During a period of 18 months beginning in January 1982, a total of 65 patients were referred to the Miami Heart Institute for evaluation of either aborted out of hospital sudden death, ventricular tachycardia resistant to standard clinically directed antiarrhythmic medication programs or high grade ventricular arrhythmia (Lown class greater than or equal to IV B) with or without syncope. After complete evaluation including cardiac catheterization in all but 1 patient, 17 patients were identified in whom no obvious cardiac disease could be found. Twelve of the 17 underwent right ventricular endomyocardial biopsy. Six of the 12 biopsies demonstrated clinically unsuspected lymphocytic myocarditis (Group A). Findings in three of the remaining six biopsies were consistent with an early cardiomyopathy and in three were completely normal (Group B). Retrospective review of the clinical, laboratory, electrophysiologic, hemodynamic and angiographic data failed to identify a marker that reliably separated Group A from Group B patients. In addition to antiarrhythmic therapy guided by laboratory electrophysiologic study, all Group A patients were treated with prednisone and azathioprine. After 6 months of immunosuppression, all patients with myocarditis were reevaluated in the hospital without antiarrhythmic medication. Ventricular tachycardia/fibrillation could not be provoked in the laboratory during repeat electrophysiologic testing in five of the six patients. Repeat myocardial biopsy after all immunosuppressive therapy had been discontinued revealed absence of inflammation associated with varying degrees of residual interstitial fibrosis. There were no deaths. It was concluded that a patient with an otherwise clinically silent lymphocytic myocarditis can present with potentially life-threatening ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARY In eight patients with chronic ventricular tachycardia and left ventricular aneurysms, we detected delayed ECG wave forms after the QRS complex from the body surface using a high-resolution ECG recorder, amplification and signal averaging. Delayed wave-form activity (D wave) extended a mean of 70 msec beyond the termination of the QRS complex. This delayed activity frequently extended to the limit of the recording window, and may thus continue throughout much of diastole. Antiarrhythmic agents never abolished the delayed activity; however, it was abolished by aneurysmectomy in four patients. Ventricular tachycardia did not recur after surgery in the four patients during a mean follow-up of 1 year. The D wave was not found in eight control patients who had chronic recurrent ventricular tachycardia nor in 11 of 12 who had aneurysms alone. The surface D wave can be readily and reproducibly detected by high-resolution electrocardiography and appears to be specific for patients with left ventricular aneurysms who also have chronic recurrent ventricular tachycardia. This delayed wave-form activity has been noted during catheter and surgical endocardial and epicardial mapping. It may represent persistence of the cardiac impulse in islands of myocardium and may be a manifestation of the delayed and fractionated activity, noted by previous investigators.

In an effort to determine the incidence of ventricular arrhythmias associated with ST segments alternans, the patterns of ST segment and T-wave electrical alternans (STEA) were analyzed in 93 patients during spontaneous Prinzmetal's angina. Twenty-eight of 93 patients, or 30% (Group I), showed STEA during episodes of ST segment elevation. SIxty-five of 93 patients, or 70% (Group II), showed no alternans during episodes of ST segment elevation. In Group I, ventricular arrhythmias, defined as all ventricular ectopic activity greater than 5 beats per minute and complex Lown grades III to V, occurred during 52 of 55 episodes, or 95%; whereas in Group II, ventricular arrhythmias occurred in only 51 of 125 episodes, or 41% (p less than 0.01). The difference in the incidence of ventricular fibrillation (VF) or ventricular tachycardia (VT) in the two groups was more striking. VT or VF occurred in 20 of 55 in Group I (36%) versus 5 of 125 in Group II (4%). Although there were no significant differences in age or sex between Group I and II patients, there was a significant difference in the magnitude of the maximum ST segment elevation (5 mm in Group I versus 3 mm in Group II, p less than 0.01). This study demonstrates that the occurrence of STEA and T wave alternans frequently heralds the onset of ventricular arrhythmias in Prinzmetal's angina. Both the arrhythmias and the alternans occur during the time of maximal ST segment elevation.

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.