Women with polycystic ovary syndrome are more likely to suffer from obesity, insulin resistance, and chronic low-grade inflammation. In fact, the excessive activation of monocytes exacerbates oxidative stress and inflammation. However, high-density lipoprotein cholesterol neutralizes the pro-inflammatory and pro-oxidant effects of monocytes. The aim of this study is to investigate whether monocyte counts to high-density lipoprotein cholesterol ratio can predict the inflammatory condition in patients with polycystic ovary syndrome. In this cross-sectional study, a total of 124 women (61 of them with polycystic ovary syndrome and 63 age-matched healthy volunteers) were included in the study population. Obese polycystic ovary syndrome patients (n = 30) with a body mass index of ≥25 kg/m2 and lean polycystic ovary syndrome patients (n = 31) with a body mass index of < 25 kg/m2 were compared to age-and body mass index-matched healthy subjects (30 obese and 33 non-obese). The monocyte counts to high density lipoprotein cholesterol values in women with polycystic ovary syndrome were significantly higher than in control subjects (p = 0.0018). Moreover, a regression analysis revealed that body mass index, the homeostasis model assessment of insulin resistance and the high sensitivity C-reactive protein levels were confounding factors that affected the monocyte counts to high density lipoprotein cholesterol values. Additionally, a univariate and multivariate logistic regression analysis demonstrated that the increased monocyte counts to high density lipoprotein cholesterol values were more sensitive than the other known risk factors (such as increased body mass index, homeostasis model assessment of insulin resistance and high sensitive C-reactive protein levels) in the prediction of the inflammation in patients with polycystic ovary syndrome. The present study demonstrated that the monocyte count to high density lipoprotein cholesterol may be a novel and useful predictor of the presence of polycystic ovary syndrome.

We aimed to investigate the predictive value of the prognostic nutritional index (PNI) regarding the development of acute kidney injury (AKI) after elective coronary artery bypass grafting (CABG). A total of 336 consecutive patients with normal serum creatinine levels undergoing CABG were enrolled in this retrospective study. AKI was defined as meeting Acute Kidney Injury Network (AKIN) criteria based on the occurrence of creatinine changes within the first 48 h after CABG surgery. The patients were grouped according to whether they developed AKI or not into an AKI (−) and an AKI (+) group. AKI developed in 88 (26.2%) of all patients. The PNI was independently predictive of AKI (OR: 0.829, 95% CI: 0.783–0.877, p < 0.001). Moreover, C-reactive protein (CRP), a history of diabetes mellitus, and positive inotropric usage were independent risk factors for AKI in the multivariate logistic regression analysis. The area under the curve (AUC) of the multivariable model, including positive inotrope support, a history of diabetes mellitus, and CRP, was 0.693 (95% CI: 0.626–0.760, p < 0.001) in predicting AKIN. When the PNI was added to the multivariable model, the AUC was 0.819 (95% CI, 0.762–0.865, z = 3.777, difference p = 0.0002). Also, the addition of the PNI to the multivariable model was associated with a significant net reclassification improvement estimated at 88.2% (p < 0.001) and an integrated discrimination improvement of 0.22 (p < 0.001). Our study demonstrated that decreasing the PNI could be associated with the development of AKI after coronary artery bypass surgery.

Carotid artery stenosis (CAS), mainly caused by carotid atherosclerosis, is related to ischemic stroke. We investigated whether C-reactive protein (CRP) to albumin ratio (CAR) was associated with increased severity of carotid stenosis in patients undergoing carotid angiography. A total of 269 patients who were undergoing carotid angiography were included in this study. The patients were divided into 2 groups with respect to the severe CAS: group 1 (stenosis < 70%, n = 189) or group II (stenosis ≥ 70%, n = 80). C-reactive protein to albumin ratio was higher in group II compared to group I (0.56 ± 0.25 vs 0.14 ± 0.01, P < .001). The CAR (odds ratio [OR]: 1.051, 95%CI: 1.027-1.076, P < .001), neutrophil to lymphocyte ratio (NLR), and total cholesterol levels were independent predictors of severe CAS. The area under the receiver operating characteristic curve (area under the curve) for the CAR to predict severe CAS was 0.798 (95% CI: 0.741-0.854, P < .001). C-reactive to protein albumin ratio was an independent risk factor of severe CAS. Therefore, CAR might be considered a potential index in the severity of carotid artery disease.

