
Introduction Despite earlier evidence, the benefit of long-term β-blockers after myocardial infarction (MI) in patients with preserved or mildly reduced ejection fraction remains unclear in the modern reperfusion era. Material and Methods We conducted a PRISMA-guided systematic review and meta-analysis by searching the PubMed, Google Scholar, and Cochrane databases, pooling results using a random effects model with 95% CIs. Results Five RCTs, including a total of 23,524 participants, were analysed. β-blocker therapy showed no significant effect on all-cause mortality (RR = 0.98, 95% CI: 0.87–1.11) or cardiovascular mortality (RR = 1.06, 95% CI: 0.83–1.36). Similarly, no significant differences were observed for secondary outcomes: major adverse cardiovascular events (MACE) (RR = 0.96, 95% CI: 0.85–1.07), recurrent MI (RR = 0.89, 95% CI: 0.78–1.02), stroke (RR = 1.27, 95% CI: 0.92–1.76), or hospitalisations for HF (HF) (RR = 0.77, 95% CI: 0.56–1.05). Conclusions Long-term β-blockers showed no reduction in mortality, recurrent MI, stroke, MACE, or HF admissions, indicating limited routine benefit.
Artificial Intelligence (AI) could be integrated into Primary Health Care (PHC) to enhance the preventive care of several diseases. This scoping review aims to provide current evidence on AI applications for the prevention of non-infectious diseases in PHC. A structured search was conducted in PubMed/Medline and Scopus databases to identify studies evaluating AI-based interventions implemented in the preventive care of non-infectious diseases in the PHC sector. AI-supported preventive care was compared to standard preventive care or non-AI-based interventions. Preventive medicine was defined as at least one primary outcome related to disease incidence, risk reduction, and early detection rates of non-infectious diseases. AI demonstrates significant potential in preventive medicine in PHC as it enables proactive, personalized, and data-driven interventions. However, its adoption requires strategies to overcome technical, ethical, and organizational barriers. Future research should address real-world implementation, cost-effectiveness, and clinician engagement to maximize clinical impact.
Introduction:Perioperative atrial fibrillation (POAF) remains the most common arrhythmic complication occurring in the setting of isolated coronary artery bypass grafting (CABG), and it is now being increasingly recognised as a marker of early postoperative morbidity, rather than a simple rhythm disturbance. The aim of the research to find the independent clinical and procedural predictors of POAF in patients with isolated CABG, as well as to assess the relationship with early clinically significant outcomes. Material and methods:In this single-centre retrospective cohort analysis, consecutive adult patients who received isolated CABG surgery between January 2022 and December 2025 were included. Patients with a history of atrial fibrillation/flutter, simultaneous cardiac surgery, and incomplete perioperative records were excluded. POAF was identified as new atrial fibrillation/flutter occurring within seven days of surgery or before discharge. Multivariate logistic regression analysis was used to evaluate independent predictors of POAF. Early postoperative outcomes were compared between patients with and without POAF. Results:In the study involving 550 patients, POAF occurred in 150 (27.3%) patients. Multivariate analysis showed that advanced age, chronic kidney disease, increased left atrial dimension, decreased left ventricular ejection fraction, prolonged cardiopulmonary bypass time, and perioperative red blood cell transfusion were significant predictors of POAF. Patients with POAF had increased rates of acute kidney injury (22.0% vs. 11.0%, p = 0.001), increased intensive care unit stay, and increased hospital stay, compared to those without POAF. There was no significant difference in in-hospital mortality. Conclusions:In the case of isolated CABG, the incidence of POAF is related to a higher incidence of early postoperative morbidity, but it is not related to in-hospital mortality. The identification of at-risk patients with the use of clinical data could contribute to the evaluation of risk stratification.
Introduction Chronic total occlusion (CTO) of the common iliac artery (CIA) represents a technically challenging subset of aorto-iliac occlusive disease, particularly when the lesion extends close to the aorto-iliac bifurcation. Although endovascular therapy has become the preferred treatment modality, the optimal access strategy for unilateral CIA CTO remains uncertain. This study aimed to evaluate the feasibility, procedural control, and clinical outcomes of a planned first-line bilateral femoral access strategy in unilateral CIA CTO. Material and methods This retrospective single-centre study included 30 consecutive patients with unilateral CIA CTO who underwent endovascular revascularisation using a first-line bilateral femoral approach between January 2020 and December 2024. Continuous contralateral diagnostic angiography was used to guide the lesion crossing and stent deployment. Lesions were classified according to the TransAtlantic Inter-Society Consensus (TASC II). Technical success was defined as residual stenosis < 30% with restoration of antegrade flow. Procedural complications and mid-term clinical outcomes were assessed. Results Most lesions were classified as TASC II C–D (86.7%). Technical success was achieved in 93.3% of cases. Periprocedural complications were infrequent and included access-site haematoma (6.7%), flow-limiting dissection (3.3%), and distal embolisation (3.3%). During a median follow-up of 13 months, symptom recurrence occurred in 20.0% of patients. Imaging performed in symptomatic patients confirmed restenosis or reocclusion in 13.3%, and target lesion revascularisation was required in 10.0% of cases. Conclusions A planned first-line bilateral femoral endovascular approach for unilateral CIA CTO is feasible and safe, achieving high technical success with low complication rates even in predominantly TASC II C–D lesions. By enhancing procedural control and bifurcation preservation, this strategy may be particularly valuable in anatomically complex cases.
