The goal of this study was to assess the effect of gallopamil on left ventricular (LV) diastolic function early after acute myocardial infarction (AMI). Gallopamil was compared with placebo and atenolol in two different groups of patients. Study patients, 2 days after experiencing their first AMI, in Killip class I and stable sinus rhythm, were randomized in a crossover, double-blind sequence to receive (a) gallopamil (50 (μg/kg over 5 min) or placebo (i.v. 10-ml bolus, with a time interval of 90 min); and (b) gallopamil (50 μg/kg over 5 min) or atenolol (5 mg over 5 min), with a time interval of 24 h. Group I and group II consisted of 28 patients (26 men and 2 women; mean age 55 ± 9 years) and of 14 patients (13 men and 1 woman; mean age 56 ± 10 years), respectively. All the patients were treated with thrombolysis within 6 h from the onset of symptoms. Doppler echocardio-graphic examinations were performed as follows: at baseline (B) and 15 min after administration of gallopamil bolus and placebo bolus, in group I; at baseline before gallopamil (BG) and atenolol (BA), and 15 min after each bolus in group II. The following echo-Doppler parameters were calculated, at each examination: the early and late transmitral peak velocity ratio (E/A), the early and late velocity integral ratio (Ei/Ai), the peak filling rate normalized to mitral stroke volume (nMPFR), and the LV is ovolumic relaxation time (IVRT), which was normalized to an 800-ms R-R cycle length in the patients in group II. Mean blood pressure (MBP) and heart rate (HR) were also measured. No patients developed electrical or mechanical complications, but two patients in group I, in whom first and second Mobitz first-degree atrioventricular block lasted only a few minutes were observed. These two patients were excluded from the study. Expressing data as mean ± SEM, E/A, Ei/Ai, and nMPFR increased after gallopamil, when compared with values for placebo in group I (1.1 ± 0.1 vs. 0.8 ± 0.1, 1.5 ± 0.1 vs. 1.1 ± 0.1, 3.9 ± 0.2 vs. 3.2 ± 0.1, respectively, p < 0.001), and with BG values in group II (1.2 ± 0.1 vs. 0.9 ± 0.1, 1.8 ± 0.2 vs. 1.3 ± 0.2, 3.9 ± 0.3 vs. 3.5 ± 0.3, respectively, p < 0.01). IVRT was shortened by gallopamil in both groups (97 ± 3 vs. 116 ± 3, in group I; 89 ± 4 vs. 116 ± 4, in group II, p < 0.001). Atenolol was associated with only a slight increase of E/A. However, the magnitude of the change of E/A induced by atenolol was much smaller than that observed after administration of gallopamil (11.8% vs. 27.8%, p < 0.01). MBP and HR showed only a slight decrease after administration of gallopamil. A greater decrease of HR was observed after atenolol administration. In conclusion, our data suggest that gallopamil administration improves echo-Doppler LV filling parameters, with only trivial changes of loading conditions, in patients with noncomplicated AMI, suggesting a possible favorable effect on LV diastolic function. On the other hand, atenolol appears to have slight or no influences on LV diastole.
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