The QRS complex during transient myocardial ischemia: studies in @entity1 with @entity5968 and in a XXXX preparation.

@entity1 @entity5968 @entity235 @entity63
We made continuous electrocardiographic recordings on magnetic tape during 15 episodes of @entity63 in five @entity1 with @entity5968 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 @entity63 . Large changes in the QRS occurred during @entity63 but the waveform quickly returned to baseline when the episode subsided. In all @entity1 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 @entity63 zone. In a given @entity1 the amplitude of ST displacement varied between episodes, presumably because of variation in the intensity of @entity63 , but the QRS changes were directionally similar in each episode. In two @entity1 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 @entity63 zone. To determine the possible mechanism for the electrocardiographic changes, @entity63 episodes of 120 to 150 sec were produced in seven @entity235 and electrocardiographic recording and analysis techniques similar to those used in @entity1 were employed. Myocardial conduction velocity was measured in three directions in the @entity63 zone and was correlated with simultaneous electrocardiographic recordings from the body surface. The electrocardiographic changes in the @entity235 preparation were virtually identical to those in the @entity1 and strongly correlated with a fall in myocardial conduction velocity. We conclude that the QRS changes during @entity5968 result from the altered excitation pattern produced by conduction delay in the @entity63 zone. The probable cause for the increase in terminal QRS voltage is delayed (and uncancelled) activation of the @entity63 zone.