Introduction Loop diuretics are a cornerstone in the symptomatic management of heart failure. There is conflicting evidence regarding potential differences between torsemide and furosemide in their effects on heart failure outcomes. Therefore, we conducted a meta-analysis of randomized controlled trials (RCTs) to compare the therapeutic efficacy of furosemide versus torsemide in the management of heart failure. Methods Medline/PubMed, Embase, and Cochrane Central Register of Controlled Trials were queried for studies comparing furosemide to torsemide in heart failure from inception to January 2023. Outcomes of interest included all-cause mortality, hospitalization due to heart failure, and weight change. Results Our analysis included 10 RCTs comprising 4011 patients, of whom 2019 were treated with furosemide and 1992 patients were treated with torsemide. There was no significant difference between the groups in terms of all-cause mortality (OR = 0.99; 95% CI: 0.97–1.02; p = 0.66; I2 = 0.03%) or heart failure hospitalization (OR = 0.96; 95% CI: 0.87–1.06; p = 0.38; I2 = 89%). Both diuretics had a significant effect on weight change: torsemide (mean difference 2.36; 95% CI: 0.5–4.22; p = 0.01; I2 = 0.0%) and furosemide (mean difference 2.48; 95% CI: 0.81–4.15; p = 0.00; I2 = 0.0%). There was no significant difference in weight change between the two diuretics (mean difference –0.15; 95% CI: –0.82–0.52; p = 0.66; I2 = 94%). Conclusions Furosemide and torsemide have similar impacts on mortality, hospitalization due to heart failure, and weight change in patients with congestive heart failure.
Introduction P2Y12 inhibitor monotherapy has emerged as a potential alternative to aspirin following dual antiplatelet therapy (DAPT) in patients undergoing percutaneous coronary intervention (PCI), but the optimal choice remains uncertain. Methods A systematic literature search compared P2Y12 inhibitors with aspirin post PCI. A random-effects model pooled odds ratios (ORs) with 95% confidence intervals (CIs) for outcomes. Results Seven studies (29,756 patients) were included. P2Y12 inhibitors significantly reduced MACE compared to aspirin [OR = 0.73; 95% CI: 0.64–0.84]. No significant difference was observed in all-cause mortality [OR = 0.90; 95% CI: 0.77–1.05], cardiac death [OR = 0.86; 95% CI: 0.68–1.09], major bleeding [OR = 1.06; 95% CI: 0.67–1.68], MI [OR = 0.78; 95% CI: 0.56–1.08], or stent thrombosis [OR = 0.71; 95% CI: 0.41–1.22]. P2Y12 inhibitors significantly reduced repeat revascularisation [OR = 0.83; 95% CI: 0.73–0.94] and stroke [OR = 0.63; 95% CI: 0.48–0.81]. Conclusions P2Y12 inhibitors may be a safer, more effective alternative to aspirin alone after PCI.
Acral ischaemia and necrosis are rare but severe complications of high-dose or prolonged vasopressor therapy in critically ill patients. Although these agents are life-saving in distributive shock, intense a-adrenergic vasoconstriction, microcirculatory failure, and coagulopathy can converge to cause irreversible digital or limb necrosis, often requiring amputation and sometimes leading to medicolegal disputes. We report two cases of vasopressor-associated acral necrosis. These cases illustrate the multifactorial pathogenesis of vasopressor-induced acral necrosis, in which profound vasoconstriction, endothelial injury, microthrombosis, and the severity of underlying shock lead to distal tissue loss despite intact large-vessel pulses. Consequences include prolonged hospitalisation, the need for staged surgical or reconstructive procedures, long-term functional deficits, and substantial psychosocial burden. The dramatic nature of limb loss after life-saving therapy frequently triggers medicolegal scrutiny regarding dosing, monitoring, and documentation. Awareness of this uncommon but devastating complication is essential.
