Origin of the giant R wave in acute transmural myocardial infarction in the pig.
An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1 min after coronary artery ligation (p less than 0.05), compared to control amplitude and peaked at 8 min (p less than 0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients +/- SEM at 1 min, r = 0.64 +/- 0.08, and at 8 min, r = 0.81 +/- 0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p less than 0.0001), and were greater in subepicardial than in subendocardial areas (p less than 0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.
Chang
W S
WS
Department of Medicine, University of Rochester Medical Center, New York 14642.
Akiyama
T
T
Richeson
J F
JF
Faillace
R T
RT
Serrino
P
P
D000818:Animals; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000503:physiopathology; D013552:Swine