In heart failure with mildly reduced (HFmrEF) or preserved ejection fraction (HFpEF), a smaller left ventricular end-diastolic diameter (LVEDD) has been associated with lower stroke volume and functional capacity. Howeve...In heart failure with mildly reduced (HFmrEF) or preserved ejection fraction (HFpEF), a smaller left ventricular end-diastolic diameter (LVEDD) has been associated with lower stroke volume and functional capacity. However, its association with clinical outcomes remains unexplored. We evaluated the prognostic impact of small LV in patients hospitalized with acute HFpEF. We performed a single-center retrospective analysis of a prospectively collected cohort of patients admitted for acute heart failure (AHF) with LVEF >40%. Small LV was defined according to ASE guidelines. The primary outcome was in-hospital mortality; secondary outcomes included worsening renal function and need for inodilators. Among 369 patients, 82 (22.2%) had a small LV. These patients had fewer traditional comorbidities but more amyloid cardiomyopathy and lower systolic blood pressure. In-hospital mortality was significantly higher in the small LV group (12.2% vs 3.5%, p = 0.002). In multivariable analysis, small LV was independently associated with mortality (adjusted OR 7.15). These findings suggest that in HFpEF or HFmrEF, small LV represents a high-risk phenotype.
Fabry disease (FD) is an X-linked lysosomal storage disease that results in the accumulation of glycosphingolipids, such as globotriaosylceramide (Gb3) in a variety of cells. FD most prominently involves cardiac, nervous...Fabry disease (FD) is an X-linked lysosomal storage disease that results in the accumulation of glycosphingolipids, such as globotriaosylceramide (Gb3) in a variety of cells. FD most prominently involves cardiac, nervous, and renal tissue, with cardiac complications representing the most common cause of death. Fabry disease has a prevalence ranging between 1:8454 to 1:117,000 among men. The higher prevalence included patients with the A143T mutation, which was shown to be a non-disease causing variant. Due to its rarity, and wide array of phenotypic presentations, especially in women, FD is often misdiagnosed. Advances in echocardiographic techniques and magnetic resonance imaging can play a crucial role in raising suspicion for Fabry disease and identifying early Fabry cardiomyopathy. Identification of end-organ involvement can, in turn, permit treatment initiation in patients who did not previously qualify for advanced therapies and in screened family members who are still too early in the disease process to manifest specific symptoms.
BACKGROUND: Arterial stiffness, reflected by pulse wave velocity (PWV), is an important cardiovascular risk marker. Physical activity (PA) may reduce arterial stiffness, but the most beneficial intensity remains unclear....BACKGROUND: Arterial stiffness, reflected by pulse wave velocity (PWV), is an important cardiovascular risk marker. Physical activity (PA) may reduce arterial stiffness, but the most beneficial intensity remains unclear. The objective this study was to analyze the relationship between different intensities of PA and arterial stiffness in adults and to verify whether these relationships are independent of sex, age, and socioeconomic status. METHODS: A total of 185 participants (104 women) were included in this study. Arterial stiffness was assessed using PWV, measured by a non-invasive oscillometric device (Arteriograph AOP). Three consecutive measurements were performed (with one-minute intervals), and the device provided the final PWV value. PA intensity (light, moderate, and vigorous) was objectively measured using an ActiGraph GT3X accelerometer. The associations between PWV and PA intensities were examined using Pearson's correlation and linear regression models, with the crude model and subsequently adding sex, age, and socioeconomic status, to estimate the magnitude of these associations. RESULTS: An inverse relationship was found between PWV and vigorous-intensity PA in the unadjusted model (β = -0.007; 95 % CI: -0.011, -0.002; p = 0.006). This association remained significant after adjustment for sex (β = -0.006; 95 % CI: -0.010, -0.001; p = 0.010), but lost significance after additional adjustment for age (β = -0.001; 95 % CI: -0.004, 0.001; p = 0.323). No associations were observed between PWV and light or moderate PA. CONCLUSION: PWV was inversely associated with vigorous-intensity PA; however, but age appears to exert a strong influence on this relationship.
