Peak aortic blood acceleration is recognized to be a sensitive index of global left ventricular performance. In the present study peak acceleration was assessed noninvasively in patients with a continuous-wave Doppler velocity meter. Peak aortic blood velocity and peak blood acceleration were measured by placing the ultrasonic transducer at the suprastemal notch. Measurements were obtained in 36 patients undergoing diagnostic cardiac catheterization. Peak velocity and acceleration were measured at rest just before left ventriculography. In patients with ejection fractions greater than 60%, peak acceleration was 19 5 m/sec/sec. In patients with ejection fractions of 41% to 60%, peak acceleration was lower, at 12 2 m/sec/sec (p < .001). In patients with ejection fractions of 40% or less, peak acceleration (8 ± 2 mlsec/sec) was markedly lower than in patients with ejection fractions greater than 60% (p <. 001). Peak acceleration showed a good linear correlation with ejection fraction (r = .90), and a better power fit (r = .93
We performed a randomized trial comparing intracoronary administration of streptokinase versus dextrose placebo within six hours after the onset of symptoms of acute myocardial infarction in 40 patients. The base-line clinical, hemodynamic, and angiographic findings were similar in the control and streptokinase-treated groups. Reestablishment of flow occurred in 12 of 20 patients treated with streptokinase and in 2 of 20 given placebo (P less than 0.05). Left ventricular function, angiographic ejection fraction, and regional wall motion, measured before and immediately after intervention, and serial radionuclide ejection fractions, measured at treatment, at 12 days, and at 5 months, were compared according to type of treatment (streptokinase vs. placebo) and outcome of therapy (reperfusion vs. no reperfusion). No statistically significant differences between groups were found. Thus, although streptokinase was more effective than placebo in achieving reperfusion, we detected no improvement of left ventricular function as a result of reestablished coronary flow.
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