The effect of insulin resistance (IR) on the fatty acid metabolism of myocardium, and therefore on the recovery of left ventricular (LV) wall motion, has not been established in patients with acute myocardial infarction (AMI). A total of consecutive 58 non-diabetic AMI patients who had successfully undergone emergency coronary angioplasty were analyzed retrospectively. They were categorized into 2 groups, normal glucose tolerance (NGT) and impaired glucose tolerance (IGT), based on a 75-g oral glucose tolerance test (OGTT). The parameters of OGTT, myocardial scintigraphy (n=58) (thallium-201 (Tl) and iodine-123-beta-methyl-iodophenylpentadecanoic acid (BMIPP)) and left ventriculography (n=24) were compared in the 2 groups after reperfusion (acute phase) and 3-4 weeks after the AMI (chronic phase). The insulin resistance (IR), estimated by the serum concentration of insulin at 120 min (IRI 120') of the OGTT and by the HOMA (the homeostasis model assessment) index, was higher in the IGT group than in NGT group. An inverse correlation was found between the recovery of regional LV wall motion in the ischemic lesion and the IRI 120' and HOMA index. Although the recovery of BMIPP uptake from the acute to the chronic phase was higher in the IGT group, it was only correlated with the degree of IRI 120', not with the HOMA. IR accompanied by IGT can negatively influence the recovery of regional LV wall motion.
The absorption of nifedipine (10 mg) and haemodynamic response were studied in 10 patients with myocardial infarction before (Phase A) and after (Phase B) a standardized breakfast. In Phase A, the peak nifedipine concentration (Cmax) and maximum haemodynamic changes were found 1 h after drug administration. In Phase B, the Cmax was lower than that in phase A (43 +/- 6 vs 136 +/- 23 ng/ml, p less than 0.001), and both Cmax and maximum haemodynamic changes were delayed to the fourth hour after administration. Nifedipine plasma concentration correlated significantly with the percent changes in systolic and diastolic blood pressure and heart rate. This study suggests that not only dose but also the time intervals between nifedipine administration and food intake are important in determining the haemodynamic effects.
The acute effects of nifedipine (20 mg sublingually) on hemodynamics and cardiac function were studied at rest and during supine bicycle exercise in 20 patients with aortic regurgitation. At rest, heart rate increased by 13%, systemic vascular resistance decreased by 34% and regurgitant index decreased by 17%. The change in systemic vascular resistance was related to its initial rest level (r = 0.82, p less than 0.001) and to the changes in forward cardiac output (r = 0.58, p less than 0.01) and regurgitant index (r = 0.60, p less than 0.01). Left ventricular end-diastolic and end-systolic volumes, stroke volume and ejection fraction were unchanged, whereas right ventricular ejection fraction increased. During exercise, nifedipine administration further increased heart rate by 8% and decreased systemic vascular resistance by 19%. Both forward stroke volume and forward cardiac output increased, but total left ventricular stroke volume was unchanged, resulting in a significant decrease in regurgitant index. Although left ventricular end-diastolic volume was slightly decreased, end-systolic volume did not increase; thus, ejection fraction was higher than that during control exercise (p less than 0.01). Right ventricular ejection fraction increased further. In aortic regurgitation, the acute administration of nifedipine improved cardiac performance and reduced regurgitation at rest and during exercise as a result of afterload reduction and increased heart rate. Whether these beneficial effects will occur during long-term therapy requires further investigation.
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