Search Results (1,352)

Background: Kounis syndrome is an allergic acute coronary syndrome precipitated by coronary vasospasm, plaque destabilization, stent thrombosis, or bypass occlusion. Cardiac surgery represents a uniquely high-risk setting due to cardiopulmonary bypass–associated inflammation and exposure to multiple pharmaceutical agents. Importantly, Kounis syndrome remains underrecognized in this context, as classical signs of anaphylaxis may be masked under general anesthesia and cardiopulmonary bypass, while ischemic manifestations may be misattributed to other perioperative conditions. Methods: A narrative review of PubMed-indexed literature was conducted to synthesize current evidence on the pathophysiology, perioperative triggers, clinical presentation, diagnostic strategies, and management of Kounis syndrome in cardiac surgery, with emphasis on intraoperative recognition and surgical decision-making. Published cases were retrieved involving perioperative cardiac surgery patients with a definite diagnosis of Kounis syndrome. Additionally, cases presenting with severe perioperative anaphylaxis and life-threatening cardiovascular involvement (grade III with cardiovascular collapse and grade IV with cardiac arrest) were included as possible Kounis syndrome, reflecting real-world diagnostic uncertainty in the intraoperative setting. Results: The literature review identified five cases of definite Kounis syndrome and ten cases of possible Kounis syndrome, including three cases with cardiovascular collapse and seven cases with cardiac arrest. Recurrent episodes were reported in several patients, particularly due to re-exposure to the triggering agent. In the context of cardiac surgery, Kounis syndrome is most frequently triggered by chlorhexidine, protamine, antibiotic prophylaxis, and anesthetic agents. The clinical presentation is often subtle during cardiopulmonary bypass. Vasoplegia, pulmonary hypertension, ventricular dysfunction, new regional wall-motion abnormalities, and hyperdynamic ventricles on transesophageal echocardiography commonly precede overt electrocardiographic changes. Diagnosis is primarily clinical and relies on intraoperative ultrasound, hemodynamic monitoring, serum tryptase, serum troponin, and, when indicated, coronary angiography. A dual-pathway approach addressing both anaphylaxis and myocardial ischemia is essential; however, one component may predominate, particularly in perioperative patients with limited clinical information, potentially leading to misdiagnosis. A multidisciplinary approach is therefore required for rapid diagnosis and individualized management. In refractory cases, cardiopulmonary bypass or ventricular assist devices may provide lifesaving support. Conclusions: Kounis syndrome remains underrecognized in cardiac surgery but carries significant morbidity. Increased clinical awareness, multidisciplinary collaboration, structured diagnostic approaches, and preventive strategies are essential to improve outcomes and reduce the risk of recurrence during future procedures. Full article

A key limitation in contemporary HF management is the marked heterogeneity of the syndrome, driven by diverse pathophysiological mechanisms that are not fully captured by traditional classifications based on left ventricular ejection fraction. Precision medicine has emerged as a promising approach to address this heterogeneity by integrating clinical characteristics, circulating biomarkers, advanced imaging, and computational phenotyping strategies. However, current frameworks predominantly emphasize myocardial dysfunction, while the contribution of vascular abnormalities remains underrepresented. The interaction between the left ventricle and the arterial system plays a fundamental role in cardiovascular performance. Arterial stiffness, commonly assessed by pulse wave velocity (PWV), represents a key determinant of vascular aging and a robust predictor of cardiovascular risk. Increasing evidence suggests that vascular dysfunction contributes significantly to the pathophysiology and clinical expression of HF, particularly in phenotypes characterized by preserved ejection fraction. This review synthesizes current evidence on precision medicine in HF and highlights the emerging role of arterial stiffness and PWV in multidimensional patient phenotyping. We propose that integrating vascular parameters into existing phenotyping frameworks may enhance risk stratification, improve mechanistic understanding, and support the development of more personalized therapeutic strategies in heart failure. Unlike previous reviews that have addressed arterial stiffness or heart failure phenotyping separately, this work uniquely integrates ventricular–vascular interaction and pulse wave velocity into a comprehensive precision medicine framework for heart failure. By bridging vascular physiology with data-driven phenotyping strategies, this review provides a novel conceptual model for incorporating arterial stiffness into multidimensional patient characterization across the full spectrum of heart failure phenotypes. Full article

