Search Results (1,260)

Monitoring cardiovascular health enables continuous and real-time risk assessment. This study utilized the Framingham Heart Study dataset to develop and evaluate machine-learning models for predicting mortality risk based on key cardiovascular parameters. Some machine-learning algorithms were applied to multiple machine-learning models. Among these, XGBoost achieved the highest predictive performance, each with an area under the curve (AUC) value of 0.83. Feature importance analysis revealed that coronary artery disease, glucose levels, and diastolic blood pressure (DIABP) were the most significant risk factors associated with mortality. The primary contribution of this research lies in its implications for public health and preventive medicine. By identifying key risk factors, it becomes possible to calculate individual and population-level risk scores and to design targeted early intervention strategies aimed at reducing cardiovascular-related mortality. Full article

Coronavirus disease 2019 (COVID-19) causes cardiovascular complications, which contributes to the high mortality rate of the disease. Emerging evidence indicates that aberrant vascular smooth muscle cell (SMC) function is a key driver of vascular disease in COVID-19. While antivirals alleviate the symptoms of COVID-19, it is not known whether these drugs directly affect SMCs. Accordingly, the present study investigated the ability of three approved COVID-19 antiviral drugs to influence SMC function. Treatment of SMCs with remdesivir (RDV), but not molnupiravir or nirmatrelvir, inhibited cell proliferation, DNA synthesis, and migration without affecting cell viability. RDV also stimulated an increase in heme oxygenase-1 (HO-1) expression that was not observed with molnupiravir or nirmatrelvir. The induction of HO-1 by RDV was abolished by mutating the antioxidant responsive element of the promoter, overexpressing dominant-negative NF-E2-related factor-2 (Nrf2), or treating cells with an antioxidant. Finally, silencing HO-1 partly rescued the proliferative and migratory response of RDV-treated SMCs, and this was reversed by carbon monoxide and bilirubin. In conclusion, the induction of HO-1 via the oxidant-sensitive Nrf2 signaling pathway contributes to the antiproliferative and antimigratory actions of RDV by generating carbon monoxide and bilirubin. These pleiotropic actions of RDV may prevent occlusive vascular disease in COVID-19. Full article

(1) Background: Comparison of clinical outcomes between patients with moderate-severe aortic valve stenosis and those with mild or no aortic valve stenosis undergoing surgical revascularization for critical limb threating ischemia (CLTI). (2) Methods: Single center retrospective analysis of consecutive patients undergoing surgical lower limb revascularization with femoro-distal bypass for critical ischemia between 2016 and 2022. All patients were evaluated preoperatively by echocardiographic examination and divided into two cohorts: group A with moderate-severe aortic valve stenosis (AVA-cm² < or =1.5 cm²) and group B with mild or absent stenosis (AVA-cm² > 1.5 cm²). Primary outcomes were major limb amputation and mortality between the two groups. The rate of major cardiovascular events (stroke, myocardial infarction, sudden cardiac death) and change in “preoperative functional status” were the secondary outcomes. Descriptive statistics for continuous variables were performed by calculating means, standard deviation (SD) medians, and interquartile range (IQR) while, for categorical variables, frequencies and percentages were performed. Intergroup comparison tests, for continuous variables, were performed by t-test or corresponding nonparametric tests (Mann-Whitney test) while, for categorical variables, Chi-square test was used. Evaluation of cut-offs for the variable AVA-fx-cm², in terms of predictive of outcome outcomes, was calculated by ROC curves. Comparison between clinical and outcome variables was performed using logistic regression models. A total of 316 patients were analyzed and divided in two groups: 50 (16%) patients with moderate or severe aortic valve stenosis (group A) and 266 (84%) with no or mild aortic valve stenosis (AVA > 1.5 cm²). Patients in group A were significantly older than those in group B (78 years vs. 74 years, p value = 0.005); no other significant comorbidity differences were found between the two groups. The mean follow-up was 1178 days (SD 991 days; 2–3869 days). There were no statistically significant differences between group A and group B in terms of major amputation rate (20% vs. 16.5%; p = 0.895) and overall mortality (48.0% vs. 40.6%; p = 0.640). In the total cohort, the statistically significant variables associated with the major amputation were systemic perioperative complication (OR 5.83, 95% CI: 2.36, 14.57, p < 0.001), bypass-related complication within 30 days of surgery (OR 2.74, 95% CI: 1.17, 6.45, p = 0.020), surgical revascularization below the knee (OR 7.72, 95% CI: 1.53, 140.68, p = 0.049), and the presence of a previous cardiovascular event (OR 2.65, 95% CI: 1.14, 6.26, p = 0.024). In patients undergoing surgical revascularization for CLTI, no significant difference in major amputation rate and overall mortality was found between subjects with mild or no aortic valve stenosis and those with moderate/severe stenosis. As expected, overall mortality was higher in older patients with worse functional status. A significantly higher rate of limb amputation was found in those subjects undergoing subgenicular revascularization, early bypass failure, or previous cardiovascular event. Full article