The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to >600 million people in 2023. Atherosclerotic vascular disease results not only from hyperlipidemia but also from ac...The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to >600 million people in 2023. Atherosclerotic vascular disease results not only from hyperlipidemia but also from acute and chronic inflammatory changes in response to arterial endothelial injury. Inflammation together with cytokines, chemokines, and acute-phase reactants play a pivotal role in atherosclerotic vascular plaque formation, progression, rupture, and thrombogenesis that lead to an acute coronary syndrome (ACS), cerebral, or peripheral arterial disease. In addition, individuals who have previously sustained an ACS or cerebral or peripheral arterial occlusion frequently have evidence of residual arterial inflammation as indicated by increased blood concentrations of the inflammatory biomarker C-reactive protein (CRP). As a consequence, chronic arterial inflammatory disease contributes to >15% of all global deaths from myocardial infarction, cerebral vascular events (transient ischemic attacks or strokes), and peripheral arterial disease. This Review Article discusses the important mechanisms by which inflammation contributes to the initiation and progression of coronary artery atherosclerosis, the biologic measurements which indicate arterial inflammation in individuals, the diagnostic techniques useful in the detection of arterial inflammation and atherosclerosis, and the clinical studies that have been performed and are currently being performed to limit the contributions of acute and chronic inflammation to the morbidity and mortality from coronary artery disease.
INTRODUCTION: The natriuresis measurement is useful to diagnose diuretic resistance (DR) and adjust furosemide doses in acute heart failure (AHF) hospitalized patients, but the utility of urinary chloride is unknown. OBJ...INTRODUCTION: The natriuresis measurement is useful to diagnose diuretic resistance (DR) and adjust furosemide doses in acute heart failure (AHF) hospitalized patients, but the utility of urinary chloride is unknown. OBJECTIVES: To correlate the urine chloride at admission (UCLA) in AHF patients with the development of DR and cardiovascular (CV) events at the 180-day outpatient follow-up. METHODOLOGY: A prospective study included patients hospitalized for AHF, without shock, creatinine >2.5 mg/dL or mechanical respiratory support at admission. They received 40 mg of intravenous furosemide at admission, UCLA was measured, and diuretic treatment was based on a protocol. DR was defined as the requirement for furosemide ≥240 mg/day, sequential nephron diuretic blocked (SNB), hypertonic saline serum, or renal replacement therapy. RESULTS: 116 patients were included, 51% were men, UCLA was 105 meq/L, and DR was developed in 17% of patients. The UCLA was associated with the development of DR (p 0.0001; AUC ROC curve 0.81; cut-off point 96 meq/L). UCLA <96 meq/L was associated with persistent congestion (p 0.01), furosemide ≥240 mg/day use (p 0.004), worsening of AHF (p 0.002) and renal function (p 0.02), use of SNB (p 0.001) and inotropic drugs (p 0.007), a longer hospital stay (p 0.02) and a higher CV death (p 0.05). At 180-day follow-up, UCLA <96 meq/L was associated with AHF readmissions (p 0.002). CONCLUSION: In AHF hospitalized patients, low UCLA was associated with DR, persistent congestion, need for more aggressive decongestion strategies, worse in-hospital clinical outcomes and more AHF hospitalizations at 6 months.
