Objectives: Performing percutaneous mitral commissurotomy (PMC) in the women with asymptomatic severe mitral stenosis (MS) who plan a pregnancy is recommended. However the data regarding this recommendation is limited in the literature. We aimed to investigate maternal and fetal outcomes of women with asymptomatic severe MS who underwent PMC before a planned pregnancy. Methods: We retrospectively analysed the procedural, pregnancy related, and fetal outcomes of 33 consecutive women with severe asymptomatic MS, age 27.97 ± 2.86 years, who underwent PMC before a planned pregnancy between 2014 and 2019. The control group comprised of 66 pregnant women, age 29.09 ± 3.00 years, without a cardiac disease. Results: The PMC procedure was successful in all patients and no major complication occurred. There were no deaths, pulmonary oedema, heart failure, atrial fibrillation, and thromboembolism during pregnancy. Maternal arrhythmia (p < .001), deterioration in NYHA class (p = .08), and use of cardiovascular medication (p < .001) was significantly higher in the study group. Maternal hospitalisation (p = .435), preeclampsia (p = 1), abortus (p = 1), fetal death (p = 1), and preterm delivery (p = .746) was similar between groups. Birth weight was significantly lower in the PMC group 2890 g (229) vs 3120 g (255) <0.001, however small for gestational age newborns were similar between groups (p = .12). Conclusions: PMC is safe in asymptomatic women with severe MS planning a future pregnancy. In selected patients with favourable valve anatomy PMC may improve maternal and fetal outcomes.

Although oxidative stress plays a key role in the pathophysiology of acute myocardial infarction (AMI), its association with clinical risk-scoring systems (SYNTAX/ACEF) remains limited. This study examined the relationships between oxidative stress biomarkers and risk scores in patients with AMI, using bootstrap validation to evaluate statistical reliability. This cross-sectional study included 207 participants: 65 with STEMI, 62 with NSTEMI, and 80 controls. Oxidative stress biomarkers (malondialdehyde [MDA], protein carbonyl [PCO], total sulfhydryl [TSH], glutathione S-transferase [GST], glutathione reductase [GR], glutathione peroxidase [GPx], and reduced glutathione [GSH]) were measured using spectrophotometry. The SYNTAX and ACEF scores were calculated for patients with AMI. Statistical analyses included Pearson correlation, multivariate linear regression, and bootstrap resampling for validation. AMI patients exhibited significantly lower antioxidant parameters (TSH, GST, GR, GPx, and GSH; all P < .001) and higher levels of oxidative stress markers (MDA and PCO; both P < .001) than controls. Strong positive correlations were observed between SYNTAX and ACEF scores in both STEMI (R = 0.72, 95% confidence interval [95% CI]: 0.65–0.78) and NSTEMI groups (R = 0.69, 95% CI: 0.61–0.76). MDA and PCO showed strong positive correlations with both scoring systems in all patient groups. Bootstrap validation revealed a hierarchy of biomarker reliability: MDA, PCO, and GST demonstrated consistent stability in all analyses, whereas GPx and GSH showed subtype-specific patterns with lower reliability, especially in NSTEMI patients. Multivariate analysis identified age, MDA, PCO, GST, GR, and GSH as independent predictors of SYNTAX score (R ² = 0.78), while only age and eGFR predicted ACEF score (R ² = 0.65). Oxidative stress biomarkers were strongly correlated with clinical risk scores in patients with AMI. Among these, MDA, PCO, and GST demonstrated the most consistent associations with anatomical complexity. While these findings suggest that integrating validated oxidative stress biomarkers into existing scoring systems may help refine prognostic accuracy and guide personalized treatment strategies for AMI, further prospective validation is required.