Background and Objectives: Heart failure (HF) and chronic kidney disease (CKD) frequently coexist and are closely interrelated, significantly affecting clinical outcomes. Among CKD-related markers, albuminuria and estimated glomerular filtration rate (eGFR) have emerged as key prognostic indicators in HF. However, their specific predictive value across different HF phenotypes—namely HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF)—remains incompletely understood. This systematic review aims to evaluate the prognostic significance of albuminuria and eGFR in patients with HF and to compare their predictive roles in HFpEF versus HFrEF populations. Materials and Methods: We conducted a systematic search of major databases to identify clinical studies evaluating the association between albuminuria, eGFR, and adverse outcomes in HF patients. Inclusion criteria encompassed studies reporting on cardiovascular events, all-cause mortality, or HF-related hospitalizations, with subgroup analyses based on ejection fraction. Data extraction and quality assessment were performed independently by two reviewers. Results: Twenty-one studies met the inclusion criteria, including diverse HF populations and various biomarker assessment methods. Both albuminuria and reduced eGFR were consistently associated with increased risk of mortality and hospitalization. In HFrEF populations, reduced eGFR demonstrated stronger prognostic associations, whereas albuminuria was predictive across both HF phenotypes. Heterogeneity in study design and outcome definitions limited comparability. Conclusions: Albuminuria and eGFR are valuable prognostic biomarkers in HF and may enhance risk stratification and clinical decision-making, particularly when integrated into clinical assessment models. Differential prognostic implications in HFpEF versus HFrEF highlight the need for phenotype-specific approaches. Further research is warranted to validate these findings and clarify their role in guiding personalized therapeutic strategies in HF populations. Limitations: The current evidence base consists primarily of observational studies with variable methodological quality and inconsistent reporting of effect estimates. Full article

Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder with significant racial and ethnic disparities in prevalence, disease severity, and outcomes. Cardiovascular complications, including pericarditis, myocarditis, valvular disease, and conduction abnormalities, contribute to increased morbidity and mortality in SLE patients. This study examines racial and ethnic disparities in cardiovascular outcomes among hospitalized SLE patients in the United States. Methods: This retrospective study utilized the National Inpatient Sample (NIS) database from 2016 to 2021 to analyze hospitalizations of adult patients (≥18 years) with a primary or secondary diagnosis of SLE. Patients were stratified into racial/ethnic groups: White, Black, Hispanic, Asian, Native American, and Other. Primary outcomes include major adverse cardiovascular events (MACEs), which are a composite of in-hospital mortality, myocardial infarction (MI), sudden cardiac death, and other SLE-related outcomes including cardiac, pulmonary, and renal involvement. Statistical analyses included multivariable logistic regression models adjusted for demographic, socioeconomic, and hospital-related factors to assess racial disparities. Results: The study included 514,750 White, 321,395 Black, and 146,600 Hispanic patients, with smaller proportions of Asian, Native American, and Other racial groups. Black patients had significantly higher odds of in-hospital mortality (OR = 1.17, 95% CI = 1.08–1.26, p < 0.001) and sudden cardiac death (OR = 1.64, 95% CI = 1.46–1.85, p < 0.001) compared to White patients. Asian patients also exhibited increased mortality risk (OR = 1.37, 95% CI = 1.14–1.63, p = 0.001) as compared to Whites. Conversely, Black (OR = 0.90, 95% CI = 0.85–0.96, p = 0.01) and Hispanic (OR = 0.87, 95% CI = 0.80–0.96, p = 0.03) patients had lower odds of MI. Racial disparities in access to care, socioeconomic status, and comorbidity burden may contribute to these differences. Conclusion: Significant racial and ethnic disparities exist in cardiovascular outcomes among hospitalized SLE patients. Black and Asian individuals face higher in-hospital all-causes mortality and sudden cardiac death risks, while Black and Hispanic patients exhibit lower MI rates. Addressing social determinants of health, improving access to specialized care, and implementing targeted interventions may reduce disparities and improve outcomes in minority populations with SLE. Full article

Introduction: The obesity paradox has been observed in patients with cardiovascular disease. The goal of this study was to evaluate whether obesity has a protective effect in patients presenting with cardiogenic shock. Method: Using a large Nationwide Inpatient (NIS) sample database, we evaluated mortality in patients with cardiogenic shock based on weight categories in adults. Results: A total of 843,020 patients over age 18 had a diagnosis of cardiogenic shock in the database. We found that overweight and obesity had the lowest mortality using univariate or multivariate analysis (overweight mortality of 20.66% vs. obesity mortality of 26.6% vs. 34.8% of normal weights). In contrast, cachexia was associated with the highest mortality in univariate analysis (cachexia 40.4%). Using multivariate analysis adjusting for age, baseline characteristics, and comorbidities, these relations remained unchanged (cachexia MVOR: 1.13; CI: 1.21–1.13; p < 0.001; overweight MVOR: 0.52, CI: 0.43–0.65; p < 0.001; obesity MVOR: 0.76, CI: 0.73–0.79; p < 0.001). After multivariate adjustment, morbid obesity had similar mortality to patients with normal weight (morbid obesity MVOR: 0.99 CI 0.95–01.03; p = 0.6) Conclusions: We observe a partial obesity paradox in patients with cardiogenic shock, showing that being overweight, followed by obesity, has the lowest mortality, whereas cachexia has the highest mortality despite multivariate adjustment. Full article

Background: Myocardial ischemia remains a major cause of morbidity and mortality worldwide. Although traditional risk factors are well-established, genetic predisposition—particularly involving MTHFR polymorphisms—has garnered increasing attention. This study investigates the association between MTHFR C677T and A1298C polymorphisms and first-episode myocardial ischemia in a Romanian population. Methods: This study included 69 adult patients with first-episode myocardial ischemia and 55 healthy controls, matched by age and sex. Participants were recruited from southeastern Romania between 2023 and 2025. Clinical data—such as blood pressure, body mass index, smoking, and alcohol consumption—were recorded. Genotyping for MTHFR C677T and A1298C polymorphisms was performed using a real-time PCR-based assay (Bosphore^® MTHFR 677-1298 Detection Kit v2), following the manufacturer’s protocol. Results: A significantly higher frequency of homozygous mutant genotypes was observed in patients with myocardial ischemia. The TT genotype of MTHFR C677T was present in 71% of patients, compared to only 7.3% of controls. Similarly, the CC genotype of A1298C was detected in 59.4% of patients, versus 7.3% in controls. These genotypic patterns suggest a strong genetic predisposition among affected individuals. The association between MTHFR polymorphisms and myocardial ischemia was particularly evident in participants over 50 years of age, indicating a possible interaction between genetic vulnerability and age-related cardiovascular risk. Conclusions: Our findings indicate a strong association between MTHFR C677T and A1298C homozygous mutant genotypes and the risk of first-episode myocardial ischemia, particularly in older adults. These results underscore the potential role of genetic screening in early cardiovascular risk stratification. Full article