OBJECTIVES: To quantify county-level mortality attributable to non-optimal temperature in the United States and examine whether social vulnerability modifies this relationship. STUDY DESIGN: Ecological time-series analys...OBJECTIVES: To quantify county-level mortality attributable to non-optimal temperature in the United States and examine whether social vulnerability modifies this relationship. STUDY DESIGN: Ecological time-series analysis from 2000-2020. METHODS: We analyzed 1,514 counties representing 91.2% of the 2010 U.S. adult population (ages 25-84), including 33,395,241 deaths (after imputation: 33,421,054) which were linked to monthly mean temperature. A two-stage modeling framework was used. First, quasi-Poisson models with natural cubic splines estimated county-specific non-linear temperature-mortality associations, with population offsets and spline-based control for seasonality. Second, coefficients and variances were pooled using random-effects multivariate meta-analysis to identify the minimum mortality temperature (MMT) and percentile (MMP). Effect modification was assessed by incorporating Social Vulnerability Index (SVI) quartiles into a multivariate meta-regression. Attributable deaths were estimated using 5,000 Monte Carlo draws and classified as heat-related (above MMT) or cold-related (below MMT); crude rates were expressed per 100,000 person-years. RESULTS: The pooled MMT was 22.7 °C (95% CI: 22.2-23.2), corresponding to the 78.4th percentile (95% CI: 76.1-80.8). Nationally, an estimated 72,361 (95% CI: 68,837-76,153) cold-attributable and 6,129 (95% CI: 5,309-7,227) heat-attributable deaths occurred annually, equivalent to 40.1 and 3.4 per 100,000 person-years. More socially vulnerable counties had higher MMTs [SVI Q4: 23.9 °C vs Q1: 21.0 °C] and higher heat- (2.0 vs 0.7) and cold-related mortality rates (40.9 vs 28.0). CONCLUSIONS: Cold accounted for most temperature-related deaths in the U.S., and social vulnerability intensified both cold- and heat-related mortality. These findings support geographically targeted, vulnerability-responsive public health strategies.
Theofilis P, Dimitriadis K, Pyrpyris N
… +9 more, Karakasis P, Dri E, Beneki E, Vordoni A, Tsioufis P, Chatzi M, Oikonomou E, Aznaouridis K, Tsioufis K
BACKGROUND: Infective endocarditis after transcatheter aortic valve implantation (TAVI-IE) is an uncommon but severe complication associated with substantial morbidity and mortality. Therapeutic strategies vary widely, s...BACKGROUND: Infective endocarditis after transcatheter aortic valve implantation (TAVI-IE) is an uncommon but severe complication associated with substantial morbidity and mortality. Therapeutic strategies vary widely, since invasive management is often precluded by prohibitive risk and conservative medical therapy may be linked to poorer outcomes. Therefore, we aimed to compare outcomes between conservative and invasive management in patients with TAVI-IE. METHODS: A systematic search of PubMed, Scopus, and Web of Science identified comparative studies evaluating conservative versus invasive treatment in TAVI-IE. The primary endpoints were all-cause in-hospital and 1-year mortality. Pooled risk ratios (RRs) with 95 % confidence intervals (CIs) were calculated using a random-effects model. Heterogeneity was quantified with I², publication bias was assessed with Egger's test, and sensitivity analyses (leave-one-out, GOSH plots) were performed. RESULTS: The search yielded 2,551 records; 15 studies met inclusion criteria for data extraction and meta-analysis. No significant differences were observed between conservative and invasive strategies for in-hospital mortality (RR 0.99, 95 % CI 0.80-1.24, p = 0.96; I² = 0 % with p = 0.67) or 1-year mortality (RR 1.03, 95 % CI 0.84-1.26; p = 0.81; I² = 11.4 % with p = 0.33). There was no evidence of publication bias (Egger's test: in-hospital, p = 0.07; 1-year, p = 0.54). Results were robust in sensitivity analyses. CONCLUSIONS: In patients with TAVI-IE, conservative and invasive treatments were associated with comparable in-hospital and 1-year mortality. These findings support individualized, multidisciplinary decision-making rather than presuming a uniform advantage of either approach.
Coronary artery disease (CAD) remains a leading cause of mortality and morbidity worldwide. Coronary artery calcification (CAC) is a well-established marker of atherosclerotic burden, and its quantification provides an o...Coronary artery disease (CAD) remains a leading cause of mortality and morbidity worldwide. Coronary artery calcification (CAC) is a well-established marker of atherosclerotic burden, and its quantification provides an objective measure of subclinical coronary atherosclerosis that can refine cardiovascular risk stratification and guide decisions regarding risk factor modification and lipid-lowering therapies. There is extensive data supporting the role of CAC scoring as an adjunct risk refinement tool, and it has been incorporated into multiple primary prevention guidelines. In addition to the Agatston method, CAC can also be quantified using non-gated computed tomography (CT) scans which are simple and widely available from non-cardiac screening strategies, including those obtained routinely for lung cancer screening. The integration of artificial intelligence and automated CAC assessment in non-gated studies is further expanding its application for risk stratification to a much larger population. This review summarizes the current tools, evidence and guidelines supporting the use of CAC to help risk stratify, optimize lipid lowering therapy, and potentially improve patient outcomes.
