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Platelets play a central role in the pathophysiology of coronary artery disease (CAD). Increased mean platelet volume (MPV) is an indicator of platelet function and associated with poor clinical outcome in patients with acute coronary syndrome (ACS). We evaluated the relationship between MPV and severity of CAD in patients with ACS. A total of 395 patients with ACS were included. Severity of CAD was assessed with the Gensini and Syntax scores. High levels of MPV were associated with the Gensini and Syntax scores, number of diseased vessels (>50%), number of critical lesions (>50% and >70%), and noncritical lesions. After multivariate analysis, high levels of MPV were independent predictors of multivessel CAD together with age. In patients with ACS, high MPV levels were associated with severity of CAD. It is possible that MPV can be a helpful marker in patients with CAD for the severity of coronary atherosclerosis.

We aimed to elucidate the relation between serum uric acid (SUA) level and severity of coronary artery disease (CAD) in nondiabetic, nonhypertensive patients (n = 246) with acute coronary syndrome (ACS). Severity of CAD was assessed by the Gensini score. One, 2, and 3 or more diseased vessels were identified in 87 (35.4%), 55 (22.4%), and 104 (42.2%) patients, respectively. Patients with hyperuricemia had higher Gensini score, high number of diseased vessels, critical lesions, and total occlusion. Serum uric acid level was significantly associated with number of diseased vessels. Serum uric acid was an independent risk factor for multivessel disease by univariate analysis. High levels of SUA associated with the severity of CAD in nondiabetic, nonhypertensive patients with ACS.

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We investigated whether the systemic immune inflammation index (SII) on admission is an independent risk factor that predicts the development of contrast-induced nephropathy (CIN) in patients with non-ST segment elevation myocardial infarction (NSTEMI) who underwent percutaneous coronary intervention (PCI). A total of 429 patients with NSTEMI were enrolled in the study. Contrast-induced nephropathy was defined as an increase in serum creatinine level of ≥0.5 mg/dL or ≥25% above baseline within 72 hour after the procedure. Patients were divided into 2 groups: with and without CIN. Demographics, clinical risk factors, angiographic and laboratory parameters, CIN incidence, and SII score were compared between the 2 groups. Non-ST segment elevation myocardial infarction patients, who developed CIN, had higher glucose levels ( P = .009), neutrophil counts ( P < .001), platelet counts ( P < .001), neutrophil-lymphocyte ratios ( P < .001), high sensitivity C-reactive protein levels ( P = .009), and SII levels ( P < .001) than those who did not develop CIN. The receiver operating characteristic curve analysis showed that at a cutoff of 933.2, the value of SII exhibited 77.6% sensitivity and 69.2% specificity for detecting CIN. Our study showed that the SII levels on admission were independently associated with CIN development after PCI in patients with NSTEMI.

We investigated whether serum bilirubin level (a marker of heme oxygenase activity) is a predictor of high levels of SYNTAX score (SXscore) in patients with acute myocardial infarction. Patients (n = 281; male 77%; mean age 60 ± 12) who were admitted with ST-elevation myocardial infarctions (STEMIs) were enrolled. Patients were divided into 2 groups. Group 1 was defined as SXscore <22 and group 2 was defined as SXscore ≥22. Total bilirubin levels were significantly higher in the high-SXscore group than in the low-SXscore group (0.86 ± 0.42 vs 1.02 ± 0.51, P = .005). A significant correlation was detected between total bilirubin and SXscore ( r = .42; P = .001). At multivariate analysis, total bilirubin (odds ratio: 1.86, 95% confidence interval 1.04-3.35; P = .038) was an independent risk factor for high SXscore in patients with STEMI. In conclusion, serum bilirubin level is independently associated with SXscore in patients with STEMI.