Introduction:Metabolic syndrome (MetSy) is associated with chronic low-grade inflammation and metabolic dysfunction, contributing to increased cardiometabolic risk. Low-volume plasma exchange (LVPE) is an emerging extracorporeal therapy designed to reduce systemic inflammation by removing circulating pro-inflammatory mediators. This study evaluated the effects of LVPE on metabolic endotoxemia, inflammation, and mineral metabolism in individuals with MetSy. Material and methods:A total of 48 adults with MetSy were enrolled, including 33 men and 15 women, with an average age of 50 years (men: 51 years; women: 48 years). All participants met established diagnostic criteria for MetSy. Each underwent four LVPE cycles using nanoporous membranes designed to selectively remove pro-inflammatory mediators while preserving essential plasma components. Biomarkers of systemic inflammation (CRP, hsCRP), endotoxemia (LBP, zonulin), and mineral metabolism (zinc, magnesium, iron) were measured before and after treatment. Results:LVPE significantly reduced CRP levels (p < 0.020), demonstrating attenuation of systemic inflammation. A downward trend in hsCRP was observed (p < 0.050), though without reaching statistical significance. LVPE did not significantly affect endotoxemia markers (LBP, zonulin) or IL-6 (all p > 0.05). A significant post-treatment increase in zinc levels was detected (p < 0.009), while magnesium and iron remained unchanged (p > 0.05). A significant correlation between LBP and CRP after treatment (p < 0.027) suggests that LVPE may modulate systemic inflammation through immune regulatory pathways rather than by directly influencing endotoxemia. Conclusions:Four cycles of LVPE effectively reduced low-grade inflammation, as indicated by decreased CRP levels, supporting its potential role as a therapeutic approach in managing inflammation in MetSy. Its effects on endotoxemia and gut permeability remain inconclusive, underscoring the need for additional research to clarify long-term and mechanistic outcomes.
Introduction Breast cancer remains the most common malignancy in women worldwide, with prognosis influenced not only by tumor-intrinsic factors but also by the tumor microenvironment. Adipokines, including visfatin, lipocalin-2, adiponectin, and chemerin, have been increasingly implicated in breast cancer biology, influencing inflammation, metabolism, angiogenesis, and the tumor microenvironment (TME). However, their precise contribution to tumor progression and their association with common prognostic markers remain unclear. The expression patterns of these adipokines were evaluated in invasive ductal carcinoma and explored their relationship with established clinicopathological parameters. Material and methods Breast cancer diagnosed cases were analyzed in 2018 at the University General Hospital of Patras. Immunohistochemistry was performed for visfatin, lipocalin-2, adiponectin, and chemerin. Marker expression was correlated with estrogen receptor (ER), progesterone receptor (PR), HER2/c-ERB2, Ki67, and lymphovascular invasion (LVI). Results Visfatin and adiponectin both showed significant associations between high Ki67 and LVI (p = 0.0049 and p = 0.00044, respectively). In addition, ER negativity was linked to LVI for these two adipokines (p = 0.0175 for both). By contrast, lipocalin-2 did not show significant correlations, although borderline values for ER and PR suggested a possible trend. Conclusions These findings point to visfatin and adiponectin as potential indicators of aggressive breast cancer phenotypes, while lipocalin-2 may follow a different biological trajectory. Larger, prospective studies are warranted to confirm these associations and clarify underlying mechanisms.
Introduction:This study aimed to determine the prevalence of dyslipidemia and to assess the predictive performance of lipid ratios, specifically the Atherogenic Index of Plasma (AIP) and the total cholesterol (TC) to high-density lipoprotein cholesterol (HDL-C) (TC/HDL) ratio, compared to body mass index (BMI) in identifying dyslipidemia among non-obese male university students. Material and methods:A cross-sectional study was conducted among 150 male students aged 20-30 years at a Saudi Arabian university. Participants underwent fasting lipid profiling, anthropometric measurements, and assessments of lifestyle behaviors including diet, physical activity, and smoking. Dyslipidemia was defined based on the NCEP-ATP III criteria. Predictive accuracy of AIP, TC/HDL ratio, and BMI was evaluated using receiver operating characteristic (ROC) curve analysis and logistic regression. Results:Dyslipidemia was detected in 60.7% of participants, despite a mean BMI of 25.3 ±4.0 kg/m², indicating that a substantial proportion of metabolically at-risk individuals were not obese. Unhealthy lifestyle behaviors were associated with an approximately eightfold increase in the odds of dyslipidemia (p < 0.001). Both AIP (AUC = 0.865) and TC/HDL ratio (AUC = 0.873) demonstrated significantly superior predictive performance compared with BMI (AUC = 0.570). More than 63% of students were classified as high-risk based on AIP levels. Cluster analysis revealed a distinct LDL-TG dominant phenotype strongly associated with unhealthy lifestyle factors. Conclusions:Lipid ratios, particularly AIP and TC/HDL, outperformed BMI in predicting early dyslipidemia among non-obese young adults. Incorporating these indices into routine screening could facilitate earlier detection of cardiovascular risk in university and preventive health settings, emphasizing the importance of targeted lifestyle interventions.