BACKGROUND: Immune checkpoint inhibitors (ICIs) have significantly advanced cancer treatment, especially in improving survival rates for patients with various malignancies such as melanoma, non-small cell lung cancer (NS...BACKGROUND: Immune checkpoint inhibitors (ICIs) have significantly advanced cancer treatment, especially in improving survival rates for patients with various malignancies such as melanoma, non-small cell lung cancer (NSCLC), and renal cell carcinoma. Despite their therapeutic promise, ICIs carry the risk of immune-related adverse events, with cardiotoxicity emerging as a notable concern. This umbrella review aims to critically evaluate the diverse data from published systematic reviews and meta-analyses, to provide a cohesive overview of ICI-associated cardiotoxicity across different cancer types and treatment regimens. METHODS: This umbrella review analytically evaluates data from systematic reviews and meta-analyses on cardiotoxicity in cancer patients receiving ICI therapy. We conducted a comprehensive search across PubMed, Scopus, and Google Scholar, from inception till Jan 2025. The JBI checklist was employed to assess the quality of included studies. RESULTS: Our analysis reveals varying cardiotoxicity risks associated with ICIs. The incidence of cardiac immune-related adverse events ranges from 0.8 % to 1.3 %, with myocarditis being the most common (0.5-0.72 % of patients). Combination therapies significantly increase risks: dual ICIs elevate myocarditis risk 3.07-fold compared to monotherapies, whereas PD-1/PD-L1 inhibitors with chemotherapy increase all-grade and severe cardiotoxicity by 53 % and 63%, respectively. NSCLC patients face a 97 % higher risk of all-grade cardiotoxicity with combination treatments. ICI-induced myocarditis carries a high mortality rate of 37.7 %. Notably, some studies report no significant increase in cardiac events, highlighting the need for further investigation to reconcile these disparate findings. CONCLUSIONS: The variability in cardiotoxicity reports highlights the complex risk landscape associated with ICI therapy. Although ICIs continue to enhance cancer care, they require careful cardiovascular monitoring and comprehensive risk management, particularly for combination therapies and patients with existing heart conditions.
N6-methyladenosine (m6A) RNA methylation has emerged as a pivotal epitranscriptomic regulator influencing cardiovascular development, homeostasis, and disease progression. As the most abundant internal modification in eu...N6-methyladenosine (m6A) RNA methylation has emerged as a pivotal epitranscriptomic regulator influencing cardiovascular development, homeostasis, and disease progression. As the most abundant internal modification in eukaryotic mRNA, m6A dynamically modulates RNA stability, translation, splicing, and degradation through the coordinated actions of "writers," "readers," and "erasers." Recent advances demonstrate that dysregulated m6A modifications contribute to major cardiovascular disorders, including cardiac hypertrophy, heart failure, arrhythmias, atherosclerosis, ischemia reperfusion injury, and cardiomyopathy. METTL3-mediated hypermethylation promotes pathological hypertrophy, autophagy imbalance, and ischemic injury. In contrast, demethylases such as FTO and ALKBH5 exert cardioprotective effects by preserving contractile function, enhancing angiogenesis, and regulating key transcripts involved in Ca²⁺ cycling, autophagy, and metabolism. m6A-dependent control of noncoding RNAs further amplifies its impact on inflammatory signaling, endothelial dysfunction, and vascular remodeling. The involvement of m6A in glucose metabolism, hypoxia responses, and vascular smooth muscle phenotypic transitions highlights its broad relevance across cardiovascular risk factors. As detection technologies advance, m6A profiling shows promise as a diagnostic biomarker and therapeutic target. Understanding epitranscriptomic regulation may unlock innovative treatment strategies and reshape the future of cardiovascular medicine.
Hypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiomyopathy, is characterized by left ventricular hypertrophy that typically manifests with asymmetric wall thickening and is not caused by a pressure ov...Hypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiomyopathy, is characterized by left ventricular hypertrophy that typically manifests with asymmetric wall thickening and is not caused by a pressure overload state or systemic disease. Despite its considerable prevalence-estimated to affect up to 1 in 200 individuals based on imaging data-it often goes undiagnosed or misdiagnosed, particularly in general clinical settings. Traditional tools, such as the electrocardiogram, although widely used, frequently yield nonspecific findings that complicate the early identification or screening of HCM. In recent years, artificial intelligence (AI) and machine learning have emerged as powerful tools with the potential to revolutionize HCM diagnosis and management. AI-driven algorithms trained on ECG and imaging data are being developed to improve early detection, risk stratification, and therapeutic monitoring in patients with or at risk for HCM. Additionally, AI has shown utility in biomarker-based prediction models, further enhancing diagnostic precision and clinical decision-making. Harnessing the power of AI may help close critical diagnostic gaps and optimize outcomes for individuals affected by HCM.
BACKGROUND: Patients with chronic coronary syndrome (CCS) often require long-term oral anticoagulation (OAC), most commonly for atrial fibrillation (AF). Evidence on the optimal antithrombotic strategy in this setting re...BACKGROUND: Patients with chronic coronary syndrome (CCS) often require long-term oral anticoagulation (OAC), most commonly for atrial fibrillation (AF). Evidence on the optimal antithrombotic strategy in this setting remains inconclusive, prompting this updated meta-analysis of randomized trials comparing OAC plus a single antiplatelet therapy (SAPT) with OAC monotherapy. METHODS: We systematically searched PubMed/MEDLINE, SciELO, Latindex, LILACS, the Cochrane Library, and ClinicalTrials.gov up to November 12, 2025. The primary efficacy endpoint was all-cause death, while secondary efficacy endpoints included cardiovascular death, acute myocardial infarction, ischemic stroke, and systemic embolism, each analyzed individually. Safety endpoints comprised major and clinically relevant non-major bleeding (International Society on Thrombosis and Hemostasis [ISTH] definition). RESULTS: Six randomized trials including 5,924 participants were analyzed. All-cause death did not differ significantly between OAC plus SAPT and OAC monotherapy (OR 1.31; 95 % CI 0.89-1.92). Dual therapy was associated with an increased risk of cardiovascular death (OR 1.42; 95 % CI 1.05-1.92), whereas rates of myocardial infarction (OR 0.98; 95 % CI 0.60-1.57), ischemic stroke (OR 0.95; 95 % CI 0.64-1.39), and systemic embolism (OR 1.00; 95 % CI 0.20-4.95) were similar between groups. Safety outcomes were markedly worse with dual therapy, which significantly increased the risk of major bleeding (OR 2.20; 95 % CI 1.51-3.22) and major or clinically relevant non-major bleeding (OR 2.30; 95 % CI 1.72-3.06). CONCLUSIONS: In patients with CCS requiring long-term OAC, dual therapy (OAC plus SAPT) did not reduce all-cause death nor ischemic events compared with OAC alone but significantly increased major bleeding and cardiovascular death. PROSPERO Registration No.: CRD420251239917.
This study provides a bibliometric overview of cardiovascular-related bibliometric research identified in the Scopus database using a title-abstract-keyword (TAK) search strategy. A total of 2,069 records were identified...This study provides a bibliometric overview of cardiovascular-related bibliometric research identified in the Scopus database using a title-abstract-keyword (TAK) search strategy. A total of 2,069 records were identified, with original articles (n = 1,130) and review papers (n = 596) representing the predominant document types. Restricting the analysis to these two categories yielded 1,726 documents, underscoring their central role in bibliometric reporting. A clear temporal growth was observed, increasing from a single publication in 1991 to 71 in 2025, with notable expansion after 2020. Authorship and institutional analyses revealed a strong concentration of contributions from China. Hu Y. was the most prolific author (13 publications), followed by Shou X. (7), while several others contributed five publications each. The China Academy of Chinese Medical Sciences (44 publications) and Beijing University of Chinese Medicine (41) were the leading institutions. China dominated global output with 229 publications, far exceeding the United States (25) and other contributing countries. Funding was primarily provided by the National Natural Science Foundation of China (84 publications). Frontiers in Cardiovascular Medicine was the leading journal (44 publications), followed by Medicine (United States) (28) and Heliyon (18). Thematically, over 300 cardiological subtopics were identified, spanning clinical areas such as heart failure, atrial fibrillation, and obesity-related cardiovascular disease, as well as emerging domains including artificial intelligence, autophagy, ferroptosis, non-coding RNAs, and digital health. Studies also addressed societal and environmental determinants such as gender disparities, air pollution, and psychosocial stress. Collectively, these findings demonstrate the accelerating adoption of bibliometric approaches in cardiovascular science and the field's transition toward interdisciplinary, technology-integrated, and data-driven research directions.
