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Twenty elderly (77 [+ or -] 0.4 y), nonobese [body mass index (in kg/m2) 26.4 [+ or -] 0.5] subjects with normal glucose tolerance were submitted to a euglycemic hyperinsulinemic (3.5 pmol.min/kg) glucose clamp in a double-blind, crossover, randomized procedure after 4 mo treatment with either vitamin E (900 mg d-[alpha]-tocopherol/d, Ephynal; Roche, Milan, Italy) or placebo. Body mass index was practically unchanged throughout the study. After the glucose clamp, insulin-mediated stimulation 2of whole-body glucose disposal (18.4 [+ or -] 0.5 vs 26.1 [+ or -] 0.6 [micro]amol.min/kg lean body mass P < 0.02) was significantly potentiated by vitamin E rather than placebo administration. Furthermore, net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003). Plasma vitamin E concentrations seem to play an important role in the modulation of insulin action in elderly people.

Mitral annular calcium (MAC) is a condition that often occurs in patients with systemic hypertension. To evaluate the effectiveness of nifedipine in preventing MAC, 223 patients with systemic hypertension of recent onset and without MAC were selected and randomly enrolled in 3 groups: group 1 (76 patients) received nifedipine; group 2 (72 patients) received enalapril; and group 3 (75 patients) received atenolol. After 5 years, these treatments significantly reduced systolic (p 5 mm) in the remaining 8 in the enalapril group and in the other 9 in the atenolol group. There was also a significant correlation in the degree of MAC, left atrial enlargement and mitral regurgitation. In addition, atrial fibrillation and atrioventricular conduction defects were associated with severe MAC. These results indicate that nifedipine is an effective drug both in the long-term management of systemic hypertension and in preventing or delaying MAC. (Am J Cardiol 1993;72:1038-1042)

Glibenclamide, a hypoglycemic suffonylurea, is a blocker of the adenosine triphosphatase-modulated potassium ion channels. The opening of these channels in the myocardial cells, induced by acute myocardial hypoxia, can be responsible for ischemic ventricular arrhythmias. To evaluate the antiarrhythmic effects of this drug 19 non-insulin-dependent diabetic patients were selected. They had coronary artery disease and evidence on Holter monitoring of ventricular premature complexes or nonsustained ventricular tachycardia, or both, induced by transient myocardial ischemia. in all patients, 24-hour electrocardiographic monitoring was performed to evaluate the number and duration of myocardial ischemic events, the frequency of ventricular premature complexes and nonsustained ventricular tachycardia per minute of ischemia and the percentage of ventricular premature complexes versus total ischemic bests. Selected patients were classified in 2 groups: group A (9 patients) received metformin (placebo) and group B (10 patients) was treated with glibenclamide. On the fourteenth day patients underwent 24-hour control monitoring. Then a crossover between the 2 groups was made and a new Holter monitoring sequence was performed at the end of the second phase. Results indicate that glibenclamide significantly (p [is not greater than] 0.001) reduced both the frequency of ventricular premature complexes and the episodes of nonsustained ventricular tachycardia during transient myocardial ischemia, but did not change the number and duration of acute myocardial ischemic attacks and did not reduce the spontaneous ventricular arrhythmias. Thus, glibenclamide appears to have an antiarrhythmic effect in preventing ventricular arrhythmias induced by transient myocardial ischemia. (Am J Cardiol 1991;67:843-847), People with diabetes have a greater risk for a number of diseases, including heart disease. When diabetics develop heart disease, they often have ventricular arrhythmias, which are irregular beating patterns of the heart ventricles. The problem appears to be related to loss of potassium ions (K+) from within cardiac cells through K+ channels. The drug glibenclamide has been shown to block K+ channels in other tissues. This study examined the effectiveness of using glibenclamide in patients suffering from diabetes who had ventricular arrhythmias caused by heart disease. Included were 19 diabetic men suffering from acute myocardial ischemia (oxygen deprivation to the heart) and associated ventricular arrhythmias as determined by Holter monitor (an ambulatory device) evaluation. The men were randomly divided into two groups; nine were treated with a placebo, and 10 were treated with glibenclamide for two weeks. The drug and placebo were then switched for another two weeks. Holter monitor evaluations were performed for 24 hours on the last day of each of the two-week periods. Myocardial ischemic episodes lasted for an average of 11 minutes per 24 hours prior to either treatment, and both groups averaged 11 minutes per 24 hours on the last day of treatment with both the placebo and the drug. Ventricular arrhythmias decreased significantly from beginning levels after the drug was given, but not after the placebo was given. Blood sugar levels remained constant throughout the study. Thus while glibenclamide has an antiarrhythmic effect, it does not have an effect on ischemia. The mechanism of the drug's action does not involve decreasing plasma glucose levels. (Consumer Summary produced by Reliance Medical Information, Inc.)