Cardio-ankle vascular index could reflect plaque burden in the coronary artery.

Cardio-ankle vascular index (CAVI) using the volume plethysmographic method is a noninvasive atherosclerotic indicator which is not influenced by blood pressure. Coronary intravascular ultrasound (IVUS) is a reliable technique to measure progression of atherosclerosis. The association between CAVI and IVUS has not been reported. The aim of this study was to evaluate the association between CAVI and the plaque burden measured by IVUS in the left main coronary artery (LMCA) in patients with coronary heart disease and normal LMCA. Cardio-ankle vascular index was significantly correlated with percentage plaque area (r = .649, P < .0001) measured by IVUS in the most diseased segment of LMCA. Cardio-ankle vascular index remained significant among cardiovascular disease risk factors included in the multiple regression analysis predicting percentage plaque area. Cardio-ankle vascular index was a good atherosclerotic indicator and associated with the plaque burden in nonculprit and angiographically normal LMCA.

Effects of nicorandil on cardiovascular events in patients with coronary artery disease in the Japanese Coronary Artery Disease (JCAD) study.

BACKGROUND: Nicorandil has cardioprotective effects in the ischemic myocardium, mimicking ischemic preconditioning, and is thus expected to improve the prognosis of ischemic heart disease (IHD). As part of the Japanese Coronary Artery Disease (JCAD) Study, a multicenter collaborative prospective observational study of a large cohort of coronary artery disease patients, the effect of nicorandil on outcome was examined. METHODS AND RESULTS: In total, 2,558 patients with nicorandil treatment and controls subjected to propensity score matching were eligible among 13,812 patients registered in the JCAD study. The mean follow-up interval was 2.7 years. The primary endpoint, death from all causes, was significantly lower, by 35% (hazard ratio 0.65, P=0.0008), in the nicorandil group than in the control group. There were also significant reductions in secondary endpoints, including cardiac death (56%), fatal myocardial infarction (56%), cerebral or vascular death (71%), and congestive heart failure (33%) in the nicorandil group, with no excess of deaths from other non-cardiovascular causes. Treatment with nicorandil reduced the number of deaths from all causes to a similar extent with or without treatment with sulfonylureas. CONCLUSIONS: The reduction in cardiovascular death with nicorandil was large in patients with IHD, which has important implications for treatment.

Comparison of atherosclerotic indicators between cardio ankle vascular index and brachial ankle pulse wave velocity.

BACKGROUND: Aortic pulse wave velocity has been used for evaluating atherosclerosis. Recently, the development of the volume plethysmographic method has made it possible to easily measure the index of the pulse wave velocity. The brachial ankle pulse wave velocity and cardio ankle vascular index are used for estimating the extent of atherosclerosis. The diagnostic usefulness of these indexes in predicting coronary artery disease was examined. METHODS: The brachial ankle pulse wave velocity, the cardio ankle vascular index, and the high-sensitivity C-reactive protein were measured in 696 patients who had chest pain and underwent coronary angiography. Measurement values of brachial ankle pulse wave velocity were compared with those of cardio ankle vascular index in terms of the baseline covariates and the number of major coronary vessels involved (vessel disease). RESULTS: The brachial ankle pulse wave velocity was significantly correlated with age, systolic blood pressure, and diastolic blood pressure but not with the high-sensitivity C-reactive protein. The cardio ankle vascular index was correlated only with age and the high-sensitivity C-reactive protein. The average of both brachial ankle pulse wave velocity and cardio ankle vascular index values was greater in 3 vessel disease group than in 0 vessel disease group. The receiver operating characteristic curve showed that the diagnostic accuracy of coronary artery disease was significantly higher in the cardio ankle vascular index than in the brachial ankle pulse wave velocity (area under the curve +/- standard error: 0.691 +/- 0.025 vs. 0.584 +/- 0.026; P < .05). CONCLUSIONS: As a means of estimating the extent of atherosclerosis in large arteries, our results show that both brachial ankle pulse wave velocity and cardio ankle vascular index are useful and that cardio ankle vascular index may have some advantages in its application to patients taking blood pressure-lowering medication because of the minimum effect of blood pressure on its measurement values. The cardio ankle vascular index has increased performance over brachial ankle pulse wave velocity in predicting the coronary artery disease.

[Suppressive effect of nicorandil in ventricular arrhythmias after reperfusion therapy in patients with acute myocardial infarction].

BACKGROUND: Nicorandil is reported to inhibit reperfusion arrhythmias in patients with acute myocardial infarction (AMI), but few studies have counted ventricular arrhythmias with Holter electrocardiograms in patients treated with nicorandil following AMI reperfusion. OBJECTIVES: In the present study, we examined the effects of nicorandil by investigating the occurrence of ventricular arrhythmia with Holter electrocardiogram monitoring after percutaneous coronary intervention with acute myocardial infarction. METHODS: Forty patients with AMI who underwent successful percutaneous coronary intervention (PCI) were enrolled and randomly assigned to nicorandil or placebo groups. Following PCI, nicorandil was infused intravenously at 6 mg/hr for 24 hr, with Holter electrocardiogram monitoring. Patients with 100 or more premature ventricular contractions (PVCs) over the 24-hour period were studied. The total number of PVCs, frequency of occurrence of ventricular tachycardia, and clinical characteristics were compared between the two groups. RESULTS: Fourteen patients in the nicorandil group and 12 patients in the placebo group exhibited 100 or more PVCs over the 24-hour period. Lesion characteristics and procedural factors did not differ between the two groups. Fewer PVCs were counted in the nicorandil group than in the placebo group(144.6 +/- 106.5 vs 286.8 +/- 159.1 beats/day, p = 0.012). The frequency of coupled PVCs was lower in the nicorandil group (6.9 +/- 6.9 vs 16.3 +/- 12.8 beats/day, p = 0.025). Although the frequency of ventricular tachycardia did not differ between the two groups, ventricular tachycardia duration was significantly shorter in the nicorandil group (3.73 +/- 2.30 vs 8.34 +/- 7.45 sec, p = 0.03). CONCLUSIONS: Our study indicates nicorandil inhibits ventricular arrhythmias following PCI for patients with AMI. Nicorandil treatment following PCI for AMI is convenient and may reduce the rate of cardiac events by inhibiting ventricular arrhythmias, thereby potentially improving the prognosis.