BACKGROUND: Diet high in sodium is an established major risk factor for cardiovascular diseases (CVDs), yet a comprehensive and updated assessment of its attributable disease burden, particularly comparing China with glo...BACKGROUND: Diet high in sodium is an established major risk factor for cardiovascular diseases (CVDs), yet a comprehensive and updated assessment of its attributable disease burden, particularly comparing China with global patterns over the last three decades, is lacking. METHODS: This study aims to quantify and compare the deaths and disability-adjusted life years (DALYs) of CVDs attributable to diet high in sodium in China and globally from 1990 to 2021. Using data from the Global Burden of Disease (GBD) Study 2021, we applied the comparative risk assessment framework to estimate the sodium-attributable CVD burden. Mortality and DALYs were analyzed as absolute numbers and age-standardized rates (ASRs). Temporal trends were assessed using estimated annual percentage changes (EAPCs), and future burden to 2046 was projected using an age-period-cohort (APC) model. RESULTS: In 2021, diet high in sodium was responsible for 1.71 million [95 % uncertainty intervals (UI): 0.36-3.81 million] global deaths and 37.77 million (95 % UI: 9.05-80.81 million) DALYs. The global age-standardized death rate (ASDR) and DALY rate (ASDAR) were 20.4 and 437.7 per 100,000, respectively. From 1990 to 2021, while absolute death counts increased by 52 %, the ASDR significantly declined (EAPC: -1.46 %). Pronounced sex and age disparities were observed, with males bearing a consistently higher burden and the elderly experiencing the highest rates but slowest improvements. In China, the 2021 ASDR (40.91/100,000) and ASDAR (837.94/100,000) were approximately double the global averages, despite substantial declines since 1990 (ASDR EAPC: -1.74 %; ASDAR EAPC: -1.85 %). Projections to 2046 indicate rising absolute numbers globally and in China, driven by demographic changes, despite continuing declines in age-standardized rates. CONCLUSION: High sodium intake remains a major contributor to the global and Chinese CVD burden, with significant sex and age disparities. Although age-standardized rates have improved, the rising absolute burden underscores the imperative for more effective, targeted salt-reduction public health strategies.
Diabetic cardiomyopathy (DCM) remains a major contributor to cardiovascular morbidity and mortality, yet its underlying mechanisms extend beyond hyperglycemia-induced metabolic stress. Emerging evidence identifies ferrop...Diabetic cardiomyopathy (DCM) remains a major contributor to cardiovascular morbidity and mortality, yet its underlying mechanisms extend beyond hyperglycemia-induced metabolic stress. Emerging evidence identifies ferroptosis, a regulated, iron-dependent lipid peroxidation process, as a central driver of diabetic myocardial injury. This review synthesizes molecular insights demonstrating how chronic hyperglycemia, oxidative stress, and mitochondrial dysfunction create a uniquely ferroptosis-prone cardiac environment. Particular emphasis is placed on the NRF2 signaling network, which orchestrates antioxidant defense through the HO-1 pathway and the SLC7A11-GSH-GPX4 axis. Diabetic impairment of AMPK/AKT-dependent NRF2 activation compromises these protective systems, accelerating lipid peroxidation, mitochondrial damage, inflammation, and cardiomyocyte death. We further evaluate emerging pharmacologic and natural NRF2 activators, including sulforaphane, curcumin, dexmedetomidine, canagliflozin, and 6-gingerol, demonstrating consistent cardioprotective, anti-ferroptotic benefits in preclinical models. Despite encouraging progress, concerns regarding long-term NRF2 overstimulation, metabolic reprogramming, and oncogenic risk underscore the need for carefully optimized therapeutic strategies. By integrating mechanistic advances with translational challenges, this review highlights NRF2-ferroptosis modulation as a promising frontier for targeted DCM therapy and future precision cardiology.
