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.
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.
Brachial artery endothelial dysfunction was shown previously in a small group of Behçet's disease (BD) patients. This study aimed to compare the endothelial function in BD patients with and without vascular involvement. The study group consisted of 25 BD patients with vascular involvement, 25 BD patients without any vascular disease and 46 healthy controls. Brachial artery flow-mediated (endothelium-dependent) dilation (FMD), nitroglycerine-induced dilation and carotid artery intima-media thickness were measured. FMD was impaired in patients with BD (10.41 +/- 3.85%) compared to healthy controls (14.41 +/- 3.39%, p < 0.001). FMD was significantly lower in BD patients with vascular involvement (8.80 +/- 3.63%) than those without any vascular disease (12.02 +/- 3.43%, p = 0.003). This study reveals that endothelial dysfunction documented by brachial artery FMD is a feature of BD, and it is more prominent in patients with vascular involvement.
Background:An experimental study showed that nebivolol is an effective agent in contrast‐induced nephropathy (CIN) prophylaxis.Hypothesis:We hypothesized that prophylactic nebivolol use had protective effects on renal function in human beings subjected to iodinated contrast agent since it has vasodilatory effect and antioxidant properties.Methods:The present study enrolled 120 patients scheduled for coronary angiography and ventriculography. All patients were hydrated with intravenous isotonic saline. The patients in group I received 600 mg N‐acetylcysteine every 12 hours for 4 days. The patients in group II received 5 mg nebivolol every 24 hours for 4 days. The patients in group III were only hydrated. The primary endpoint was the occurrence of CIN. The secondary endpoint was the change in serum creatinine (Cr) levels at 2 days and 5 days after the contrast exposure.Results:Nine (22.5%) patients in group I developed CIN, as did 8 patients (20.0%) in group II and 11 patients (27.5%) in group III (P = 0.72). Changes in mean Cr level from baseline to day 2 were not statistically significant in all groups. However, we detected a statistically significant increase in mean Cr levels at day 5 compared with baseline levels in group I and group III (from 1.42 ± 0.13 to 1.52 ± 0.26, p2 = 0.02; and from 1.43 ± 0.14 to 1.55 ± 0.30, p2 = 0.01, respectively). Although an increase was detected in mean Cr level from baseline to the 5‐day Cr level in group II, this did not reach statistical significance (from 1.40 ± 0.12 to 1.48 ± 0.23, P = 0.06).Conclusions:Pretreatment with nebivolol is protective against nephrotoxic effects of contrast media. © 2012 Wiley Periodicals, Inc.The authors have no funding, financial relationships, or conflicts of interest to disclose.
The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.
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