Background: Even though medication and interventional therapy have improved the death rate for non-ST elevation myocardial infarction (NSTEMI) patients, these patients still have a substantial residual risk of cardiovascular events. Early identification of high-risk individuals is critical for improving prognosis, especially in this patient group. The focus of recent research has switched to finding new related indicators that can help distinguish high-risk patients. For this purpose, we examined the relationship between the pan-immune-inflammation value (PIV) and the severity of coronary artery disease (CAD) defined by the SYNTAX score (SxS) in NSTEMI patients. Methods: Based on the SxS, CAD patients were split into three groups. To evaluate the risk variables of CAD, multivariate logistic analysis was employed. Results: The PIV (odds ratio: 1.003; 95% CI: 1.001–1.005; p = 0.005) was found to be an independent predictor of a high SxS in the multivariate logistic regression analysis. Additionally, there was a positive association between the PIV and SxS (r: 0.68; p < 0.001). The PIV predicted the severe coronary lesion in the receiver-operating characteristic curve analysis with a sensitivity of 91% and specificity of 81.1%, using an appropriate cutoff value of 568.2. Conclusions: In patients with non-STEMI, the PIV, a cheap and easily measured laboratory variable, was substantially correlated with a high SxS and the severity of CAD.

Stroke is a significant contributor to morbidity and mortality. The present study investigated how the systemic immune inflammation index (SII) could be used to predict the likelihood of developing carotid artery stenosis (CAS), which can be seen using carotid artery angiography (CAAG). This study comprised 418 individuals who underwent CAAG for CAS. SII was calculated by multiplying the platelet count by the neutrophil/lymphocyte ratio (NLR). The patients were divided into two groups: non-critical and critical CAS (stenosis below %70 and above ≥70%, respectively). Compared with the non-critical CAS, the critical CAS group had greater high sensitivity C-reactive protein levels (4.5 [3.1-5.7] vs 3.9 [2-5] [mg/L], P < .001), NLR (4.1 [2.9-7.5] vs 2.9 [1.8-3.7], P < .001), platelet/lymphocyte ratio (233 [110-297] vs 119 [96-197], P < .001), and SII (860 [608-2455] vs 604 [458-740], P < .001). Receiver Operating Characteristic Curve analysis demonstrated the best cutoff value of 672.3 for SII to predict the critical CAS with 71.2% sensitivity and 60.1% specificity. According to our study, an increase in SII is an independent predictor of the severity of CAS in patients undergoing CAAG.

We investigated the relationship between the newly-defined systemic immune-inflammation index and the new-onset atrial fibrillation in patients undergoing coronary artery bypass grafting. This study included 392 patients who underwent coronary artery bypass grafting. We divided the participants into two groups as those with and without new-onset atrial fibrillation. Prior to coronary artery bypass grafting, we evaluated blood samples, including systemic immune-inflammation index, and other laboratory parameters of the patients. We formulized the systemic immune-inflammation index score as platelet × neutrophil/lymphocyte counts. The findings revealed that new-onset atrial fibrillation occurred in 80 (20.4%) of 392 patients during follow-ups. Such patients had higher systemic immune-inflammation index, neutrophil/lymphocyte ratio, and C-reactive protein levels than those who did not develop new-onset atrial fibrillation (P<0.001, P 712.8 predicted new-onset atrial fibrillation with a sensitivity of 85% and a specificity of 61.2% (area under the curve: 0.781, 95% confidence interval: 0.727-0.835; P<0.001). Overall, systemic immune-inflammation index, a novel inflammatory marker, may be used as a decisive marker to predict the development of atrial fibrillation following coronary artery bypass grafting.