The prognosis of patients with MI has improved significantly with the recognition that early reperfusion is critical, particularly since timely percutaneous coronary intervention (PCI) became widely adopted. The invasive...The prognosis of patients with MI has improved significantly with the recognition that early reperfusion is critical, particularly since timely percutaneous coronary intervention (PCI) became widely adopted. The invasive reperfusion era also reshaped MI diagnostics, shifting the paradigm from Q-wave vs. Non-Q-wave MI to ST-Elevation Myocardial Infarction (STEMI) vs. Non-ST-Elevation Myocardial Infarction (NSTEMI). The current ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) paradigm have long been the cornerstone of myocardial infarction (MI) care but fail to identify many patients with acute coronary occlusion (ACO), delaying treatment and worsening outcomes. This limitation is increasingly important, since NSTEMI now represents the majority of presentations accounting for roughly 70% of AMI worldwide and many of these occlusive events are managed with delays contributing to worse outcomes. Adding to this challenge, substantial inter-physician variability in ECG interpretation for ACO has been demonstrated. In this review, we highlight recent advances using the artificial intelligence in the evaluation of patients presenting with ECG changes suggestive of NSTEMI and evaluate its role in the detection of NSTEMI patients with acute coronary occlusion.
INTRODUCTION: Sodium-glucose cotransporter-2 (SGLT2) inhibitors have shown significant reduction in cardiovascular mortality and heart failure hospitalization in patients with chronic heart failure. Despite their benefit...INTRODUCTION: Sodium-glucose cotransporter-2 (SGLT2) inhibitors have shown significant reduction in cardiovascular mortality and heart failure hospitalization in patients with chronic heart failure. Despite their benefits in chronic heart failure, their use during episodes of acute decompensation remains under investigation. METHODS: A comprehensive literature search was performed using PubMed, Google Scholar, and ClinicalTrials.gov from database inception through September 3, 2025. The predefined endpoints were all-cause mortality, heart failure hospitalizations, and a composite of cardiovascular mortality or heart failure worsening. Outcomes were pooled using a random effects Mantel-Haenszel model. The DerSimonian and Laird method was used for estimation of τ. We reported effect sizes as risk ratios (RR) with 95 % confidence interval (CI). RESULTS: A total of eight randomized controlled trials, encompassing 4,714 patients, were included in the analysis. Among patients hospitalized with decompensated heart failure, treatment with SGLT2 inhibitors compared with standard care only (control group) was associated with a significant decrease in all-cause mortality (RR 0.72; 95 % CI, 0.58-0.90; P < 0.01; I² = 0 %), and in the composite outcome of cardiovascular mortality or heart failure rehospitalization (RR 0.68; 95 % CI, 0.53-0.86; P < 0.01; I² = 28 %). However, no significant reduction was observed in heart failure rehospitalization as an isolated outcome (RR 0.92; 95 % CI, 0.82-1.03; P = 0.16; I² = 0 %). CONCLUSION: SGLT-2 inhibitors during hospitalization for acute decompensated heart failure is effective and led to decrease in all-cause mortality and a composite endpoint of cardiovascular mortality or heart failure hospitalizations.
Cardiovascular diseases (CVDs) remain the leading global cause of morbidity and mortality, with growing evidence highlighting the immune system as a central regulator of disease initiation and progression. Recent advance...Cardiovascular diseases (CVDs) remain the leading global cause of morbidity and mortality, with growing evidence highlighting the immune system as a central regulator of disease initiation and progression. Recent advances have uncovered pivotal roles for innate lymphoid cells (ILCs) and trained innate immunity (TI) in shaping cardiovascular homeostasis and inflammation. This review synthesizes current knowledge on the development, tissue residency, and functional specialization of ILC subsets, including ILC1/NK cells, ILC2, and ILC3, as well as their divergent contributions to atherosclerosis, myocardial infarction, heart failure, myocarditis, and pericarditis. ILC1 and NK cells promote vascular inflammation and plaque progression, whereas cardiac-resident ILC2s exert reparative, anti-inflammatory, and atheroprotective effects. Parallel evidence shows that TI, driven by metabolic stressors such as hyperglycemia, oxidized LDL, smoking, and a Western diet, induces persistent myeloid reprogramming that amplifies vascular inflammation and accelerates CVD. We further highlight their potential as diagnostic biomarkers and therapeutic targets, including cytokine-directed interventions, modulation of the IL-33/ILC2 axis, and epigenetic therapies. Together, these insights position ILC biology and TI as transformative frameworks for advancing precision immunocardiology.
