Objective This study examines the predictive value of the novel systemic immune-inflammation index (SII) in patients with ST-segment elevation myocardial infarction (STEMI).Methods A total of 1660 patients with STEMI who underwent primary percutaneous coronary intervention (pPCI) were enrolled in the study. In-hospital and 3-year outcomes were compared between the four groups (Q1-4). The SII was calculated using the following formula: neutrophil*platelet/lymphocyte.
ResultsThe frequency of in-hospital cardiogenic shock, acute respiratory failure, acute kidney injury, ventricular arrhythmia, stent thrombosis, recurrent myocardial infarction, major adverse cardiac events and mortality were significantly higher in the high SII groups (Q3 and Q4). Logistic regression models demonstrated that Q3 and Q4 had an independent risk of mortality and Q4 had an independent risk of cardiogenic shock compared to Q1. Receiver operating characteristic analysis showed that the best cutoff value of SII to predict the in-hospital mortality was 1781 with 66% sensitivity and 74% specificity. Kaplan-Meier overall survivals for Q1, Q2, Q3 and Q4 were 97.6, 96.9, 91.6 and 81.0%, respectively. Cox proportional analysis for 3-year mortality demonstrated that Q3 and Q4 had an independent risk for mortality compared to Q1.Conclusion SII, a novel inflammatory index, was found to be a better predictor for in-hospital and long-term outcomes than traditional risk factors in patients with STEMI undergoing pPCI.
Plasma fibrinogen is a readily measurable systemic inflammatory marker and is independently associated coronary severity and complexity in patients with CAD.
Echocardiographic EFT is an inexpensive, simple, and readily available marker that may be used to asses the severity of chronic heart failure in patients with NICMP.
Aortic dilatation due to inflammation may lead to an increase in C-reactive protein (CRP) levels. We investigated the possible relationship between CRP-to-albumin ratio (CAR) and presence and progression of abdominal aortic aneurysms (AAAs). The study included 150 patients previously diagnosed with AAA (diameter 40-54 mm) and 100 normal controls. Clinical and laboratory parameters and maximal cross-sectional AAA diameters (measured by computed tomography angiography) were obtained from all participants at baseline assessment as well as after 1 year for those with an AAA. The patients with AAA had significantly higher serum CAR compared with controls at baseline (P < .001). Increased serum CAR was found to be an independent predictor of the presence of AAA (odds ratio: 3.162, 95% CI: 1.690-5.126, P = .001) after multivariate logistic regression analysis. There was a significant increase in aortic diameter and CAR after 1 year in the patients with AAA ( P < .001; P = .003); a significant correlation was found between changes in the diameter of AAAs and CAR ( r = 0.414; P = .005). Serum CAR may be useful as an inflammatory biomarker for the presence and progression of AAA.
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