Background: Congenital heart disease (CHD) represents a major cause of perinatal morbidity and mortality, and fetal echocardiography is essential for its early diagnosis and management. Maternal smoking has been suggested as a potential teratogenic factor affecting fetal cardiovascular development; however, findings regarding its association with CHD remain inconsistent. This study aimed to evaluate the relationship between maternal smoking during pregnancy and the risk of CHD. Methods: A total of 2715 pregnant women and 2784 fetuses who underwent fetal echocardiography at ≥20 weeks’ gestation between 1 January 2024 and 1 November 2025 were analyzed. Pregnancies complicated by known chromosomal or syndromic abnormalities, significant teratogenic exposure, duplicate assessments, or nonstandard examinations were excluded. Maternal smoking status during pregnancy was recorded and categorized according to daily cigarette consumption. The prevalence of CHD and the distribution of CHD subtypes were evaluated and compared according to smoking status. Fetal cardiac diagnoses were classified based on the classical morphological classification system. Results: A total of 2715 pregnancies (2784 fetuses) were analyzed, including 2530 fetuses in the non-smoking group and 254 in the smoking group. Congenital heart disease was detected in 12.5% of fetuses in the non-smoking group and 14.2% in the smoking group, with no statistically significant difference (p = 0.442). According to the classical morphological classification, the distribution of fetal echocardiographic pathologies did not differ significantly between groups (p = 0.607). Septal defects were the most common subtype in both groups. Although conotruncal defects were proportionally more frequent in the smoking group, this difference did not reach statistical significance. After reclassifying daily cigarette consumption into four exposure categories, no association was detected between maternal smoking and CHD risk (OR = 1.04; 95% CI: 0.86–1.26; p = 0.691). Conclusion: In this cohort referred for fetal echocardiographic evaluation, no association was detected between maternal smoking during pregnancy and the risk of congenital heart disease or alterations in CHD subtype distribution. No consistent dose–response relationship was observed. These findings suggest that no association was detected between maternal smoking exposure and CHD. Further large-scale prospective studies are needed to clarify phenotype-specific associations. Full article

Nonobstructive coronary artery disease (NOCAD) is increasingly recognized as a heterogeneous condition characterized by diverse pathophysiological mechanisms despite the absence of flow-limiting stenosis. We sought to establish a rule-based dominant imaging phenotype framework integrating functional, structural, and inflammatory dimensions derived from multiparametric coronary computed tomography angiography (CCTA). In this retrospective cohort of 485 patients with NOCAD, CT-derived fractional flow reserve (CT-FFR), quantitative plaque burden and high-risk plaque features, and perivascular fat attenuation index (FAI) were assessed. Using predefined percentile thresholds and hierarchical rules, patients were categorized into function-, structure-, inflammation-dominant, or low-risk phenotypes. During a median follow-up of 36 months, 56 patients (11.5%) experienced major adverse cardiovascular events (MACE). After multivariable adjustment, function dominance was associated with the highest risk (hazard ratio [HR] 4.054, 95% confidence interval [CI] 1.984–8.281; p < 0.001), followed by structure dominance (HR 3.129, 95% CI 1.410–6.944; p = 0.005), whereas isolated inflammation dominance did not show a statistically significant independent association with events, with wide confidence intervals indicating limited precision. These findings suggest a graded pattern of prognostic associations across functional and structural abnormalities in NOCAD and support a phenotype-oriented interpretation of CCTA metrics reflecting distinct biological axes of coronary pathology. Full article