BACKGROUND: Exosomes, nanoscale extracellular vesicles (30-150 nm) carrying bioactive molecules (e.g., miRNAs, proteins), have emerged as pivotal mediators in cardiovascular diseases (CVDs), offering potential as diagnos...BACKGROUND: Exosomes, nanoscale extracellular vesicles (30-150 nm) carrying bioactive molecules (e.g., miRNAs, proteins), have emerged as pivotal mediators in cardiovascular diseases (CVDs), offering potential as diagnostic biomarkers and therapeutic vectors. Despite growing interest, a comprehensive analysis of global research trends, hotspots, and translational gaps in exosome applications for CVDs remains limited. METHODS: We conducted a ten-year (2016-2025) bibliometric analysis of 2617 publications from the Web of Science Core Collection, employing integrative tools (LDGAS and KMVS) to map research distribution, collaborations, and citation trends. Data was analyzed for contributions by country, institution, journal, and author, with a focus on mechanistic insights, clinical applications, and technological innovations. RESULTS: Global publications surged post-2016, with China leading in output (50 % of top institutions) and the USA/Europe dominating citation impact (e.g., Harvard Medical School: 7.83 citations/paper). Three key themes emerged: exosomal regulation of oxidative stress, inflammation, and angiogenesis; engineered exosomes (e.g., inflammation-targeting macrophage exosomes and stem cell-derived exosomes; circulating miRNAs (e.g., miR-21-5p in heart failure). Challenges include heterogeneous exosome isolation methods (<5 % studies reach preclinical trials) and imbalanced collaborations (China-USA partnerships dominated, 83 %). CONCLUSIONS: Exosome research in CVDs demonstrates transformative potential but requires standardized protocols, diversified clinical trials, and strengthened global partnerships. Prioritizing AI-driven biomarker discovery and interdisciplinary synergy will accelerate clinical translation.
Atrial fibrillation (AF) and heart failure (HF) frequently coexist, which leads to adverse clinical outcomes and a significant increase in the risk of both ischemic stroke and major bleeding. Although still valuable due...Atrial fibrillation (AF) and heart failure (HF) frequently coexist, which leads to adverse clinical outcomes and a significant increase in the risk of both ischemic stroke and major bleeding. Although still valuable due to their widespread adoption, traditional risk scores (e.g. CHADS-VASc, HAS-BLED) may not adequately capture group-specific differences in the context of substantial therapeutic and demographic changes that have occurred in recent years. This review summarizes emerging risk factors for stroke and bleeding, focusing on clinical and structural markers, and highlighting the novel biomarker-based approach. Factors such as chronic kidney disease, poor nutritional status, metabolic-associated fatty liver disease, frailty, and polypharmacy appear to substantially modify the risk. Biomarkers, including natriuretic peptides, high-sensitivity cardiac troponins, and growth differentiation factor-15, along with various markers of inflammation and hypercoagulability, provide valuable prognostic information. Incorporating echocardiographic measures, such as left atrial size, morphology, and appendage flow, together with electrocardiographic factors, including AF type and episode duration, may further refine stroke and bleeding prediction. New risk models, such as those based on novel biomarker strategies and machine learning, offer promising results in predicting stroke and bleeding when compared to traditional and well-validated risk scores. A better understanding and integration of these emerging risk factors can enhance existing risk stratification tools, guiding clinicians toward a more individualized decision-making process, while improving strategies for preventing stroke and major bleeding in this specific and vulnerable population.