Contrast-induced nephropathy (CIN) is associated with increased mortality and morbidity. The present study investigated the role of systemic immune inflammation index (SII) in predicting the risk of developing CIN after carotid artery angiography (CAAG). This study included 262 patients who underwent CAAG for symptomatic carotid artery stenosis (CAS). Simultaneous carotid stenting was applied to 232 of these patients. CIN was defined as an increase in serum creatinine level ≥.5 mg/dL or ≥25% above baseline within 72 hours after the procedure. The SII score was calculated as platelet × neutrophil/lymphocyte counts. Patients who developed CIN, had higher glucose ( P = .009), total cholesterol ( P < .001), low density lipoprotein cholesterol (<.001), and high sensitivity C-reactive protein ( P = .001) levels, as well as greater neutrophil counts ( P < .001), platelet counts ( P < .001), neutrophil–lymphocyte ratio ( P < .001), and SII score ( P < .001) than those who did not develop CIN. The Receiver Operating Characteristic analysis showed that at a cutoff of 519.9, the SII exhibited 80% sensitivity and 64% specificity for detecting CIN. SII levels on admission were independently associated with CIN development after CAAG in patients with CAS.

Background/Objectives: Postoperative new-onset atrial fibrillation (AF) (PNOAF) is the most common complication after coronary artery bypass graft (CABG), and its incidence has been reported as up to 50% in studies. In this study, we investigated whether there was a relationship between PNOAF and the neutrophil percentage to albumin ratio (NPAR) levels after on-pump CABG. Methods: A total of 454 patients who underwent CABG were included in the study. NPAR was calculated by dividing the neutrophil count by the albumin value. Results: It was determined that 93 patients developed PNOAF (20.4%). When the patient groups that developed and did not develop PNOAF were compared in terms of laboratory findings, C-reactive protein (CRP) values (4.0 mg/L (2.8–7.9) vs. 2.9 mg/L (1.1–6.7), <0.001), neutrophil/lymphocyte ratio (NLR) (2.2 (1.2–4.2) vs. 1.4 (0.7–3.1), <0.001), platelets-to-lymphocyte ratio (112 (72–177) vs. 92 (69–122), <0.001) and NPAR (2.29 (1.68–3.8) vs. 1.09 (0.79–1.81), <0.001), were found to be statistically significantly higher in the group that developed PNOAF. ROC analysis showed that the cut-off value for NPAR for the development of PNOAF was 1.86 with 78% sensitivity and 72% specificity (area under the ROC curve = 0.778, 95% CI (0.728–0.828), p < 0.001). Conclusions: NPAR, which can be detected by a simple venous blood test, has shown a strong predictive value for PNOAF in patients with CABG.

Background and Aim: Vitamin D deficiency is common and may contribute to cardiovascular diseases. We hypothesized that serum 25-hydroxyvitamin D [25(OH)D] levels would be inversely associated with inflammation and with diastolic dysfunction. We therefore investigated the link between serum vitamin D levels (i) echocardiographic measures and (ii) inflammatory parameters. Methods: The cross-sectional study included 281 patients who were referred to coronary angiography for stable angina pectoris. Patients were recruited between December 2010 and November 2011. Patients with established congestive heart failure, gout, chronic kidney disease (estimated glomeruler filtration rate <60 mL/min per 1.73 m²), and acute infection were not included. We measured serum 25(OH)D levels, C-reactive protein and fibrinogen levels. A radioimmunoassay procedure was used to measure 25(OH)D (DiaSorin, Stillwater, MN). We also performed standardized left ventricular (LV) echocardiograms, and echocardiographic data were used for classification of systolic and diastolic dysfunction. We analyzed the relation between serum levels of 25(OH)D and inflammatory markers and echocardiographic measures of LV mass and diastolic dysfunction. Results: At baseline, subjects had a mean age of 59.5 ± 10 years, and 43.4% were women. Left ventricular mass index, left atrial diameter, isovolumic relaxation time, and E/E′ ratio were significantly higher in patients with lower 25(OH)D levels. In ordinal logistic regression analysis, higher 25(OH)D was negatively associated only with LV mass index (odds ratio [OR], 0.965; 95% confidence interval [95% CI], 0.939–0.992; P = 0.015), isovolumic relaxation time (OR, 0.962; 95% CI, 0.939–0.985; P = 0.001), E/E′ ratio (OR, 0.874; 95% CI, 0.811–0.942; P = 0.008), and C-reactive protein (OR, 0.802; 95% CI, 0.668–0.962; P = 0.021). Conclusions: Serum levels of 25(OH)D are significantly associated with LV diastolic dysfunction and LV mass index, although the effect size is rather small. Longitudinal studies in larger populations are needed to establish firmly or refute a causal relationship between vitamin D levels and diastolic dysfunction and LV mass index.