Systemic sclerosis (SSc) is a complex autoimmune connective tissue disease characterized by microvascular dysfunction, immune activation, and progressive fibrosis affecting multiple organs, including the heart. Myocardial involvement represents an important but frequently underrecognized manifestation of SSc and may develop even in the absence of overt clinical symptoms. Cardiac manifestations include ventricular dysfunction, arrhythmias, conduction abnormalities, and heart failure, contributing substantially to morbidity and mortality. The underlying pathophysiology involves coronary microvascular dysfunction, immune-mediated myocardial inflammation, and progressive myocardial fibrosis, which often precede clinically apparent cardiac disease. This review aims to summarize the current understanding of myocardial involvement in SSc and to provide a comprehensive overview of contemporary multimodality cardiovascular imaging techniques for its detection, characterization, and risk stratification. A comprehensive overview of the current literature was conducted focusing on established and emerging cardiovascular imaging modalities for the evaluation of myocardial involvement in SSc. Particular attention was given to echocardiography, cardiac magnetic resonance (CMR), nuclear imaging techniques including positron emission tomography (PET) and single-photon emission computed tomography (SPECT), and cardiac computed tomography (CT). Recent advances in imaging biomarkers, parametric mapping, myocardial strain analysis, and emerging technologies such as artificial intelligence (AI), radiomics, and molecular imaging were also considered. Multimodality cardiovascular imaging plays a central role in the early detection and comprehensive assessment of myocardial involvement in SSc. Advanced imaging techniques enable improved identification of subclinical myocardial dysfunction, microvascular impairment, inflammation, and fibrosis. An integrated imaging approach combining echocardiography, CMR, nuclear imaging, and CT may facilitate earlier diagnosis, enhance risk stratification, and ultimately improve cardiovascular outcomes in patients with SSc. Full article

Background/Objectives: Cardiovascular complications remain the leading cause of mortality among patients with end-stage renal disease (ESRD) treated with maintenance hemodialysis (HD). Global longitudinal strain (GLS) is a sensitive echocardiographic marker of left ventricular systolic dysfunction that enables the detection of transient contractile abnormalities consistent with intradialytic myocardial stunning. This study aimed to assess intradialytic GLS dynamics during a single HD session and to identify predictors of GLS deterioration. Methods: Forty-three patients were enrolled. Transthoracic echocardiography, electrocardiography, and pulse wave analysis were performed before HD, at mid-session, and after HD. Biochemical assessment included, among others, plasma osmolality, electrolytes, and biomarkers of oxidative stress and endothelial dysfunction. Results: Three distinct intradialytic GLS trajectories were identified: GLS worsening (GLSw, 46.5%), GLS stable (GLSs, 34.9%), and GLS improvement (GLSi, 18.6%). In the GLSw group, independent predictors of GLS deterioration included a decrease in left atrial volume index (LAVI, p = 0.0002), an increase in left ventricular end-systolic volume index (LVESVI, p = 0.0067), diabetes mellitus (p = 0.0094), and an increase in the malondialdehyde-to-creatinine ratio (MDA/CREA, p = 0.0055). In the GLSi group, GLS improvement was associated with a decrease in plasma osmolality (p = 0.0326) and asymmetric dimethylarginine (ADMA, p = 0.0279), as well as an increase in the subendocardial viability ratio index (SEVRI, p = 0.0004) and caspase-1 (p = 0.0005). Conclusions: Intradialytic GLS trajectories are heterogeneous and reflect individual susceptibility to GLS deterioration. Modifiable adverse factors likely include oxidative stress, osmotic stress, fluid overload, uremic toxin- and ion-disturbance-related stress, and impaired coronary microvascular reserve. Future prospective studies are needed. Full article

