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Biomedical subjects

F Rengo

Publications and source records attributed to F Rengo.

277 records · Page 16Linked to original sources
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Effect of gallopamil on myocardial microperfusion in patients with stable effort angina: a randomized, cross-over, double-blind, placebo-controlled trial.

We evaluated the efficacy and safety of daily administration of gallopamil 150 mg/day and its effects on myocardial perfusion in a medium-term, randomized, double-blind, cross-over, placebo-controlled trial. We studied 19 patients (17 males and 2 females; mean age 57 +/- 6.8 years) with stable effort angina, angiographically documented coronary artery disease and reversible perfusion defects during exercise thallium-201 myocardial scintigraphy of at least one segment of the left ventricle. After 2 weeks of a single-blind placebo run-in period, during which each patient underwent at least 2 exercise tests and a 48-hour Holter ECG recording, all patients were treated with either placebo or gallopamil 50 mg t.i.d. for 28 days. At the end of this period, patients crossed over to the alternate regimen. This phase was double blind. After treatment with placebo or gallopamil, patients underwent exercise tests, 24-hour Holter ECG recording and thallium-201 myocardial scintigraphy. Weekly angina frequency and trinitroglycerin (TNT) consumption and safety were also evaluated. No patients dropped out of the study because of major side effects. The number of total ischemic and symptomatic events recorded at 24-hour ECG monitoring, weekly angina frequency and TNT consumption were significantly reduced during gallopamil treatment. After gallopamil administration, exercise duration significantly increased (run-in: 419 +/- 116 s, placebo: 420 +/- 118 s, gallopamil: 511 +/- 144 s; p < 0.05), and ST segment depression was significantly reduced (run-in: -1.3 +/- 0.3 mm, placebo: -1.3 +/- 0.3 mm, gallopamil: -0.94 +/- 0.68 mm; p < 0.01), while heart rate, systolic blood pressure and rate-pressure product were unchanged at rest, at submaximal and at peak exercise. Qualitative and quantitative evaluation of myocardial perfusion and the myocardial uptake percentage of thallium-201 in ischemic zones were significantly improved by gallopamil treatment. These findings demonstrate that gallopamil can improve myocardial perfusion and reduce myocardial oxygen consumption.

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[Efficacy and tolerance of aniracetam in elderly patients with primary or secondary mental deterioration].

The study was carried out on 60 patients (mean age 69.9 +/- 10.3 years) suffering from slight-moderate brain pathology primary or secondary to vascular forms. Patients were treated with 1500 mg/day per os of Aniracetam or placebo. Drug efficiency evaluation was performed utilizing the following psychometric tests: Blessed Scale, figures repetition test, Benton test, Corsi test, Rey test, Pieron test, phrases construction test, verbal fluency test. They were carried out during basal visit after two and four month treatment. In Aniracetam treated group the score showed a significant improving during the first and second control. In placebo treated group no change statistically considerable happened in any test. Aniracetam has proved to be a useful drug in slight-moderate brain decay treatment of the elderly.

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Effect of flecainide acetate on reperfusion- and barium-induced ventricular tachyarrhythmias in the isolated perfused rat heart.

Flecainide acetate is a new antiarrhythmic drug which suppresses different kinds of experimental arrhythmias. We studied the efficacy of flecainide acetate on reperfusion- and barium-induced ventricular tachyarrhythmias in the isolated perfused rat heart by monitoring heart rate, coronary flow rate, left ventricular systolic pressure, dp/dtmax, and the voltage of the epicardial electrogram. Seventy-five male rats were randomized into 5 groups. In group I, after a 15 min period of stabilization, hearts were perfused by ischemic perfusion and then reperfused. In group II, flecainide acetate (10(-6) M) was given after stabilization and before ischaemic perfusion. In group III, barium chloride (10(-3) M) was given after stabilization. In group IV, flecainide acetate was given after stabilization and before barium chloride administration. In group V, acetylcholine chloride (10(-6) M) was given after stabilization and before barium chloride administration. In group I, we noted during ischemia a reduction in heart rate, coronary flow rate, left ventricular systolic pressure and dp/dtmax and an increase in the voltage of the epicardial electrogram. In group II, after administration of flecainide acetate, we observed a reduction in heart rate, left ventricular systolic pressure and dp/dtmax; during the ischaemic period there was no difference in these parameters with respect to group I. Reperfusion induced ventricular arrhythmias in 12 out of 15 hearts in group I and in only 3 out of 15 in group II (p less than 0.005). Barium induced ventricular arrhythmias in the 15 hearts studied in group III as well as in group IV. On the contrary, acetylcholine chloride in group V prevented the occurrence of barium-induced ventricular arrhythmias (p less than 0.005 vs group III and IV). Thus, flecainide acetate is able to reduce reperfusion-induced ventricular arrhythmias, but is unable to reduce barium-induced ventricular arrhythmias, presumably because of a different mechanism of these two types of arrhythmias.

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Electrical and mechanical actions of magnesium sulfate during ischemia and reperfusion on isolated perfused rat heart.

Experimental and clinical studies have shown the action of magnesium salts on myocardial tissue and its antiarrhythmic action on digitalis-induced ventricular arrhythmias. We have evaluated the effects of magnesium sulfate (2.5 mM) on heart rate (HR), coronary flow rate (CFR), left ventricular systolic pressure (LVSP), dP/dt max and voltage epicardial electrogram (VEE) during ischemia and reperfusion in isolated perfused rat heart. Forty-five male rats were randomized into 3 groups. In the control group, after a 15 min period of stabilization, hearts were perfused by ischemic perfusion for 30 min and then reperfused. In group I, magnesium sulfate was given after stabilization and before the ischemic period. In group II, calcium concentration was increased by 0.5 mM and magnesium sulfate was given after stabilization and before the ischemic period. In the control group, we observed during ischemia a reduction in HR, CFR, LVSP, dP/dt max and an increase in VEE. In group I, after the administration of magnesium sulfate, we noted a decrease in HR, LVSP, dP/dt max, VEE and during the ischemic period there was no difference in these parameters with respect to the control group. In group II, the increase of extracellular calcium concentration caused an increase in LVSP, dP/dt max and the administration of magnesium sulfate abolished these effect, bringing the values back to basal values. Reperfusion provoked ventricular arrhythmias in 11/15 and 12/15 hearts in the control group and group II respectively, and only 3/15 in group I (p less than 0.005 group I vs control and group II). Thus, our results demonstrated that magnesium sulfate has varied effects on electrical and mechanical parameters and prevents reperfusion arrhythmias according to the hypothesis of a calcium-antagonist mechanism of magnesium.

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