Red cell distribution width as a novel prognostic marker in patients undergoing primary angioplasty for acute myocardial infarction.

OBJECTIVES: Red cell distribution width (RDW), a measure of red blood cell size heterogeneity, was evaluated in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Higher RDW is associated with mortality in patients with symptomatic cardiovascular disease, heart failure, and also in the general population. We hypothesized that admission RDW would be predictive of adverse outcomes in patients after primary PCI. METHODS: Two thousand five hundred and six consecutive STEMI patients (mean age 56.6±11.8 years; 2075 males, 431 females) undergoing primary PCI were retrospectively enrolled into this study. Admission RDW was measured as part of the automated complete blood count. Patients were grouped as elevated or nonelevated RDW using the upper limit of normal value of 14.8% and were followed for in-hospital and long-term outcomes for a mean period of 1.8±1.3 years (median 21 months). RESULTS: A higher in-hospital mortality rate was observed among patients with elevated admission RDW (mean 16.1±1.6%) compared with those with nonelevated RDW (mean 13.4±0.8%) (7.6 vs. 3.6%, P<0.001). The long-term cardiovascular prognosis was worse for patients with elevated admission RDW (Kaplan-Meier, log-rank P<0.001). We used Cox proportional hazard models to examine the association between RDW and adverse clinical outcomes. After discharge, there were 129 deaths during follow-up. A significant association was noted between elevated admission RDW level and the adjusted risk of cardiovascular mortality (hazard ratio: 1.831, 95% confidence interval: 1.034-3.24, P=0.03). In addition, elevated admission RDW was also an independent predictor of cardiovascular mortality in the nonanemic subpopulation of patients (hazard ratio: 2.703, 95% confidence interval: 1.208-6.048, P=0.016). CONCLUSION: A high admission RDW level in patients with STEMI undergoing primary PCI was associated with increased risk for in-hospital and long-term cardiovascular mortality.

Comparison of primary percutaneous coronary intervention and streptokinase for acute isolated inferior ST elevation myocardial infarction with a predicted low risk profile.

BACKGROUND: Primary percutaneous coronary intervention (PCI) is the treatment of choice for acute myocardial infarction, especially for high-risk patients, but the data for low-risk patients are conflicting. A very low-risk subgroup of acute inferior myocardial infarction can be identified by electrocardiographic and clinical criteria during admission. We aimed to compare the outcomes of primary PCI and streptokinase treatment in this subgroup, which has not been evaluated separately before. MATERIAL/METHODS: We retrospectively analyzed in-hospital and 10-month follow-up outcomes of 97 patients with inferior acute myocardial infarction and clinical and electrocardiographic criteria predicting low risk who have been treated with primary PCI or streptokinase. RESULTS: Forty-eight patients received streptokinase, and 49 had undergone primary PCI. Both during the in-hospital period and follow-up, the groups did not differ in the end points of death, reinfarction, or stroke (in-hospital: 2.1% versus 4.1%, P=.57; follow-up: 8.9% versus 8.9%, P=1.000). Length of hospital stay was longer in the streptokinase group (6.5+/-2.5 versus 9.1+/-3.7 days, P=.001). Rate of repeat revascularization was reduced in the PCI group at 10 months (28.9% versus 55.6%, P=.002). CONCLUSIONS: When streptokinase and primary PCI are compared in isolated inferior acute myocardial infarction patients with a low-risk profile, there are no differences for in-hospital and long-term rates of death, reinfarction, or stroke. Primary angioplasty reduces the length of initial hospital stay, and reduces repeat admissions by decreasing the need for subsequent revascularization procedures. Large-scale studies are needed to reach a final conclusion.

The relationship between nonalcoholic fatty liver disease and the severity of coronary artery disease in patients with metabolic syndrome.

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is an important complication of metabolic syndrome (MS). We investigated the possible relationship between NAFLD and angiographical severity of coronary artery disease (CAD) in patients with MS. STUDY DESIGN: This prospective study included 80 patients (35 men, 45 women; mean age 63+/-10 years; range 42 to 80 years) with a diagnosis of MS according to the ATP III criteria. All patients underwent abdominal ultrasonography to detect NAFLD. Coronary angiography was performed for stable angina pectoris (n=48), unstable angina pectoris (n=21), and prognostic reasons (n=11). The severity of CAD was assessed by the number of vessels involved (vessel score) and the severity score (Gensini score). Significant stenosis was defined as 70% or greater reduction in lumenal diameter. RESULTS: Ultrasonography revealed NAFLD in 43 patients (53.8%). Patients with NAFLD had significantly higher body mass index, waist circumference, and serum triglyceride level, and significantly lower HDL-cholesterol level (p<0.001). Coronary angiography showed significantly higher vessel (2.5+/-0.9 vs 1.0+/-1.0) and CAD severity scores (90.2+/-40.0 vs 36.4+/-28.9) in patients with NAFLD (p<0.001). Univariate analysis showed that the presence of NAFLD (r=0.61, p<0.001), grade of NAFLD (r=0.42, p<0.001), and patient age (r=0.36, p=0.002) were significantly correlated with the CAD severity score. In multivariate linear regression analysis, the presence of NAFLD was the only independent factor affecting the CAD severity score (beta: 1.35, p<0.001). CONCLUSION: The presence of NAFLD is associated with more severe CAD, requiring that patients with MS be investigated for the presence of NAFLD and those with NAFLD be attentively followed-up for the presence and severity of CAD.

Effects of folic acid and N-acetylcysteine on plasma homocysteine levels and endothelial function in patients with coronary artery disease.

OBJECTIVE: Hyperhomocysteinaemia is related with premature coronary artery disease and adverse cardiac events in patients with coronary artery disease (CAD). It is assumed that hyper-homocysteinaemia causes endothelial dysfunction. In this study, the effect of folic acid and oral N-acetylcysteine (NAC) therapies on plasma homocysteine levels and endothelial function were evaluated in hyperhomocysteinaemic patients with CAD. METHODS AND RESULTS: 60 patients were randomized to either folic acid 5 mg or NAC 600 mg or placebo daily for eight weeks. Brachial artery endothelial functions were studied by using high-resolution ultrasound and assessed by measuring endothelium-dependent dilation (EDD) and endothelium-independent dilation (NEDD). Folic acid and NAC therapies decreased plasma homocysteine (from 21.7 +/- 8.7 micromol/l to 12.5 +/- 2.5 micromol/l, P < 0.001; from 20.9 +/- 7.6 micromol/l to 15.6 +/- 4.3 micromol/l, P = 0.03, respectively), and increased EDD (6.7 +/- 6.1% P = 0.002, 4.4 +/- 2.6% P < 0.001, respectively) compared with placebo. There was no significant difference in improving EDD between the folic acid and the NAC group (6.7 +/- 6.1%, 4.4 +/- 2.6%, P = 0. 168). In the univariate analyses there was an inverse correlation between the post-treatment homocysteine level and the percent change in EDD with folic acid therapy (r= -0.490, P = 0.028), but there was no correlation with the NAC therapy (r = 0.259, P = 0.333) CONCLUSION: In patients with hyperhomocysteinaemic CAD, folic acid and NAC lowered plasma homocysteine levels and improved endothelial function. The effects of both treatments in improvement of EDD were similar.