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.
PURPOSE:To analyze the effect of maintenance hemodialysis on left ventricular diastolic function in patients with end-stage renal disease.METHODS: Study population consisted of 42 patients with end-stage renal disease. Before an arteriovenous fistula was surgically created, the patients were evaluated by conventional and Doppler echocardiography and Doppler tissue imaging. Then, the patients undergoing hemodialysis treatment when the arteriovenous fistula was compleated. After the first hemodialysis session (mean 76.14 ¡ 11.37 days) the second echocardiographic evaluations were performed. RESULTS:Mean age was 58 ¡ 13 years and 21 (%50) of the patients were female. After maintenance hemodialysis treatment; peak early (E) and peak late (A) diastolic mitral inflow velocities and E/A ratio were not significantly change however the deceleration time of E wave and left atrial diameter were significantly increased. Also there was no change in the early (Em) and late (Am) diastolic myocardial velocities and Em/Am ratios of lateral and septal walls of left ventricular. E/Em ratio was decreased insignificantly. Pulmonary vein velocities and right ventricular functions are remained almost unchanged after hemodialysis treatment.
BackgroundThe prognostic significance of changes in mean platelet volume (MPV) during hospitalization in ST segment elevation myocardial infarction (STEMI) patients underwent primary percutaneous coronary intervention (pPCI) has not been previously evaluated. The aim of this study was to determine the association of in-hospital changes in MPV and mortality in these patients.MethodsFour hundred eighty consecutive STEMI patients were enrolled in this retrospective study. The patients were grouped as survivors (n = 370) or non-survivors (n = 110). MPV at admission, and at 48–72 h was evaluated. Change in MPV (MPV at 48–72 h minus MPV on admission) was defined as ΔMPV.ResultsAt follow-up, long-term mortality was 23%. The non-survivors had a high ΔMPV than survivors (0.37 (− 0.1–0.89) vs 0.79 (0.30–1.40) fL, p < 0.001). A high ΔMPV was an independent predictor of all cause mortality ((HR: 1.301 [1.070–1.582], p = 0.008). Morever, for long-term mortality, the AUC of a multivariable model that included age, LVEF, Killip class, and history of stroke/TIA was 0.781 (95% CI:0.731–0.832, p < 0.001). When ΔMPV was added to a multivariable model, the AUC was 0.800 (95% CI: 0.750–0.848, z = 2.256, difference p = 0.0241, Fig. 1). Also, the addition of ΔMPV to a multivariable model was associated with a significant net reclassification improvement estimated at 24.5% (p = 0.027) and an integrated discrimination improvement of 0.014 (p = 0.0198).ConclusionsRising MPV during hospitalization in STEMI patients treated with pPCI was associated with long-term mortality.
In patients with coronary artery disease (CAD), though aspirin inhibits platelet activation and reduces atherothrombotic complications, it does not always sufficiently inhibit platelet function, thereby causing a clinical situation known as aspirin resistance. As hyperuricemia activates platelet turnover, aspirin resistance may be specifically induced by increased serum uric acid (SUA) levels. In this study, we thus investigated the association between SUA level and aspirin resistance in patients with CAD. We analyzed 245 consecutive patients with stable angina pectoris (SAP) who in coronary angiography showed more than 50% occlusion in a major coronary artery. According to aspirin resistance, two groups were formed: the aspirin resistance group (Group 1) and the aspirin-sensitive group (Group 2). Compared with those of Group 2, patients with aspirin resistance exhibited significantly higher white blood cell counts, neutrophil counts, neutrophil-to-lymphocyte ratios, SUA levels, high-sensitivity C-reactive protein levels, and fasting blood glucose levels. After multivariate analysis, a high level of SUA emerged as an independent predictor of aspirin resistance. The receiver-operating characteristic analysis provided a cutoff value of 6.45 mg/dl for SUA to predict aspirin resistance with 79% sensitivity and 65% specificity. Hyperuricemia may cause aspirin resistance in patients with CAD and high SUA levels may indicate aspirin-resistant patients. Such levels should thus recommend avoiding heart attack and stroke by adjusting aspirin dosage.
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