Cirrhosis is no longer viewed solely as an isolated hepatic disorder but rather as a complex multisystemic disease that affects cardiovascular, renal, pulmonary, metabolic, and immune systems. One of its most clinically relevant but under-recognized consequences is cardiac dysfunction, manifesting as cirrhotic cardiomyopathy, portopulmonary hypertension, right ventricular (RV) failure, and impaired myocardial strain. Oxidative stress (OS) has recently emerged as a fundamental mechanistic link between hepatic fibrogenesis and myocardial remodeling, acting through mitochondrial injury, NADPH oxidase activation, nitric oxide dysregulation, iron-mediated ferroptosis, and inflammatory cytokines. These alterations lead to diastolic dysfunction, autonomic imbalance, myocardial fibrosis, electrophysiological abnormalities (including QTc prolongation), and impaired RV–pulmonary artery coupling. Redox biomarkers such as malondialdehyde (MDA), NOX2-derived peptides, GSH/GSSG ratio, sST2, NT-proBNP, and 8-isoprostanes hold promise in detecting early subclinical cardiac involvement in cirrhosis. Novel antioxidant therapies, including mitochondrial-targeted molecules, NOX inhibitors, and ferroptosis blockers, may improve myocardial remodeling and hemodynamic stability. This review explores the central role of redox imbalance in the cardiohepatic syndrome and its potential utility in diagnosis, monitoring, and therapy. Full article

Background: Chronic kidney disease (CKD) associated vascular calcification (VC) is a leading cause of cardiovascular mortality, partially driven by osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation cellular process. However, the precise role and mechanism of CMA in CKD-associated vascular calcification remain unknown. Methods: We studied calcified arteries from CKD patients and rats fed on a high-phosphate diet using histological and ultrastructural methods. VSMCs’ calcification was induced by a calcification medium containing high phosphate and calcium. CMA activity was measured by a KFERQ reporter and lysosomal staining. The expression of LAMP2a and HSP90AA1 was knocked down by siRNA, overexpressed by plasmid, and activated by QX77.1. Bioinformatic analysis, protein interaction studies, immunofluorescence and co-immunoprecipitation were performed to investigate the potential mechanism of CMA in VC. Results: The expression of LAMP2a was increased in human calcified radial artery tissues (n = 3, p < 0.05) and rats’ calcified aortic tissues (n = 3, p < 0.01), accompanied by lysosomal abnormalities. The activity of CMA was increased during the osteogenic transdifferentiation of VSMCs, as indicated by increased expression of RUNX2 and reduced expression of SM22α (p < 0.05). LAMP2a knockdown attenuated VSMCs’ calcification (p < 0.05), whereas pharmacological activation of CMA aggravated calcification in VSMCs (p < 0.01). Bioinformatic screening identified HSP90AA1 as a candidate involved in CMA in vascular calcification. Elevated HSP90AA1 expression was observed in human calcified radial artery tissues (n = 3, p < 0.01) and rat calcified aortic tissues (n = 3, p < 0.01), which promoted osteogenic transdifferentiation of VSMCs (p < 0.05). HSP90AA1 interacted with LAMP2a and positively regulated its expression (p < 0.01). Conclusions: These findings support an association between CMA activation and CKD vascular calcification. It suggests that HSP90AA1 facilitates vascular calcification in chronic kidney disease involving chaperone-mediated autophagy. Full article

Background: Cardiovascular risk in chronic kidney disease (CKD) remains high despite frequently normal conventional lipid parameters. The extent to which lipid patterns vary across CKD severity and metabolic complications remains incompletely characterized. Therefore, this study evaluated lipid patterns and their associations with renal function and CKD-related metabolic complications. Methods: This retrospective cross-sectional study included 229 CKD patients from the nephrology clinic at King Saud Medical City. Single-time-point laboratory data and clinical variables were extracted from medical records. Patients were stratified by KDIGO eGFR stage, uremia, and phosphate status. Lipid parameters were analyzed using nonparametric tests, multivariable regression, and ROC analysis. Results: Among 229 CKD patients, the most prevalent lipid abnormalities were low HDL-C (49.8%) and elevated remnant cholesterol (RC) (31.4%). HDL-C was reduced and RC increased with declining eGFR, while TC, LDL-C, and TG remained unchanged. In uremia, HDL-C remained reduced and RC increased, with additional reductions in TC and LDL-C, whereas TG did not differ. No significant lipid changes were observed with hyperphosphatemia. In multivariable analyses, HDL-C was positively associated with eGFR (β = 48.8, q = 0.003) and inversely associated with BUN (β = −14.3, q = 0.0014), while RC showed an inverse association with eGFR (β = −19.9, q = 0.0005) and a positive association with BUN (β = 3.37, q = 0.0315). These relationships remained independent of age, sex, BMI, smoking status, hypertension, and type 2 diabetes. ROC analysis further demonstrated the moderate discriminatory ability of HDL-C and RC for identifying CKD stages and uremia. Conclusions: Alterations in HDL-C and RC were independently associated with renal function and uremic status. These findings suggest that lipoprotein composition may reflect metabolic disturbances accompanying CKD progression. Full article

