Circulation, Vol 55, 574-577, Copyright © 1977 by American Heart Association
MJ Kleinfeld and JJ Rozanski
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.
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Alternans of the ST segment in Prinzmetal's angina
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