Carvedilol plus NAC decreased POAF incidence and duration of hospitalization compared with metoprolol and decreased POAF incidence compared with carvedilol.

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Arrhythmias have been reported to occur frequently in symptomatic patients with mitral valve prolapse (MVP). The mechanisms causing ventricular arrhythmias in patients with MVP have not been fully investigated. The purpose of this study was to determine the clinical, echocardiographic and heart rate variability parameters, and plasma concentrations of electrolytes and inflammatory markers in predicting ventricular arrhythmias in patients with MVP. A total of 58 consecutive patients with MVP were included in this study. We performed electrocardiography, echocardiography, holter analysis, routine biochemical tests including plasma concentrations of electrolytes and inflammatory markers, and evaluated the clinical characteristics. Ventricular arrhythmia defined as occurrence of any of the followings: ventricular premature contractions (VPCs), VPC couplets, and ventricular tachycardia documented by holter analysis, continuous monitoring or by electrocardiography. Twenty patients (34%) had ventricular arrhythmias, and 38 (66%) patients had no ventricular arrhythmias. Seventeen patients had VPC, 2 patients had VPC couplets and 1 patient had ventricular tachycardia. Univariable predictors of ventricular arrhythmias included isovolumetric relaxation time and the occurrence of moderate to severe mitral regurgitation. Multivariable logistic regression analysis showed that occurrence of moderate to severe mitral regurgitation was the only independent predictor of ventricular arrhythmias (relative risk: 8.42, 95% confidence interval: 1.49-47.64, p = 0.01). Present study showed that the only independent predictor of ventricular arrhythmias in patients with MVP is the occurrence of moderate to severe mitral regurgitation.

Previous studies have reported increased platelet activation and aggregation in patients with obstructive sleep apnea (OSA). Continuous positive airway pressure (CPAP) treatment has been shown to decrease platelet activation. We aimed to study the effects of nasal CPAP therapy has on MPV values in patients with severe OSA. Thirty-one patients (21 men; mean age 53.8 ± 9.2 years) with severe OSA (AHI > 30 events/hour) constituted the study group. An age, gender and body mass index (BMI) matched control group was composed 25 subjects (14 men; mean age 49.6 ± 8.5 years) without OSA (AHI < 5 events/hour). We measured MPV values in patients with severe OSA and control subjects and we measured MPV values after 6 months of CPAP therapy in severe OS patients. The median (IQR) MPV values were significantly higher in patients with severe OSA than in control group (8.5 [8.3-9.1] vs. 8.3 [7.5-8.8] fL; p = 0.03). The platelet counts were significantly lower in patients with severe OSA than in control group (217.8 ± 45.9 vs. 265.4 ± 64.0 × 10⁹/L; p = 0.002). The six months of CPAP therapy caused significant reductions in median (IQR) MPV values in patients with severe OSA (8.5 [8.3-9.1] to 7.9 [7.4-8.2] fL; p < 0.001). Six months of CPAP therapy caused significant increase in platelet counts when compared with baseline values (217.8 ± 45.9 to 233.7 ± 60.6 × 10⁹/L; p < 0.001). We have found that the MPV values of patients with severe OSA were significantly higher than those of the control subjects and 6 months CPAP therapy caused significant reductions in the MPV values in patients with severe OSA.

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