No abstract

During the course of AMI, SES implantation adversely affects endothelium-dependent vasomotor function in resistance and epicardial coronary arteries after the ischemia-reperfusion in association with a reduction in myocardial VEGF secretion.

The impairment of FMD in the brachial artery at the time of follow-up was independently and closely associated with late ISR in native coronary arteries. The noninvasive assessment of FMD at the time of follow-up might be useful for identification of late ISR.

We determined time course of stabilization of echolucent carotid plaques by statin therapy in patients with acute coronary syndrome (ACS). Treatment with 4 mg/d pitavastatin (n = 33) or placebo (n = 32) was initiated within 3 days after onset of ACS in 65 patients with echolucent carotid plaque. Vulnerable carotid plaques were assessed by measuring plaque echolucency using carotid ultrasound with integrated backscatter (IBS) analysis before and 1 month after treatment in all patients. The calibrated IBS value (intima-media IBS value minus adventia IBS) of vulnerable carotid plaques favorably changed at 1 month after treatment in both groups, but the echolucency at 1 month improved more in the pitavastatin than in the placebo group (pitavastatin group: -18.7 +/- 3.3 dB at pretreatment versus -12.7 +/- 2.3 dB at 1 month *P < 0.001; placebo: -19.0 +/- 3.5 dB versus -16.9 +/- 3.2 dB, P < 0.05, *P < 0.01 versus the value at 1 month in placebo group). Levels of CRP, VEGF, and TNFalpha at 1 month were significantly lower in pitavastatin than placebo group. In conclusion, pitavastatin improved carotid plaque echolucency within 1 month of therapy in patients with ACS, in association with decrease in the inflammatory biomarkers related to vulnerable plaques.

Background Because metabolic syndrome is associated with cardiovascular diseases, its association with the risk of paroxysmal atrial fibrillation (PAF) and/or atrial flutter (PAFL) was examined in the present study. Methods and Results A prospective analysis was performed in 592 consecutive hospitalized patients without obvious structural heart diseases. Sinus rhythm was confirmed by electrocardiography in all patients. PAF/PAFL occurred in 32 (5%) and metabolic syndrome was present in 127 (21%) of the patients enrolled. PAF/PAFL occurred in 12 (9%) of the patients with metabolic syndrome, but only 20 (4%) of patients without metabolic syndrome (p=0.02). Multivariate logistic regression analysis showed that metabolic syndrome was a significant risk factor for PAF/PAFL that was independent of left atrial diameter (>44 mm) or age (>70 years) (odds ratio (OR) 2.8, 95% confidence interval (CI) 1.3-6.2, p<0.01). Among the 5 components of the metabolic syndrome, body mass index ≥25 kg/m 2 was the most strongly associated with PAF/PAFL (OR; 3.0, 95% CI 1.2-7.4, p=0.02). Conclusions Metabolic syndrome is highly associated with PAF/PAFL in patients without structural heart diseases and obesity may be an underlying mechanism for the higher prevalence. (Circ J 2007; 71: 252 -255)