Background: Cardiovascular disease remains a leading cause of morbidity and mortality after kidney transplantation. The relative contribution of metabolic abnormalities and inflammatory burden to cardiac remodeling and subsequent clinical outcomes in kidney transplant recipients (KTRs) remains incompletely understood. Methods: In this retrospective cohort study, 152 KTRs underwent comprehensive cardiovascular evaluation at a stable post-transplant time point (12 ± 4 months after transplantation). Metabolic phenotype was assessed using metabolic syndrome and indices of insulin resistance and atherogenic dyslipidemia (TyG index, TG/HDL ratio, and atherogenic index of plasma [AIP]). Inflammatory status was evaluated using hs-CRP and complete blood count-derived indices. Echocardiographic damage composite (EDC) was defined as the presence of left ventricular hypertrophy, diastolic dysfunction, or left atrial enlargement. Patients were followed for major adverse clinical outcome (MACO), defined as cardiovascular event, graft failure, or death, and major adverse cardiovascular and cerebrovascular events (MACCE). Results: At baseline, 78 patients (51.3%) met criteria for EDC. EDC was strongly associated with higher TyG, AIP, TG/HDL, LDL/HDL ratio, and metabolic syndrome, whereas inflammatory markers showed no association. In multivariable logistic regression adjusted for age, sex, eGFR, and proteinuria, TyG remained independently associated with EDC (OR 1.13 per 0.1 increase, 95% CI 1.05–1.21; p = 0.001), independent of hs-CRP. Similar results were observed when AIP was evaluated in place of TyG (OR 10.39, 95% CI 2.22–48.71; p = 0.003). During follow-up, 78 patients developed MACO and 49 developed MACCE. In Cox regression analysis, graft dysfunction and inflammatory markers independently predicted MACO, whereas TyG was no longer significant. In contrast, TyG remained an independent predictor of MACCE after adjustment for confounders and inflammatory markers (HR 1.10 per 0.1 increase, 95% CI 1.04–1.16; p < 0.001). Similar results were observed when AIP was tested in place of TyG (HR 10.8, 95% CI 3.06–38.11; p < 0.001). Echocardiographic damage did not independently predict outcomes after adjustment. Conclusions: In KTRs, metabolic abnormalities reflecting insulin resistance and atherogenic dyslipidemia are closely associated with cardiac remodeling one year after transplantation and remain specifically linked to subsequent cardiovascular events. In contrast, systemic inflammation and graft dysfunction are the primary determinants of overall adverse clinical outcomes. Simple metabolic indices such as TyG and AIP may provide practical tools for cardiovascular risk stratification in this population. In Cox proportional hazards models, TyG (HR 1.102, 95% CI 1.043–1.164, p = 0.001) and AIP (HR 10.8, 95% CI 3.06–38.11, p < 0.001) were independently associated with cardiovascular events during follow-up, underscoring the role of atherogenic dyslipidemia in cardiovascular risk. Full article

