A b s t r a c tBackground: The balance of oxidant and antioxidant status plays a key role in the coronary artery diseases (CAD). Thiol is one of the most important antioxidant barriers in humans, and thiol/disulphide homeostasis is a novel oxidative stress marker. Aim:We aimed to investigate the relation of serum thiol levels and thiol/disulphide homeostasis with the presence and severity of CAD. Methods:A total of 161 patients who underwent coronary angiography owing to stable angina pectoris were consecutively enrolled. They were divided into three groups. Group I -47 age-and gender-matched subjects with normal coronary angiography (control); group II -71 newly diagnosed CAD patients with noncritical stenosis; and group III -43 newly diagnosed CAD patients with critical stenosis. Serum native thiol, total thiol, and disulphide levels were measured, and disulphide/thiol ratios were calculated. Gensini scores were calculated in CAD patients.Results: While the highest thiol levels were found in group I, the lowest one was observed in group III (p < 0.001). Total and native thiol levels were significantly lower in group II than in group I (p < 0.001 for each), but they increased considerably in group II compared with group III (p = 0.031 and p = 0.028, respectively). Disulphide levels decreased in group II and III compared with group I (p < 0.001 for each). No statistically significant changes were observed in disulphide/thiol ratios (p > 0.05). Gensini scores were negatively correlated with total and native thiols, and positively with age and dyslipidaemia.Stepwise linear regression analyses showed that native thiol was an independent predictor in the final model for Gensini score. Receiver operating characteristic curve analysis demonstrated that thiol values of 310.7 or below could predict CAD with 89% sensitivity and 85% specificity (AUC = 0.918; 95% CI 0.870-0.965). Conclusions:While the disulphide/thiol ratio did not change significantly, decreased native thiol levels were associated with the presence and severity of CAD. This result indicates that the reduction of thiols may be an important factor in the development of CAD.
Objective: Concentric or eccentric left ventricular hypertrophy (LVH) is an independent prognostic factor of major cardiovascular events in hypertension (HT). A high neutrophil to lymphocyte ratio (NLR) is correlated with high mortality and poor prognosis in cardiovascular disease. This study was performed to investigate the associations between NLR and different left ventricular (LV) geometric patterns in patients with newly diagnosed HT. Methods:The study population consisted of 222 patients with newly diagnosed HT (mean age: 53.2 ± 10.0 years). Echocardiographic examination was performed in all patients. Four different geometric patterns were determined in hypertensive patients according to the left ventricular mass index (LVMI) and relative wall thickness (RWT). Results:The baseline demographic characteristics were similar in all groups. The NLR and platelet to lymphocyte ratio (PLR) were higher in the eccentric hypertrophy and concentric hypertrophy groups compared to the normal geometry and concentric remodeling groups (p < 0.05, for all). NLR was positively and significantly correlated with LVMI (r = 0.508, p < 0.001). Linear regression analysis showed that LVMI was independently correlated with NLR (β = 5.440, p < 0.001), systolic blood pressure (β = 0.284, p < 0.001), ejection fraction (β = -0.201, p < 0.001), E/A (β = -2.270, p = 0.24), and high-density lipoprotein cholesterol (β = -0.245, p < 0.001). Conclusions:We demonstrated that patients with newly diagnosed HT with LVH had significantly higher NLR and PLR compared to those without LVH. In addition, NLR predicted LVH in hypertensive patients. The results of this study suggested that inflammation plays a role in the pathogenesis of LVH in hypertensive subjects.
Introduction: Inflammation and platelet activation play a central role in the initiation and progression of the atherosclerosis process. The Platelet-to-lymphocyte ratio (PLR) is a new prognostic marker in coronary artery disease. The PLR is a significant independent predictor of longterm mortality after none-ST elevated myocardial infarction (NSTEMI). We aimed to evaluate the relationship between PLR and no-reflow (NR) in patients with NSTEMI. Material and methods: The present study included 173 patients with NSTEMI. The patients were classified into two groups as follows: 115 patients in the NR group and 58 patients in the normal reflow group. NR was defined as coronary thrombolysis in myocardial infarction (TIMI) flow grade ≤ 2 after vessel recanalization with primary percutaneous coronary intervention. The PLR was calculated from the complete blood count. Results: The PLR values of the patients with NR were significantly higher than those of patients with normal reflow (108.6 (14.6-511.3) vs. 91.7 (17.2-225.3), p = 0.01). Also, neutrophil-to-lymphocyte ratio (NLR) was significantly higher in the NR group than the normal-reflow group (3.0 (0.3-16.5) vs. 2.3 (0.01-12.5), p = 0.02). The Correlation between the PLR and NLR was positive and significant (r = 0.68, p < 0.001). Conclusion: This study showed that PLR is an independent predictor of NR in patients with NSTEMI.
Aim: Acute coronary syndrome (ACS) is an ischemic cardiac disease that could result in myocardial necrosis with prolonged ischemia. Omentin (intelectin-1) is a new biomarker that is released from adipose tissue. It is associated with coronary artery disease (CAD) and has an acute ischemic injury-reducing effect. This study aimed to assess the omentin levels in patients with unstable angina pectoris (USAP), Non-ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevated myocardial infarction (STEMI). Methods: This case-control prospective study included 59 patients with ACS and 22 healthy subjects. MB fraction of creatine kinase (CKMB), troponin, myoglobin, and omentin levels were measured from venous blood obtained from each patient within six hours after the onset of symptoms. Plasma omentin levels were determined with an omentin enzyme-linked immunosorbent assay kit. Results: The patient group was older than the control group (P<0.05) but there was no difference between the groups in terms of gender (P>0.05). The rate of smoking was higher in the patient group, and the patient group was heavier than the control group (P>0.05). Omentin levels were similar in ACS patients and control subjects (6.0 (1.7) vs. 6.3 (1.3), P=0.40). There was no significant correlation among CKMB, troponin, myoglobin, and omentin levels. Moreover, omentin levels were similar in ACS subgroups (P=0.58). There was no significant correlation between body mass index and omentin levels (r =-0.186, P=0.09). Conclusion: This study revealed that there was no significant relationship between omentin and myoglobin levels in ACS patients. The potential usefulness of blood concentrations of omentin levels in understanding the relationship with ACS warrants further studies.
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