Nicorandil protects against lethal ischemic ventricular arrhythmias and up-regulates endothelial nitric oxide synthase expression and sulfonylurea receptor 2 mRNA in conscious rats with acute myocardial infarction.

Nicorandil is an adenosine triphosphate sensitive K (K-ATP) channel opener and a nitric oxide donor. K-ATP channels and nitric oxide are important factors in ischemic preconditioning, which in turn suppresses reperfusion arrhythmias. The present study sought to evaluate whether nicorandil suppresses ischemic-induced ventricular arrhythmias and enhances sulfonylurea receptors (SUR 2; subunit of K-ATP channel), endothelial nitric oxide (eNOS), and inducible nitric oxide (iNOS) expression in the left ventricle after myocardial infarction without reperfusion. Thirty male Sprague-Dawley rats at 7 weeks of age were separated into three groups, as follows. Acute myocardial infarction was induced in twenty rats by ligating the left main coronary artery. Ten of these twenty rats were continuously administered nicorandil at 3 mg/kg/day i.p. The other ten rats were left untreated. The ten controls were untreated and sham-operated. After coronary ligation, ventricular arrhythmias were evaluated from stored ECG signals. At 24 hours after treatment, eNOS, iNOS, and SUR2 mRNA levels and eNOS, iNOS expression in the left ventricle were determined by reverse transcription polymerase chain reaction (RT-PCR) and by immunohistochemical staining, respectively. Nicorandil suppressed the total number of ventricular arrhythmias from 1 to 2 hours, the total duration of ventricular tachycardia from 2 to 3 hours, and that of ventricular fibrillation from 1 to 2 and from 4 to 5 hours after coronary ligation. Nicorandil improved the survival rate 24 hours after coronary ligation. Levels of SUR2 mRNA increased only in left ventricles treated with nicorandil, particularly in the non-ischemic myocardium. eNOS mRNA was enhanced 2.2-fold in the area at risk in infarcted controls compared to sham-operated rats. In the non-ischemic area and area at risk of rats treated with nicorandil compared to sham-operated rats, eNOS mRNA was enhanced 3.3- and 2.7-fold, respectively. Staining indicated that the highest concentrations of eNOS occurred in the endothelium and myocardium of the non-ischemic area of rats treated with nicorandil. iNOS mRNA was present in both the area at risk and the non-ischemic area only in infarcted rats, and levels thereof were higher in the area at risk than in the non-ischemic area. However, there was no difference in iNOS mRNA levels between nicorandil-treated rats and controls. iNOS exhibited stronger staining in the area at risk than in the non-ischemic area of both nicorandil-treated and infarcted controls, with no differences between these two groups of rats. The mechanisms of protection against lethal ventricular tachyarrhythmia in nicorandil may increase nitric oxide release by upregulated eNOS expression through the opening of K-ATP channels and/or a K-ATP channels opener itself after acute myocardial infarction.

Association of plasma atrial natriuretic peptide, N-terminal proatrial natriuretic peptide, and brain natriuretic peptide levels with coronary artery stenosis in patients with normal left ventricular systolic function.

PURPOSE: To examine whether coronary artery stenosis affects plasma levels of atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide (proANP), and brain natriuretic peptide (BNP) in patients with normal left ventricular systolic function. METHODS: We studied 104 consecutive patients with normal left ventricular function and suspected coronary artery stenosis. Plasma natriuretic peptide levels were measured by immunoradiometric assays. RESULTS: Plasma levels of ANP, N-terminal proANP, and BNP were higher in patients with (n = 65) than in those without (n = 39) coronary artery stenosis, whereas hemodynamic variables were similar. Patients who had coronary artery stenosis with only distal lesions (n = 36) had higher levels of all three natriuretic peptides than did patients with no coronary artery stenosis. N-terminal proANP levels were significantly higher in patients who had coronary artery stenosis with proximal lesions (n = 29) than in patients who had coronary artery stenosis with only distal lesions and those with no coronary artery stenosis. Multiple logistic regression analysis revealed that N-terminal proANP, but not ANP or BNP, was independently associated with coronary artery stenosis after adjusting for clinical and demographic variables (odds ratio per 100 fmol/mL increase = 1.9; 95% confidence interval: 1.9 to 2.6; P = 0.01). However, the sensitivity, specificity, and positive and negative predictive values of each peptide were not sufficiently high to be used for prediction. CONCLUSION: N-terminal proANP may be associated with clinically important coronary artery stenosis in patients with normal left ventricular systolic function, but its clinical usefulness may be limited.