Background: Chronic kidney disease (CKD) is associated with increased cardiovascular morbidity and mortality, even at early stages. Postmenopausal women represent a particularly vulnerable population due to estrogen deficiency, which promotes adverse cardiovascular remodeling. However, data specifically characterizing the cardiac phenotype of hypertensive postmenopausal women with mild-to-moderate CKD remain limited. Methods: We conducted a prospective observational cohort study including 413 hypertensive postmenopausal women consecutively referred to a tertiary center between 2019 and 2022. Participants were stratified into a CKD group with stage 3 CKD (estimated glomerular filtration rate of 30–59 mL/min/1.73 m²; n = 213) and a control group without CKD (n = 200). All subjects underwent comprehensive clinical evaluation, laboratory testing, and standardized transthoracic echocardiography. The prevalence of left ventricular hypertrophy (LVH), left ventricular diastolic dysfunction (LVDD), and chronic coronary syndromes (CCS) was assessed. Multivariable logistic regression analyses were performed to evaluate independent associations between CKD and cardiovascular abnormalities. Results: Compared with controls, women with CKD showed a significantly higher prevalence of LVH (46.7% vs. 21.5%), LVDD (55.8% vs. 36.0%), and CCS (15.5% vs. 7.5%) (all p < 0.01). The coexistence of LVH and LVDD identified a high-risk cardiac phenotype that was markedly more frequent in the CKD group (41.3% vs. 12.5%). After adjustment for age, body mass index, blood pressure, duration of hypertension, smoking status, and antihypertensive therapy, stage 3 CKD remained independently associated with LVH, LVDD, and CCS. Conclusions: In hypertensive postmenopausal women, mild-to-moderate CKD is associated with a substantial burden of cardiac structural and functional abnormalities exceeding that attributable to hypertension alone, supporting early cardiovascular screening and an integrated cardiorenal approach. Full article

Photoplethysmography (PPG) has emerged as an attractive modality for non-invasive cardiovascular monitoring due to its low cost, unobtrusive nature, and ubiquity in consumer wearable devices. Despite its potential, existing PPG-based arrhythmia detection systems remain limited in scope: (i) most target only atrial fibrillation, (ii) temporal localization of abnormal segments is rarely provided, and (iii) deep learning models lack explainability, hindering adoption in clinical workflows. We present a comprehensive and fully integrated framework for multi-class arrhythmia detection, segmentation, and explainability based on PPG waveforms, Heart Rate Variability (HRV), and structured clinical metadata. The proposed system introduces a CLIP-style contrastive learning module aligning PPG waveforms with clinical variables and rhythm-state textual descriptions using BioBERT; a multitask U-Net architecture performing 4-class classification and 1D segmentation; a Retrieval-Augmented Generation (RAG) pipeline leveraging Gemini Flash large language models to produce guideline-grounded diagnostic reports; and a real-time Streamlit-based web platform supporting inference, visualization, and database storage. The system significantly improves classification accuracy (from 86.27% to 91.19%) and segmentation Dice (from 0.5815 to 0.7167). These results demonstrate the feasibility of a robust, multimodal, and explainable PPG-based arrhythmia monitoring system for real-world applications. Full article

Background and Objectives: Rates of obesity have been consistently increasing in recent years across all age groups, with a notable rise among young people. Obesity represents a persistent inflammatory condition and a key contributor to various chronic health problems, such as cardiovascular disorders, metabolic abnormalities, cancer, and psychological conditions. The move from high school to university is a transitional phase accompanied by specific pressures that can affect both body weight control and mental health in students. This cross-sectional investigation aimed to investigate potential associations between excess weight and the presence of depressive and anxiety symptoms in university populations. Methods: This cross-sectional analysis included 5298 students enrolled at universities across ten geographic areas of Greece. Participants filled out questionnaires concerning demographic information and lifestyle behaviors. Levels of depression and anxiety were measured using the Beck Depression Inventory (BDI-II) and the short form of the State Anxiety Inventory (STAI-6), respectively. Measurements of height and body weight were obtained to compute Body Mass Index (BMI). Results: The presence of overweight or obesity among students was significantly and independently related to female sex, urban residence, living independently, tobacco use, and lower academic performance (p = 0.0103, p = 0.0102, p = 0.0203, p = 0.0075, and p = 0.0168, respectively). Individuals reporting insufficient physical activity had 85% higher odds of being overweight or obese (p = 0.0068). Similarly, participants experiencing depressive or anxious symptomatology had more than double odds of excess body weight compared with those without such symptoms (p = 0.0015 and p = 0.0012, respectively). Furthermore, poor Mediterranean diet adherence was linked to more than a twofold increase in the odds of overweight or obesity (p = 0.0005). Conclusions: These findings offer considerable evidence that symptoms of depression and anxiety may serve as significant contributors to the development of overweight and obesity among university students. Additional longitudinal studies are strongly encouraged to substantiate these observations. Full article