Trimethylamine-N-oxide (TMAO), a metabolite produced by gut microbiota, has been linked to cardiovascular disease; however, its role in acute decompensated heart failure (ADHF) remains unclear. In this prospective observational study involving 102 ADHF and 60 stable heart failure (SHF) patients, plasma TMAO levels were correlated with clinical, echocardiographic, and laboratory parameters. TMAO levels were higher in ADHF compared with SHF (median 452.9 vs 372.4 ng/mL; P < .001), showing a positive correlation with B-type natriuretic peptide (BNP) and creatinine, and an inverse correlation with left ventricular ejection fraction (LVEF), estimated glomerular filtration rate (eGFR), hemoglobin, and high-density lipoprotein (HDL) cholesterol. TMAO demonstrated fair diagnostic ability for identifying ADHF (area under the curve [AUC] = 0.751), although weaker ( P = .006) than BNP (AUC = 0.875). Multivariate analysis identified both TMAO and BNP as important discriminators. Additionally, TMAO levels were higher in ischemic than in non-ischemic heart failure ( P = .047). These findings suggest that elevated TMAO is associated with ADHF and markers of disease severity. Because TMAO levels are influenced by renal function and anemia, it may be a context-dependent adjunct to natriuretic peptides rather than a standalone diagnostic marker. Further studies are needed to determine any additional value for diagnosis and risk stratification.

Background: Obstructive sleep apnea syndrome (OSAS) is linked to pulmonary hypertension and cardiovascular risk, yet simple echocardiographic indices related to cardiopulmonary hemodynamics and cardiometabolic burden are limited. We evaluated ePLAR and epicardial adipose tissue (EAT) thickness as complementary, noninvasive echocardiographic markers associated with OSAS presence and severity in newly diagnosed patients. Methods: In this cross‐sectional study, 63 polysomnography‐confirmed OSAS patients and 63 controls with a similar distribution of age, sex, and major comorbidities underwent transthoracic echocardiography. OSAS severity was classified as mild, moderate, or severe. ePLAR (TRVmax/E/e′) and EAT were measured. Diagnostic performance was assessed by ROC analysis (apparent discrimination), and prediction models for severe OSAS were fitted using Firth penalized logistic regression with bootstrap optimism correction. Results: OSAS patients had higher EAT (0.62 ± 0.11 vs. 0.53 ± 0.06 cm) and ePLAR (0.37 ± 0.09 vs. 0.23 ± 0.04 m/s) than controls (both p < 0.001). Within OSAS, both measures increased stepwise with severity ( p < 0.001). In internally validated models, adding ePLAR and/or EAT to age/sex/BMI improved discrimination for severe OSAS. Conclusions: EPLAR and EAT were associated with OSAS presence and severity and showed good apparent discrimination for severe OSAS in this cohort; these findings are hypothesis‐generating and require external validation in clinically representative populations before any clinical implementation. Trial Registration: This study was observational and cross‐sectional in design and was not registered in a clinical trial registry because it was not an interventional clinical trial.

Objective: To determine the prevalence of toxoplasmosis in cardiac patients and investigate the relationship between toxoplasmosis and cardiac diseases. Methodology: The study included 170 patients followed up in the cardiology department (patient group) and 167 individuals without any disease who were not receiving any immunosuppressive treatment (control group). Blood samples obtained from the study participants were analyzed for anti-Toxoplasma gondii immunoglobulin G (IgG) levels via enzyme-linked immunosorbent assay. Results: Anti- T. gondii IgG was detected in 41.2% of the patient group and 29.3% of the control group. Statistical analysis showed a significant correlation between anti- T. gondii IgG seropositivity in the patient and control groups. In the patient group, anti- T. gondii IgG was detected in 65.7% of those with a history of myocardial infarction (MI), 49.4% of those undergoing coronary angiography, and 48.6% of those undergoing stenting. In the statistical evaluation of patients with a history of coronary angiography, stenting, and MI, and toxoplasmosis seropositivity, significant relationships were found separately (p = 0.016, p = 0.014, and p = 0.001, respectively). Conclusions: Patients with cardiac diseases were found to be at a higher risk for toxoplasmosis compared to healthy individuals. In individuals with cardiac diseases, it is recommended that patients should be monitored for toxoplasmosis at regular intervals and necessary precautions should be taken, considering that latent infection may be reactivated in case of immune system failure.