Long-term vitamin-K antagonist use and coronary artery calcification.

BACKGROUND: The aim of this study was to investigate the impact of vitamin K antagonist (VKA) therapy on coronary artery calcification (CAC) by comparing long-term VKA users with metallic prosthetic valves (MPVs) and VKA-free patients undergoing coronary calcium scoring for cardiovascular (CV) risk stratification. METHODS: A total of 108 patients (43 VKA users with MPV and 65 gender-, age-, and risk-factor-matched VKA-free patients) were included in the study. CAC was determined via computed tomography (CT) and quantified on the basis of the Agatston score. The VKA group comprised patients who had an MPV for longer than 5 years, which entailed long-term VKA use. RESULTS: Long-term VKA users had more calcified coronary arteries compared with the control group (178.1 ± 278 vs. 61.1 ± 130.6, p = 0.01). There was no difference between groups in terms of traditional CV risk factors. The mean duration of VKA use was 15 ± 7 years for the patients with MPV. There was no correlation between the duration of VKA use and mean Agatston score (r = 0.2, p = 0.215). CONCLUSION: With its unique selection of patient groups, our study extends the findings of previous research that long-term VKA use is related to CAC as detected via CT scanning. The longer and more potent VKA regimen required for MPV patients is the primary cause of CAC in this group.

Relationship between neutrophil-to-lymphocyte ratio and impaired myocardial perfusion in cardiac syndrome X.

OBJECTIVE: Myocardial tissue perfusion is decreased in patients with cardiac syndrome X (CSX). Systemic inflammation appears to be an important contributor to the diseased microvascular network of these patients. The neutrophil-to-lymphocyte ratio (NLR) is a surrogate marker of inflammation. Accordingly, we evaluated this biomarker concerning the microvascular circulation of CSX patients. PATIENTS AND METHODS: This study included 60 consecutive patients (54.1 ± 7.8 years of age, 49 females) with CSX (typical chest pain, positive exercise stress test results, and normal coronary angiograms) and 60 consecutive age- and sex-matched control subjects. In all coronary territories, epicardial coronary flow was assessed by the Thrombolysis In Myocardial Infarction frame count (TFC) method, and myocardial tissue perfusion was assessed by the myocardial blush grade (MBG) method. Normal myocardial perfusion was accepted as an MBG score of 3 in all coronary territories. RESULTS: Patients with CSX had higher NLRs than those of control subjects (1.98 ± 0.77 vs 1.72 ± 0.55, respectively; p = 0.04). Among patients with CSX, those with impaired myocardial perfusion had higher NLRs than those with normal myocardial perfusion (2.13 ± 0.82 vs 1.71 ± 0.59, respectively; p = 0.028). There was a negative correlation between the NLR and total MBG score (p = 0.027, r = -0.29). Logistic regression analysis showed that the NLR was an independent and negative predictor of myocardial tissue perfusion (p = 0.027; Beta, -1.057; odds ratio, 2.878; 95% confidence interval, 1.129-7.335). CONCLUSIONS: Patients with CSX have high NLRs, and inflammation seems to be associated with distorted myocardial perfusion in these patients.

Independent relationship of serum uric acid levels with leukocytes and coronary atherosclerotic burden.

BACKGROUND AND AIM: Epidemiological studies have shown that increased serum uric acid (SUA) level is associated with coronary artery disease (CAD). Leukocytes have been shown to play an important role in the atherosclerotic process. The aim of the study was to investigate whether there is any relationship among SUA, leukocyte counts and coronary atherosclerotic burden in patients who are suspected of having CAD. METHOD AND RESULTS: We enrolled 690 eligible patients who had undergone coronary angiography between October 2005 and June 2006 in a consecutive manner. The relationship of SUA with total and differential leukocyte counts and CAD was investigated. Serum uric acid levels (5.57+/-1.64 vs 4.63+/-1.27 mg/dl, p<0.001) and leukocytes were higher in patients with CAD than those with normal coronary arteries (NCA). When we divided the patients into four groups according to the quartiles of SUA, we found that the monocyte count was prominently related with SUA (478+/-165, 553+/-177, 565+/-199 and 607+/-229 mm(-)(3), Q1-Q4, p<0.001). In multivariate analysis, SUA was an independent predictor of CAD (OR, 1.270; 95% CI, 1.087-1.484, p=0.003). When we performed multiple linear regression analyses to determine the independent predictors of inflammatory cells in blood, we found a strong, positive and independent relationship between SUA with neutrophils (beta+/-SE: 206+/-60, p=0.001) and monocytes (beta+/-SE: 35+/-7, p<0.001). CONCLUSION: Our study results demonstrated that neutrophils and monocytes which play an important role in inflammation and atherosclerosis were independently related with SUA. This finding suggests an important epidemiologic relation and may provide a possible causative mechanism of SUA in atherosclerotic process.