Introduction:Hypertrophic cardiomyopathy (HCM) is a common genetic cardiac disorder associated with significant morbidity and mortality. Cardiac myosin inhibitors (MIs), including mavacamten and aficamten, offer a novel therapeutic approach for HCM. Methods:An online database search was performed from inception to September 2024. We selected randomized controlled trials (RCTs) that compared mavacamten with placebo/guideline medical treatment for HCM. Results:Six RCTs involving 1,081 participants were analyzed. Cardiac myosin inhibitors significantly reduced left ventricular outflow tract (LVOT) gradients at rest (-70.22 mm Hg, 95% CI: -85.42 to -55.03) and during the Valsalva maneuver (-61.44 mm Hg, 95% CI: -71.10 to -51.78). Patients experienced improved functional status, with a pooled risk ratio (RR) of 2.21 (95% CI: 1.75 to 2.80, p < 0.05) for at least one NYHA class improvement and an enhanced Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) (+7.80 points, 95% CI: 4.58 to 11.02, p < 0.05). Biomarkers, including NT-proBNP (-69.41 pg/ml, 95% CI: -87.06 to -51.75, p < 0.05) and cardiac troponin I (cTnI) (-42.66 ng/l, 95% CI: -48.47 to -36.85, p < 0.05), showed significant reductions. Reductions in left ventricular ejection fraction (LVEF) were observed, with aficamten demonstrating a greater reduction (-10.35%, 95% CI: -13.48 to -7.21) compared to mavacamten (-2.50%, 95% CI: -6.21 to 1.20). Safety analyses showed no significant increase in treatment emergent adverse events (TEAEs) (RR = 1.02, 95% CI: 0.92 to 1.14), serious adverse events (SAEs) (RR = 0.69, 95% CI: 0.37 to 1.28), or atrial fibrillation (RR = 0.77, 95% CI: 0.27 to 2.23). Conclusions:MIs significantly improve symptomatic, functional, and biomarker outcomes in symptomatic HCM while maintaining an acceptable safety profile, highlighting their potential as a transformative treatment option. Further studies are warranted to evaluate long-term efficacy and safety.
Cardiopulmonary bypass (CPB) is one of the most groundbreaking medical innovations in history, enabling safe and effective heart surgery by temporarily replacing the function of the heart and lungs. This article begins with ancient concepts of cardiopulmonary function, then traces the evolution of CPB through important physiological and anatomical discoveries, culminating in the development of the modern heart-lung machine. In addition to examining the contributions of significant figures such as Galen, Ibn al-Nafis, William Harvey, and John Gibbon, we also explore the ethical and technical challenges encountered in the early days of open-heart surgery. The historical trajectory of pneuma illustrates the transition from speculative medical theories to empirical science. While no longer relevant in modern physiology, pneuma has left an enduring legacy in medical terminology and holistic perspectives on health, highlighting the deep connections between ancient and contemporary medical thought.
Introduction:Isolated cardiac sarcoidosis (ICS) is characterized by a lack of the apparent extra-cardiac involvement seen in systemic cardiac sarcoidosis (SCS) and is being increasingly recognized as a distinct clinical phenotype of cardiac sarcoidosis. This systematic review and meta-analysis pooled data from published literature to assess any differences in outcomes of ICS vs. SCS patients. Methods:Studies were identified from PubMed/Medline, Embase, and the Cochrane Library. Risk ratios were calculated using the Mantel-Haenszel method in a random effects model. Heterogeneity was assessed using the Higgins I 2 statistic. Leave-one-out sensitivity analysis was also performed. The primary outcome was a composite of MACE, including cardiac death, ventricular arrhythmias, or hospitalization for heart failure. The secondary outcomes included sudden cardiac death, arrhythmias, and heart-failure-related hospitalizations. Results:The analysis included 7 studies and 918 CS patients (28.9% ICS and 71.1% SCS). Increased risk for arrhythmias (RR = 3.06, 95% CI: 0.98 to 9.55, p = 0.05, I 2 = 67%) in patients with ICS compared to SCS was observed. No significant difference was observed for composite outcome (RR = 1.43, 95% CI: 0.93 to 2.18, p = 0.10, I 2 = 0%), HF-related hospitalizations (RR = 6.83, 95% CI: 0.47 to 100.33, p = 0.16, I 2 = 80%), or cardiac death (RR = 1.85, 95% CI: 0.49 to 7.08, p = 0.37, I 2 = 0%) between the two groups. Conclusions:Although ICS patients were more likely to experience arrhythmias, no significant difference was observed between ICS and SCS patients for composite outcome, cardiac death, or hospitalizations due to heart failure.