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease associated with high morbidity and mortality. Both pulmonary and extrapulmonary comorbidities significantly influence disease progression and patient outcomes. Despite current therapeutic options, effective treatments remain limited. Quercetin, a naturally occurring flavonoid, has emerged as a promising compound due to its antioxidant, anti-inflammatory, and antifibrotic properties. Preclinical and clinical studies have demonstrated its ability to modulate key molecular pathways involved in IPF, including Nrf2, SIRT1/AMPK, and the regulation of fibrosis-associated microRNAs (miRNAs). Furthermore, quercetin shows therapeutic potential across a range of IPF-related comorbidities, including chronic obstructive pulmonary disease, pulmonary hypertension, lung cancer, cardiovascular disease, diabetes, and psychiatric disorders. Under these conditions, quercetin acts via epigenetic modulation of miRNAs and regulation of oxidative stress and inflammatory signaling pathways. This review highlights the multifunctional role of quercetin in IPF and its comorbidities, emphasizing its gene regulatory mechanisms and potential as an adjunctive or alternative therapeutic strategy. Full article

Background and Objectives: Cardiac transplantation is currently the elective treatment choice in end-stage heart failure, and cellular rejection is a predictive factor for morbidity and mortality after surgery. We proposed an evaluation of the clinicopathologic factors involved in the mechanism of rejection. Materials and Methods: This study included 146 patients who underwent transplantation at the Institute of Cardiovascular Diseases and Transplantation in Targu Mures between 2010 and 2023, and we evaluated the function and structure of the myocardium after surgery by using endomyocardial biopsy. Results: Overall, 120 men and 26 women underwent transplantation, with an approximately equal proportion under and over 40 years old (48.6% and 51.4%). Evaluating the degree of acute cellular rejection according to the International Society for Heart and Lung Transplantation classification showed that most of the patients presented with acute cellular rejection (ACR) and antibody-mediated rejection (AMR) grade 0, and most cases of ACR and AMR were reported with mild changes (13% or 10.3% patients). Therefore, the most frequent histopathologic diagnoses were similar to lesions unrelated to rejection (45.2% of patients) and ischemia–reperfusion lesions (25.3% patients), respectively. Conclusions: Although 82.2% of the transplanted cases showed no rejection (ISHLT score 0), non-rejection-related lesion-like changes were present in 45.2% of cases, and because more of the non-rejection-related criteria could be detected, it may be necessary to adjust the grading of the rejection criteria. The histopathologic changes that characterize rejection are primarily represented by the mononuclear inflammatory infiltrate; in our study, inflammatory changes were mostly mild (71.9%), with myocyte involvement in all cases. These changes are associated with and contribute to the maintenance of the rejection phenomenon. Full article

This study investigated associations of inflammation-based biomarkers with endothelial dysfunction and lipids and their predictive value for clinical outcome parameters in patients with giant cell arteritis (GCA). A total of 138 patients with inactive GCA were retrospectively analyzed to investigate potential differences in inflammatory biomarkers regarding clinical GCA subtypes and potential correlations between inflammatory parameters with markers of endothelial dysfunction and lipid parameters. Additionally, the predictive role of inflammatory biomarkers for clinical outcomes, including disease relapse, all-cause mortality, cardiovascular events, and glucocorticoid adverse effects, was analyzed. GCA individuals without concomitant symptoms of polymyalgia rheumatica and those who received initial glucocorticoid pulse therapy exhibited significantly higher levels of white blood cells and neutrophils (all with p < 0.05). No other significant differences were observed between inflammatory biomarkers and clinical GCA subtypes. Additionally, significant correlations were identified between selected inflammation-based ratios and specific markers of endothelial dysfunction and lipid parameters (all with p < 0.05). Elevated white blood cells and neutrophils were significant and independent predictors of disease relapse in GCA (all with p < 0.05) in multiple logistic regression analysis. No significant associations were found between any other inflammatory biomarker and the occurrence of cardiovascular events, mortality, or glucocorticoid-related adverse effects. In patients with inactive GCA, selected inflammatory parameters correlated with endothelial dysfunction and dyslipidemia and may be predictive of disease relapse. Full article

