We made continuous electrocardiographic recordings on magnetic tape during 15 episodes of ischemia in five patients with variant angina to determine the characteristics of the QRS changes. Orthogonal leads were used and the electrocardiograms were analyzed visually and by digital computer. Changes were quantified by subtracting baseline electrocardiograms from those obtained during ischemia. Large changes in the QRS occurred during ischemia but the waveform quickly returned to baseline when the episode subsided. In all patients there was prolongation of the QRS duration and an increase in QRS voltage during the terminal 40 msec of the waveform in the lead(s) showing the most marked ST displacement. The increase in the terminal QRS could be represented by a vector directed toward the ischemic zone. In a given patient the amplitude of ST displacement varied between episodes, presumably because of variation in the intensity of ischemia, but the QRS changes were directionally similar in each episode. In two patients there was also a smaller change involving the initial 40 msec of the QRS that could be represented by a vector directed away from the ischemic zone. To determine the possible mechanism for the electrocardiographic changes, ischemic episodes of 120 to 150 sec were produced in seven dogs and electrocardiographic recording and analysis techniques similar to those used in patients were employed. Myocardial conduction velocity was measured in three directions in the ischemic zone and was correlated with simultaneous electrocardiographic recordings from the body surface. The electrocardiographic changes in the dog preparation were virtually identical to those in the patients and strongly correlated with a fall in myocardial conduction velocity. We conclude that the QRS changes during variant angina result from the altered excitation pattern produced by conduction delay in the ischemic zone. The probable cause for the increase in terminal QRS voltage is delayed (and uncanceled) activation of the ischemic zone.Circulation 71, No. 5, 901-911, 1985. WE HAVE investigated the QRS changes during spontaneous ischemia in patients with variant angina by performing a detailed analysis of electrocardiograms from orthogonal leads. To

Studies of patients during variant angina have revealed that there are specific changes in the terminal part of the QRS complex that provide information regarding the location of the ischemia. Extending these studies to acute myocardial infarction, the electrocardiogram (ECG) obtained from 32 patients within 5 h of the onset of chest pain was analyzed to determine if similar inferences could be made. A preinfarction ECG was available from each patient for comparison and 30 patients underwent coronary arteriography within 3 weeks of the infarction. The 10 patients with anterior infarction had a decrease (p less than 0.05) in the S wave in leads V2 (0.80 +/- 0.50 mV) and V3 (0.65 +/- 0.43 mV). In 23 patients with inferior infarction an increase (p less than 0.05) in the R wave of lead III (0.47 +/- 0.35 mV), S wave of lead aVL (0.31 +/- 0.23 mV) and R wave of lead aVF (0.37 +/- 0.30 mV) occurred. A strong positive correlation between the R wave changes in leads III and aVF and the S wave in lead aVL (r = 0.94 and 0.91, respectively) suggests that the R and S wave changes in these leads are expressions of the same phenomenon and indicates that the terminal QRS complex is chiefly affected. Eight of 23 patients with inferior infarction and ST depression in the anterior precordial leads had a normal left anterior descending coronary artery. All had an increase in S wave amplitude in leads V2 and V3. Eight patients had inferior infarction, ST depression in anterior leads and severe lesions in the left anterior descending artery or anterior wall motion abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

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