Introduction:Myocardial injury, indicated by elevated troponin levels, is common among patients hospitalized with COVID-19. This study aimed to evaluate the correlation between the degree of myocardial injury in myocarditis patients and imaging parameters of systolic and diastolic cardiac function and clinical outcome over a 6-month follow-up period. Material and methods:Atotal of 59 COVID-19 myocarditis patients with elevated high-sensitivity troponin levels (hs-cTnI) were included. Demographic data, laboratory results, and clinical outcomes were collected from hospital electronic health records. All patients underwent cardiac magnetic resonance imaging (cMRI) and a comprehensive echocardiographic evaluation at baseline and at the 6-month follow-up. Results:COVID-19 myocarditis was confirmed in all patients undergoing cMRI. The mean hs-cTnI level among the patients was 281.27 ±400.86 ng/l. Hs-cTnI elevation showed a significant positive correlation with left ventricular global longitudinal strain (LVGLS) values (p < 0.001, r = 0.6) but not with right ventricular global longitudinal strain (RVGLS) values (p = 0.155, r = 0.187). Reduced LVGLS values were significantly associated with late gadolinium enhancement (LGE) (p < 0.001, r = 0.509) in cMRI and with the administration of antiviral medications, including treatment of remdesivir (p < 0.001, r = 0.62) indicative of more severe disease. Conclusions:The increase in hs-cTnI levels in COVID-19 myocarditis patients is associated with future impairment in left ventricular systolic function and deterioration of left ventricular myocardial strain. These findings highlight the importance of monitoring cardiac function in patients with acute myocarditis following COVID-19 infection during long-term follow-up.
Cardiovascular diseases (CVDs) are the leading cause of global morbidity and mortality, with oxidative stress and redox imbalance playing pivotal roles in their initiation and progression. In this comprehensive review, we explore the molecular mechanisms by which reactive oxygen and nitrogen species disrupt vascular homeostasis, promote endothelial dysfunction, and drive adverse cardiac remodeling. We highlight key redox-sensitive pathways, including NADPH oxidase activation, mitochondrial dysfunction, endothelial nitric oxide synthase uncoupling, and endoplasmic reticulum stress. Emerging oxidative stress biomarkers, such as 8-iso-prostaglandin F2α, oxidized low-density lipoprotein, and myeloperoxidase, are critically examined for their diagnostic and prognostic relevance. Additionally, we discuss therapeutic strategies targeting oxidative stress, ranging from conventional antioxidants to novel mitochondrial-directed and enzyme-specific interventions. Despite advances in understanding the redox landscape of CVDs, challenges remain in translating these insights into effective clinical therapies. Future research integrating omics technologies, precision medicine, and combined lifestyle-pharmacological approaches may offer new opportunities for redox-based cardiovascular interventions.
Systemic sclerosis (SSc) is an autoimmune disorder causing immune dysregulation, leading to microvascular damage and fibrosis. Cardiovascular involvement begins with endothelial dysfunction and progresses to vasospasm, ischemia, and fibrosis, impairing cardiac function. Common manifestations include myocardial fibrosis, conduction abnormalities, heart failure, and valvular dysfunction, affecting 15–35% of patients and contributing to 27.2% of SSc-related deaths. High-risk factors include male gender, older disease onset, African American ethnicity, diffuse cutaneous SSc, and poor quality of life. Subclinical cardiac dysfunction is common but underdiagnosed, and cardiovascular complications worsen outcomes. Pulmonary arterial hypertension is a major cause of morbidity and mortality and requires early diagnosis and multidisciplinary management. Treatments include calcium channel blockers, phosphodiesterase inhibitors, endothelin receptor antagonists, and prostacyclin analogs. Imaging (echocardiography, cardiac MRI, stress tests) and biomarkers (troponin, NT-proBNP, endothelin-1) help in diagnosis and monitoring. Early recognition and comprehensive management improve patient outcomes.