Aim: The frontal QRS-T (fQRS-T) angle serves as an electrocardiography indicator that visually represents the disparity between the frontal QRS axis and the T axis. The heterogeneity between cardiac depolarization and repolarization rises with an increase in the fQRS-T angle. Prior research has demonstrated a relationship between the fQRS-T angle and the extent of atherosclerosis, along with the risk of cardiovascular mortality. The non-alcoholic fatty liver disease fibrosis score (NFS) is a non-invasive scoring tool used to quantify the degree of liver fibrosis in individuals with non-alcoholic fatty liver disease (NAFLD). Non-alcoholic fatty liver disease increases the risk of atherosclerotic cardiovascular disease, which can be predicted using the NFS. The objective of this study is to examine the potential correlation between the fQRS-T angle and NFS in patients with stable angina pectoris. Materials and Methods: This cross-sectional study included 177 (48 women) non-alcoholic patients who underwent coronary angiography due to stable angina pectoris. Individual NFS values were calculated using clinical and laboratory data. Patients were categorized into two groups based on a NFS threshold value of 0.67. Following a minimum fasting period of 12 h, biochemical laboratory parameters were acquired using a peripheral venous sample, and electrocardiographic data were recorded. Results: The univariate logistic regression analysis revealed significant associations between hypertension (p = 0.018), coronary artery disease (p = 0.014), neutrophil (p = 0.024), hemoglobin (p = 0.038), and low-density lipoprotein (LDL, p = 0.007) with the NFS. The electrocardiographic variables related to the score included the QRS duration (p = 0.015), Pmax (p = 0.026), QTC interval (p = 0.02), and fQRS-T angle (p < 0.001). In the multivariate logistic regression analysis, NFS was independently associated with LDL (OR: 0.984, 95% CI: 0.970–0.998, p = 0.024) and fQRS-T angle (OR: 3.472, 95% CI: 1.886–6.395, p < 0.001). Conclusions: The FQRS-T angle may exhibit a distinct correlation with NAFLD. Extensive investigations should validate this link, since the fibrosis score can serve as an effective tool for monitoring patients prior to the onset of clinical symptoms associated with liver fibrosis. Full article

Aging is a multifaceted biological process characterized by a progressive decline in cellular function and physiological resilience, increasing the risk of multiple chronic conditions. Chronic lung diseases frequently manifest within the aging population and are closely intertwined with systemic dysfunctions across cardiovascular, musculoskeletal, and neurological systems. In this review, we explore the biological mechanisms linking aging, multiple chronic conditions patterns, and chronic lung disease, with a particular focus on inflammaging and cellular aging. We also highlight shared pathological pathways such as oxidative stress, mitochondrial dysfunction, and the dysregulation of repair processes that underlie both natural aging and the accelerated aging seen in chronic lung disease. Additionally, we discuss the systemic impact of multiple chronic conditions on patient outcomes, including increased frailty, diminished physical capacity, cognitive impairment, and elevated mortality risk. This review advocates for a comprehensive, patient-centered approach that combines early detection, personalized pharmacological therapies targeting inflammatory and senescent pathways, and non-pharmacological interventions such as pulmonary rehabilitation, exercise, and dietary optimization. Emerging therapeutics, including senolytics and anti-inflammatory agents, present promising avenues for mitigating age-related lung decline and managing multiple chronic conditions. Full article

