Onuk T.,Siyami Ersek Cardiothoracic and Vascular Surgery Center |
Gungor B.,Siyami Ersek Cardiothoracic and Vascular Surgery Center |
Karatas B.,Siyami Ersek Cardiothoracic and Vascular Surgery Center |
Ipek G.,Siyami Ersek Cardiothoracic and Vascular Surgery Center |
And 7 more authors.
Clinical Laboratory | Year: 2015
Background: The prognostic relevance of hematological parameters in cardiovascular diseases has been well demonstrated. The purpose of the present study is to investigate the association between the hematological parameters, particularly neutrophil to lymphocyte ratio (NLR), and outcomes of aortic dissection (AD). Methods: Two hundred patients diagnosed with AD were retrospectively recruited and compared with 76 subjects with ascending aortic dilatation (AAD) and 92 subjects with normal aortic diameters. The independent relation between hematological parameters and in-hospital mortality was analyzed by regression analysis. Results: The NLR was significantly higher in the AD group compared to the AAD and control groups (median 8.83 [8.13] vs. median 1.95 [1.10] vs. median 1.71 [0.77], respectively; p = 0.01). The NLR was higher in the de-ceased (n = 57) compared to the surviving patients (n = 143) (median 10.37 [10.86] vs. median 7.84 [8.17]; p = 0.01). Receiver operating curve (ROC) analysis revealed that a NLR measurement higher than > 8.78 predicted in-hospital mortality for patients with acute aortic dissection with a sensitivity of 67.4% and a specificity of 57.2% (AUC: 0.672; p = 0.01). In multivariate logistic regression analysis, increased aortic diameter, acute dissection, and increased levels of NLR remained as the independent markers of in-hospital mortality within the study population. Conclusions: In patients with AD, NLR levels were increased compared to patients with AAD and controls and were independently associated with in-hospital mortality. This finding implicates that admission hematological parameters may have clinical importance in evaluating the mortality risk in patients with AD. Source