acid metabolism also plays major roles in diabetic cardiomyopathy and atherosclerosis. Specific amino acid intake or catabolism might influence oxidative stress, inflammation, and fibrosis, among related processes, thus indirectly highlighting their potential as novel targets for metabolic interventions. However, the mechanisms and clinical relevance of amino acid metabolism in these diseases remain incompletely understood and warrant further investigation.
Hypertensive disorders of pregnancy (HDP), the third leading cause of maternal mortality worldwide, account for approximately 16% of all maternal deaths. The incidence and mortality rates of HDP vary across regions. This study was aimed at examining global trends in HDP prevalence from 1990 to 2021, identifying major risk factors associated with HDP-related mortality, and assessing the influence of dietary habits on HDP risk. Using data from the 2021 global burden of disease (GBD) study, we conducted a cross-sectional analysis across 204 countries and 21 regions. The estimated annual percentage change was used to evaluate trends in incidence, disability-adjusted life years (DALYs), and mortality associated with HDP. Mendelian randomization analysis was applied to investigate the causal relationships between dietary habits and HDP risk. In addition, projections of HDP prevalence were made through 2035 according to GBD data. Although the absolute number of HDP cases has risen, HDP incidence, DALYs, and mortality rates have declined globally. Regional, age-related, and socioeconomic disparities persist, and low-income countries are disproportionately affected because of limited healthcare resources. Behavioral risks, maternal and child malnutrition, and iron deficiency were identified as risk factors for HDP-related mortality. Despite the overall decline in HDP incidence, DALYs, and mortality rates over the past 3 decades, the persistent high burden in low socio-demographic index regions highlights the urgent need for targeted health interventions. Addressing broader socioeconomic determinants is essential to sustainably decrease the global effects of HDP.
Osteoprotegerin (OPG), a glycoprotein in the tumor necrosis factor superfamily, regulates bone metabolism by suppressing the formation and activation of osteoclasts. Nonetheless, increasing evidence underscores its physiological importance, particularly in cardiovascular diseases (CVDs). Elevated OPG levels are associated with atherosclerosis, arterial calcification, and heart failure, thus indicating their involvement in cardiac remodeling and vascular pathology. OPG regulates calcification and vascular homeostasis by restricting the transdifferentiation of vascular smooth muscle cells into osteogenic phenotypes. OPG expression is aberrant in illnesses posing cardiovascular risk, such as aortic valve stenosis, chronic renal disease, and diabetes. Beyond structural regulation, OPG interacts with inflammatory and apoptotic mediators, including RANKL and TRAIL, in signaling pathways linking bone metabolism, inflammation, and vascular dysfunction. Myocardial infarction, left ventricular remodeling, and mortality are associated with elevated circulating OPG and altered OPG/TRAIL ratios. This review discusses molecular and clinical insights regarding OPG’s multifaceted role in CVDs, highlighting its potential as a regulator of disease etiology and a predictive biomarker. In cardiovascular medicine, understanding the OPG/RANKL/TRAIL axis has potential to facilitate targeted therapy and risk stratification.