Cardiovascular and metabolic diseases (CMDs) are the leading causes of global mortality. While university students represent a critical demographic for early intervention, conventional univariate screenings often fail to capture the synergistic interactions between lipid abnormalities and adiposity. This study aimed to identify and characterize multidimensional cardiometabolic phenotypes in Ecuadorian university students using multivariate exploratory techniques. A cross-sectional study was conducted with 365 students from the Coastal (n = 193) and Andean (n = 172) regions of Ecuador. Lipid profiles (TC, HDL-c, LDL-c, triglycerides), body composition (body fat percentage, visceral fat via bioelectrical impedance), and blood pressure were analyzed. Data were processed using HJ-Biplot analysis for dimensional reduction and a hybrid clustering approach (Hierarchical and K-means) for population segmentation. The HJ-Biplot explained 72.3% of the total variance. The first principal component (PC1, 49.2%) was associated with morphometric size (weight, height), while the second (PC2, 23.1%) was dominated by adiposity markers (body fat and visceral fat). Three distinct clusters were identified: Cluster 0 (27.1%, predominantly female) represented a low-risk profile with the highest HDL-c (57.5 mg/dL); Cluster 1 (26.6%, majority male) exhibited an intermediate-risk profile with the highest triglycerides (117.9 mg/dL); and Cluster 2 (46.3%, almost exclusively male and Andean-dominant) presented the highest risk, characterized by the lowest HDL-c levels (41 mg/dL) and older age. In conclusion, cardiometabolic risk is heterogeneously distributed across sex and geographical regions. Multivariate profiling allows for the detection of early metabolic vulnerability that remains undetected in traditional screenings. These findings support the implementation of targeted public health strategies tailored to the specific phenotypic and regional characteristics of the university population in Ecuador. Full article

Background and Objectives: The interaction between the brain and heart has become more interesting in the last 20 years. The most common cardiac complications after stroke are myocardial infarction, heart failure, arrhythmias, electrocardiographic disturbances, repolarization disorders, and sudden cardiac death. The prolonged Tpeak–Tend interval is an indicator of the electrical heterogeneity of the myocardium (abnormal repolarization) that causes malignant arrhythmias. We aimed to investigate whether the Tpeak–Tend interval, which reflects the heterogeneity of repolarization, is prolonged in stroke and its relationship with short-term mortality. Materials and Methods: Individuals over the age of 18 who presented with hemorrhagic or ischemic stroke were included in the study. Demographic characteristics, laboratory and imaging findings of the patients were recorded. ECGs were obtained at the time of admission to the hospital and 24 h later. Patients were followed for in-hospital mortality. Results: 89 (82.4%) of the patients had ischemic stroke, 19 (17.6%) had hemorrhagic stroke. It was determined that Tp-eV2 and Tp-eV5 at hospital admission were significantly longer than the 24th hour values. A total of 92.01 (16.3) ms at Tp-eV2 admission, 84.1 (16.3) ms after 24 h (p = 0.003), 91.9 (7.3) msTp-eV5 at admission, and 81.6 (17.8) ms (p = 0.000) after 24 h. In multivariate logistic regression analysis of in-hospital mortality, Tp-eV2 (HR: 0.96 (95% CI 0.93–0.99) p = 0.008) was determined as an independent predictor among cardiovascular parameters. Conclusions: Tp-e intervals were prolonged in both leads V2 and V5 in patients with stroke. Prolongation of lead V2 in the Tp-e interval is an independent indicator of short-term mortality among cardiovascular parameters. Full article