No abstract

We investigated whether the neutrophil to lymphocyte ratio (NLR) can predict stent thrombosis (STh) and high mortality rate in patients with ST-segment elevation myocardial infarction (STEMI). We analyzed data of 102 patients with STh and 450 patients with STEMI admitted to 2 high volume hospitals. Preprocedural NLR was significantly higher in patients with STh (P < .001). There was a significantly higher mortality rate in patients with high NLR during hospitalization (P < .001). Also, in the STh group there was a significantly higher mortality rate in patients with high NLR (P < .001). In receiver-operating characteristic analysis, NLR >4.8 had 56% sensitivity and 68% specificity for predicting STh. The NLR >4.9 had 70% sensitivity and 65% specificity for predicting in-hospital mortality. On multivariate regression analysis, NLR was found to be significantly related to STh. In patients with STEMI, preprocedural high NLR is associated with both STh and higher mortality rates.

CIN was observed in 20.5% of patients. Advanced age, male gender, elevated creatinine, uric acid and phosphate levels, and low glomerular filtration rate were correlated with the development of CIN. Correlation analysis also showed a significant association between the ALP level and the development of CIN (126.1 ± 144.9 vs. 97.2 ± 46.9, p = 0.004). Univariate regression analysis also showed the impact of ALP on the development of CIN (OR 1.004, 95% CI 1.001–1.007, p = 0.02). Conclusions: Our outcomes indicate a possible active role of ALP in the mechanism of CIN. An elevated ALP level may predict the development of CIN.

Elevated ALP levels are associated with higher Gensini scores and a more severe form of CAD.

Contrast-induced nephropathy (CIN) accounts for 10% of hospital-acquired renal failure, causes a prolonged in-hospital stay and represents a powerful predictor of poor clinical outcome. The underlying mechanism of the CIN development remains unclear and seems to be multifactorial. The potential link between platelet indices such as mean platelet volume (MPV) and platelet distribution width (PDW) with CIN is unknown. Herein, we aimed to investigate the correlation between MPV and PDW levels with the development of CIN. The incidence of CIN (20.5%) was prospectively evaluated in 430 patients with diagnosis of acute coronary syndrome. Initial creatinine (1.13 ± 0.25 vs. 1.05 ± 0.27 mg/dl, P = 0.01) and PDW (40.1 ± 20.2 vs. 34.5 ± 19.9%, P = 0.02) levels and the total volume of contrast media used (121 ± 61 vs. 94 ± 42 ml, P = 0.01) were higher in patients who developed CIN. MPV was similar between the two groups (P = 0.80). In a univariate regression analysis, age, increased creatinine, uric acid, phosphate, PDW levels and higher total volume of contrast media used were significantly correlated with CIN incidence. However, in a multivariate analysis, only total volume of CM used [odds ratio (OR) 1.011, 95% confidence interval (CI) 1.006-1.016; P = 0.01], increased age (OR 1.026, 95% CI 1.00-1.052; P = 0.05) and increased PDW levels (OR 1.009, 95% CI 1.00-1.022; P = 0.04) remained as the independent predictors of CIN. Among platelet indices, PDW, but not MPV, was associated with CIN development. The clinical significance of such link remains unclear, but may indicate involvement of platelet activation in CIN pathogenesis.