IntroductionNeutrophil-to-lymphocyte ratio (NLR), which is an essential marker of inflammation, has been shown to be associated with adverse outcomes in various cardiovascular diseases in the literature. In this study we sought to evaluate the association between NLR and prognosis of acute pulmonary embolism (APE).Material and methodsWe retrospectively evaluated blood counts and clinical data of 142 patients with the diagnosis of pulmonary embolism (PE) from Ondokuz Mayis University Hospital between January 2006 and December 2012. The patients were divided into two groups according to NLR: NLR < 4.4 (low NLR group, n = 71) and NLR ≥ 4.4 (high NLR group, n = 71).ResultsMassive embolism (66.2% vs. 36.6%, p < 0.001) and in-hospital mortality (21.1%, 1.4%, p < 0.001) were higher in the high NLR group. In multivariate regression analysis NLR ≥ 5.7, systolic blood pressure (BP) < 90 mm Hg, serum glucose > 126 mg/dl, heart rate > 110 beats/min, and PCO2 < 35 or > 50 mm Hg were predictors of in-hospital mortality. The optimal NLR cutoff value was 5.7 for mortality in receiver operating characteristic (ROC) analysis. Having an NLR value above 5.7 was found to be associated with a 10.8 times higher mortality rate than an NLR value below 5.7.ConclusionsIn patients presenting with APE, NLR value is an independent predictor of in-hospital mortality and may be used for clinical risk classification.

Chronic smoking in young, healthy people causes significant alterations in the longitudinal diastolic myocardial function parameters as assessed by color tissue Doppler imaging.

Patients with chronic renal failure on regular hemodialysis program show significant alterations at LV longitudinal myocardial function parameters assessed by color TDI.

Coronary slow flow phenomenon leads to significant alterations in the myocardial deformation parameters of the left ventricle as assessed by STE. Specifically, circumferential deformation parameters are affected in CSFP patients.

Atherosclerosis is a complex process mediated by leukocytes, macrophages and various inflammatory markers. Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p<0.001). In the correlation analysis, serum galectin-3 showed significant correlation with the Gensini score (r=0.715, p<0.001), number of diseased vessels (r=0.752, p<0.001) and serum hs-CRP level (r=0.607, p<0.001). In addition, multivariate logistic regression analysis showed that the serum galectin-3 levels were significant and independent predictors of the presence of angiographic CAD (OR=3.933, 95% CI 2.395 to 6.457; p<0.001). In the present study, the serum galectin-3 levels were higher in the patients with CAD than in healthy controls. Also, serum galectin-3 levels showed a significant positive correlation with the severity of CAD. An increased serum galectin-3 level may be considered an important activator and a marker of the atherosclerotic inflammatory process in CAD.