Contrast-induced nephropathy (CIN) is acute kidney failure that occurs after exposure to contrast agent. There is no sensitive biomarker to predict the development of CIN. In a retrospective study, we investigated the predictive value of the fibrinogen to albumin ratio (FAR) to determine the risk of CIN in patients (N = 246) who underwent carotid angiography. Contrast-induced nephropathy was defined as a 0.5 mg/dL or 25% increase in serum creatinine levels 48 to 72 hours following exposure to a radiocontrast agent. Patients were grouped according to whether they developed CIN or not, that is, CIN(–) and CIN(+) groups, respectively. Contrast-induced nephropathy developed in 39 (15.8%) of all the patients. The fibrinogen levels, neutrophil to lymphocyte ratio (NLR), and FAR in the CIN (+) group were higher than in the CIN (−) group (P < .001). Multivariate analysis showed that age, diabetes, NLR, platelet–lymphocyte ratio, and FAR were independent risk factors for CIN. The area under the curve (AUC) of FAR was 0.800 for the prediction of CIN, and the best cutoff value was 57.4 with sensitivity, specificity, positive predictive value, and negative predictive value of 74.4%, 60.8%, 26.4%, and 92.7%, respectively. The FAR may be useful as a predictor of CIN.

The purpose of the study was to investigate whether the addition of left ventricular ejection fraction (LVEF) to the MELD score enhances the prediction of mortality in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). This retrospective study analyzed 846 consecutive patients with ACS undergoing PCI who were not receiving previous anticoagulant therapy. The patients were grouped as survivors or non-survivors. The MELD score and LVEF were calculated in all patients. The primary end point was all-cause death during the median follow-up of 28 months. During the follow-up, there were 183 deaths (21.6%). MELD score was significantly higher in non-survivors than survivors (10.1 ± 4.4 vs 7.8 ± 2.4, p < 0.001). LVEF was lower in non-survivors compared with survivors (41.3 ± 11.8% vs. 47.5 ± 10.0%, p < 0.001). In multivariate analysis, both MELD score and LVEF were independent predictors of total mortality. (HR: 1.116, 95%CI: 1.069–1.164, p < 0.001; HR: 0.972, 95%CI: 0.958–0.986, p < 0.001, respectively). The addition of LVEF to MELD score was associated with significant improvement in predicting mortality compared with the MELD score alone (AUC:0.733 vs 0.690, p < 0.05). Also, the combining LVEF with MELD score improved the reclassification (NRI:24.6%, p < 0.001) and integrated discrimination (IDI:0.045, p < 0.001) of patients compared with MELD score alone. Our study demonstrated that the combining LVEF with MELD score may be useful to predict long-term survival in patients with ACS who were undergoing PCI.

Cardiovascular disease is the most common cause of death in adult population in the world. The disease includes numerous problems, many of which are related to a process called atherosclerosis. Atherosclerosis is a condition that develops when a substance called plaque builds up in the walls of the arteries. This plaque narrows the arteries, making it harder for blood to flow through. If a blood clot forms, it can stop the blood flow. This can cause a heart attack or stroke. There are many risk factors associated with cardio vascular disease (CVD). While some risk factors cannot be changed, such as family history, some of them can be modified with treatment such as abnormal blood lipid and sugar levels, obesity, smoking, and high blood pressure. Research makes it clear that abnormal blood lipid (fat) levels have a strong correlation with the risk of coronary artery disease, heart attack and coronary death. Cholesterol plays detrimental roles in the pathogenesis of atherosclerosis and CVD. In this chapter, we aim to summarize the relationship between blood cholesterol levels and CVD.