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Objectives: The purpose of this study was to evaluate the long-term prognostic value of ST segment depression on the electrocardiogram (ECG) in patients with acute myocardial infarction., Background: The prognostic importance of ST segment depression on the ECG has been studied in small groups of patients with infarction, but larger numbers are needed., Methods: Coronary care unit ECGs of 1,234 patients who survived the coronary care unit with acute Q wave (n = 896) or non-Q wave (n = 338) myocardial infarction were analyzed for the presence of ST segment depression. Patients were followed up for up to 4 years., Results: ST segment depression was present in 607 patients. Those with ST segment depression had a 1-year mortality rate of 10.3% compared with a rate of 5.6% for those without ST segment depression (p = 0.002). This effect was seen in both the Q wave and non-Q wave subgroups. Of the 437 patients with anterior ST segment elevation, those with ST segment depression in other regions had a 13.6% 1-year mortality rate compared with a rate of 6.9% for those with no ST segment depression (p = 0.0005). Of the 514 patients with inferior ST segment elevation, those with ST segment depression in other leads had an 11.0% 1-year mortality rate compared with a 1.8% rate for those with no ST segment depression (p = 0.0001). The Cox proportional hazards model showed that ST segment depression was an independent predictor of mortality over the follow-up period., Conclusions: ST segment depression on the admitting ECG in patients with acute myocardial infarction is a predictor of increased mortality in the year after infarction.

The effect of diltiazem on long-term outcome after acute myocardial infarction (AMI) was assessed in 2,377 patients enrolled in the Multicenter Diltiazem Post-Infarction Trial and subsequently followed for 25 +/- 8 months. The study population included 855 patients (36%) with at least 1 prior AMI before the index infarction and 1,522 patients (64%) with a first AMI, of whom 409 (27%) had a first non-Q-wave AMI, 664 (44%) a first inferior Q-wave AMI, and 449 (30%) a first anterior Q-wave AMI. This post hoc analysis revealed that, among patients with first non-Q-wave and first inferior Q-wave AMI, there were fewer cardiac events during follow-up in the diltiazem than in the placebo group, and that the reverse was true for patients with first anterior Q-wave AMI or prior infarction. The diltiazem:placebo Cox hazard ratio (95% confidence limits) for the trial primary end point (cardiac death or nonfatal reinfarction, whichever occurred first) was: first non-Q-wave AMI-0.48 (0.26, 0.89); first inferior Q-wave AMI-0.66 (0.40, 1.09); first anterior Q-wave AMI-0.82 (0.51, 1.31); and prior AMI-1.11 (0.85, 1.44). Use of cardiac death alone as an end point gave an even more sharply focused treatment difference: first non-Q-wave AMI-0.46 (0.18, 1.21); first inferior Q-wave AMI-0.53 (0.27, 1.06); first anterior Q-wave AMI-1.28 (0.68, 2.40); prior infarction-1.26 (0.90, 1.77). Further analysis revealed that these differences in the effect of diltiazem in large part reflected the different status of the 4 electrocardiographically defined subsets in terms of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was performed to determine the sensitivity of thallium imaging vs ECG monitoring for detecting coronary artery spasm noninvasively following intravenous ergonovine administration as compared to simultaneous coronary angiography. Thirty-two patients with insignificant coronary artery disease and chest pain underwent 12-lead ECG monitoring, thallium imaging, and coronary arteriography following the administration of 0.05, 0.1, 0.2, and 0.3 mg of ergonovine given 5 minutes apart or until chest pain occurred. One minute following the last dose of ergonovine, 2.5 mCi of thallium-201 was injected intravenously, and a final ECG was recorded and repeat coronary arteriography performed. Within 10 minutes following the injection of thallium, imaging was performed in the 40-degree and 70-degree left anterior oblique and anterior projections. The ECG, thallium study, and coronary arteriogram were read blindly and results were compared. The ECG, angiogram, and thallium study were read as positive if the following occurred, respectively: greater than or equal to 1 mm ST segment elevation, depression, or T wave reversal; greater than 50% vessel narrowing,; and reversible perfusion defect. Five patients were excluded from analysis because of either catheter-induced spasm, suboptimal thallium studies, or protocol violations. Of the 27 patients included for analysis, six had chest pain, five had a positive angiogram, five had a positive thallium study, and one had a positive ECG. The sensitivity of thallium vs ECG monitoring was 80% vs 25%, and the accuracy was 92% vs 80%. We conclude that thallium imaging greatly increases the noninvasive detection of ergonovine-induced coronary spasm as compared with the ECG with no loss of accuracy.

Risk stratification using clinical and historical variables plus early low level exercise testing was performed in 141 patients with a first non-Q wave myocardial infarction. The 111 patients who performed the exercise test had a 3.6% cardiac mortality rate in the first year compared with 13.3% in the 30 patients who could not exercise (p = 0.063), and a 1 year incidence rate of recurrent cardiac events (cardiac death or recurrent nonfatal myocardial infarction) of 10.8% compared with 23.3% (p = 0.127). Patients who developed ischemia (ST depression or angina) during the test had an increased incidence of cardiac events in the year after the infarction (odds ratio greater than 3, p less than 0.05). When patients were subgrouped by the presence or absence of pulmonary congestion, the discriminatory value of the exercise test was seen to reside primarily in the cohort with pulmonary congestion. For example, ST depression during exercise in this group identified patients with a 71% incidence of cardiac events in the year after the infarction compared with 5.3% for those without ST depression (odds ratio 45, p = 0.002). In the patients without pulmonary congestion, the exercise test had no discriminatory value. It is concluded that early low level exercise testing has a limited role after an uncomplicated non-Q wave infarction, but is useful in patients with clinical markers of higher risk.

Twelve patients completed a double-blind, crossover antiarrhythmic drug trial in which 300 mg of quinidine, 500 mg of procainamide, 100 mg of phenytoin, or placebo was given four times daily on subsequent weeks. Analysis of 24-hour Holter tapes with a computerized analysis system (Argus/H) permitted accurate counting of premature ventricular complexes (PVCs) subclassified according to coupling interval. No antiarrhythmic agent demonstrated a significant overall reduction in the number of PVCs, but both quinidine and procainamide showed a statistically significant (p less than 0.05) reduction of PVCs with coupling intervals less than 400 msec. This effect was noted both in isolated PVCs (quinidine only) and in PVCs that were part of a couplet or run (both drugs). These findings demonstrate that clinically important effects of procainamide and quinidine can occur in the absence of an overall reduction in the number of PVCs.