Two-dimensional echocardiography and gated radionuclide ventriculography were performed in 93 patients (66 men, 27 women; mean age 61 years) with 95 episodes of acute myocardial infarction within 48 hours and at 10 days after infarction. Electrocardiographic sites of infarction were: 35 anterior, 49 inferoposterior and 11 nonlocalized. Abnormal motion of the anterior wall, septum or apex was seen in 97 and 100% of anterior infarctions by radionuclide ventriculography and echocardiography, respectively. Abnormal motion of an inferior or posterior wall segment was seen in 91% of inferoposterior infarctions by echocardiography versus 61% seen by radionuclide ventriculography. Ejection fractions determined by echocardiography and radionuclide ventriculography correlated well (r = 0.82) and did not change from the first 48 hours to 10 days after infarction (0.48 +/- 0.14). Similarly, wall motion score showed minimal change from the first 48 hours to 10 days. In-hospital mortality was 37 and 42% in patients with an ejection fraction of 0.35 or less by echocardiography and radionuclide ventriculography, respectively. No mortality was seen in patients with an ejection fraction above 0.40 by either test. The echocardiographic wall motion score was also predictive of mortality (40 versus 2%; score less than or equal to 0.50 versus greater than 0.50). The 1 year mortality rate in the 81 short-term survivors was 17%. Mortality was lowest in patients with an ejection fraction above 0.49 or wall motion score above (0.79 (2 to 5%) and worse in those with an ejection fraction below 0.36 or wall motion score below 0.51 (36 to 63%) by either technique. Thus in acute myocardial infarction, echocardiography and radionuclide ventriculography provide a comparable assessment of left ventricular function and wall motion in anterior infarction. Echocardiography appears more sensitive in detecting inferoposterior wall motion abnormalities. Both techniques are capable of identifying subgroups of patients with a high risk of death during the acute event and with an equally high mortality rate over a 1 year follow-up period.

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To compare the steady-state kinetic profiles and ectopy-suppression rates of two sustained-release forms of quinidine with those of a conventional quinidine preparation, 18 patients with ventricular ectopy were studied in randomized crossover fashion. The drugs were conventional quinidine sulfate 300 mg q6h, sustained-release quinidine sulfate 600 mg q12h, and sustained-release quinidine gluconate 648 mg q12h. Following baseline electrocardiographic ambulatory monitoring, each drug was given for three days, with repeat ambulatory monitoring and serial plasma drug level determinations performed on the third day. There were no washout periods between treatments. Plasma quinidine levels were assayed by both enzyme multiplied immunoassay technique (EMIT) and quinidine-specific high-performance liquid chromatography (HPLC) methods. Using actual steady-state HPLC values, there were no differences in the area under the plasma concentration-time curve (AUC) among the three treatments; the dose-corrected AUC was greater for quinidine gluconate than for the other two preparations. Using EMIT values, mean plasma quinidine levels from the conventional quinidine sulfate regimen were greater during the last five hours of the 12-hour study interval. A consistently strong inverse relationship between EMIT plasma quinidine levels and hourly ectopy rates was present in only one of eight (13%) responders. Diurnal variation of quinidine kinetics was observed after two days of each treatment; trough values at midnight were slightly lower than trough values at noon. Among patients demonstrating at least 70% suppression of premature ventricular contractions (PVCs), there were no differences in ectopy rates or ectopy-suppression rates among treatments. Dosing sustained-release quinidine sulfate 600 mg or quinidine gluconate 648 mg q12h was clinically acceptable in the small number of responders studied.