Objective:Obesity causes subclinical inflammation. Leukocyte count and high-sensitivity C-reactive protein (hs-CRP) are used to indicate inflammation in clinical practice. Also, inflammatory markers are evaluated as important indicators of cardiovascular risk in patients with obesity and metabolic syndrome (MetS). We aimed to investigate the usage of the neutrophil-lymphocyte ratio (NLR) as an inflammatory marker in obese patients with and without MetS.Methods:The study included a total of 1267 patients. The patients were assigned groups according to degree of obesity and status of MetS. Metabolic and inflammatory markers were compared between groups, and correlation analysis was performed.Results:Leukocyte count and hs-CRP were significantly different (p<0.001), but NLR was not different between body mass index (BMI) groups (p=0.168). Both lymphocyte and neutrophil counts were significantly increased with increased degree of obesity (p<0.001, p=0.028, respectively). Leukocyte, neutrophil, and lymphocyte counts and hs-CRP level showed a significant correlation with BMI (r=0.198, p<0.001; r=0.163, p<0.001; r=0.167, p<0.001; r=0.445, p<0.001, respectively), whereas NLR was not correlated with BMI (r=0.017, p=0.737). Only a significant association between a MetS severity of 5 and 4 with hs-CRP level was observed (p=0.028), whereas there was no statistically significant association for leukocyte count and NLR (p=0.246; p=0.643, respectively).Conclusion:NLR was not a good indicator of inflammation, while leukocyte and hs-CRP were more useful biomarkers to indicate inflammation in non-diabetic patients with obesity and MetS.
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.
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