Systemic lupus erythematosus (SLE) is a multisystem auto-immune disease that may affect any organ/system, including the cardiovascular system. Several studies have shown that SLE is associated with an increased risk of cardiovascular disease (CVD), even though most of the patients who have lupus are young women. In this review, we present that apart from the traditional risk factors, there are more appropriate SLE-related indices such as imaging parameters, auto-antibodies, disease manifestations, medications, and genetic factors that might represent useful tools to create an algorithm for early identification of SLE patients at increased risk of CVD. Early recognition and appropriate treatment of patients at increased CVD risk might reduce morbidity/mortality and improve the quality of life of patients with SLE. Full article

Background: The atherogenic index of plasma (AIP), a prognostic indicator for cardiovascular disease, has not been fully explored in relation to clinical outcomes in patients receiving peritoneal dialysis. This study aims to elucidate the relationship between baseline AIP levels and all-cause mortality, cardiovascular mortality, and the peritonitis risk in this population. Methods: This retrospective cohort study included incident peritoneal dialysis patients in our center from 1 January 2006 through 31 December 2021. The end of the follow-up time was 31 December 2023. The participants were stratified by baseline AIP levels. Kaplan–Meier curves, Cox regression analyses, and subgroup analyses were used to evaluate associations with clinical outcomes. Results: The average age of the 2460 participants in this study was 45.9 years, and 1456 (59.2%) of them were men. Diabetic nephropathy (19.5%) was the second most common kidney disease, after primary glomerulonephritis (60.8%). The higher AIP tertile group was significantly associated with increased risks of all-cause mortality, cardiovascular mortality, and peritonitis compared to the lowest AIP group, as evidenced by the Kaplan–Meier curves and the multivariate analyses. Continuous AIP levels also showed a positive correlation with the all-cause mortality and peritonitis risk, even after controlling for covariates. Conclusions: Our study highlights AIP as a predictive marker for adverse outcomes in PD patients, emphasizing its potential utility in risk stratification and clinical management. Full article

Over the past three turbulent decades, research has profoundly reshaped our understanding of chronic Toxoplasma gondii infection—traditionally regarded as harmless in immunocompetent individuals—unveiling its surprising impact on human health, performance, and behavior. This review emphasizes the effects of chronic Toxoplasma infection on physical and mental health, cognitive performance, and behavioral changes, highlighting key findings from studies investigating these domains, with a particular focus on both ultimate and proximate mechanisms underlying the observed effects. To this end, the primary focus will be on human studies; however, animal model studies will also be thoroughly considered when necessary and appropriate, to provide context and additional important information. Research demonstrates that chronic Toxoplasma infection may contribute to a broad spectrum of physical health issues. Ecological studies have revealed correlations between toxoplasmosis prevalence and increased morbidity and mortality from various conditions, including cardiovascular diseases, neurological disorders, and certain cancers. Large-scale cross-sectional studies have further shown that infected individuals report a higher incidence of numerous health complaints and diagnosed diseases, suggesting a significant impact on overall physical well-being. In addition to physical health, lifelong Toxoplasma infection (subclinical toxoplasmosis) has been implicated in cognitive impairments and behavioral changes. Studies have reported associations between infection and poorer performance in areas such as reaction time, processing speed, working memory, and executive function. Many of these behavioral changes likely relate to worsened health and a shift towards a “fast life history strategy.” These cognitive deficits can have significant implications for daily functioning and performance. Furthermore, the role of Toxoplasma infection in the development or exacerbation of mental health disorders has been extensively investigated. Meta-analyses, ecological studies, and large-scale observational studies have demonstrated associations between Toxoplasma infection and an increased risk of disorders such as schizophrenia and obsessive–compulsive disorder. While the precise mechanisms underlying these associations remain under investigation, research suggests that neuroinflammation and alterations in neurotransmitter systems are likely to play a role. Far from being harmless, subclinical toxoplasmosis is increasingly recognized as a hidden factor influencing human health, behavior, and cognitive performance—with implications that extend well beyond the individual to public health at large. Further research is warranted to elucidate the complex interplay between Toxoplasma infection, host physiology, and the development of various physical, cognitive, behavioral, and mental health conditions. Full article