acetylstrophanthidin and Myocardial-Infarction

We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocardial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on this parameter. The reflex chronotropic response to arterial baroreceptor stimulation was assessed in 29 patients with uncomplicated acute myocardial infarction in control conditions (72-96 h after symptom onset) and 30 min after acetylstrophanthidin administration. To check for spontaneous baroreflex sensitivity variations, 24 patients with the same characteristics were evaluated at the same time intervals before and after a 10-cc bolus of saline placebo. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in RR intervals. Mean baseline baroreflex sensitivity value for the whole study population was 7.4 +/- 4.5 ms/mmHg and was unchanged, 7.0 +/- 4.5 ms/mmHg, after acetylstrophanthidin (P = NS). Mean baroreflex sensitivity values were also comparable dividing patients according to the site of infarction both before and after acetylstrophanthidin. Despite the lack of difference in mean baroreflex sensitivity values between the two studies, at a post hoc analysis an inverse relation was found in the total study population between baseline baroreflex sensitivity values and their changes after acetylstrophanthidin (r = -0.62; P < 0.005). The inverse relation was also evident separately in anterior (r = -0.57; P < 0.05) and in inferior (r = -0.70; P < 0.005) myocardial infarction patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Baroreflex; Blood Pressure; Female; Heart Rate; Humans; Male; Middle Aged; Myocardial Infarction; Stroke Volume; Strophanthidin; Time Factors

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecti

Topics: Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Chronic Disease; Dogs; Electrocardiography; Electrophysiology; Heart Conduction System; Lidocaine; Myocardial Infarction; Pericardium; Procainamide; Skin; Strophanthidin

The peripheral arterial and venous responses to rapidly active acetylstrophanthidin (rather than the much slower digitalis) were studied in patients with acute myocardial infarction without congestive heart failure. In eight control patients placebo did not change mean blood pressure (BP), calf blood flow (CBF), calf vascular resistance (CVR), or calf venous volume (CVV). Seventeen patients received 10 mg IV acetylstrophanthidin. In these patients BP increased 5.3%, CBF decreased 18.2%, and CVR increased 29.2%. Venous capacitance was not changed. Acetylstrophanthidin induced no significant change in cardiac output, systemic vascular, resistance, pulmonary capillary wedge pressure, or right atrial pressure. In patients with acute myocardial infarction not complicated by congestive heart failure, digitalis may promote limb vasoconstriction and increase blood pressure, but it does not adversely affect cardiac function.

Topics: Electrocardiography; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Strophanthidin