R-wave amplitude variations during acute experimental myocardial ischemia: an inadequate index for changes in intracardiac volume.

Abstract

SUMMARY The role of intracardiac volume in controlling electrocardiographic R-wave amplitude changes during acute myocardial ischemia was studied in 24 open-chest dogs. The R-wave amplitude in surface ECG leads 2, V. and Frank X, Y and Z leads were correlated with hemodynamic, echocardiographic and angiographic changes in a 5-minute circumflex coronary artery ligation and reperfusion model. After coronary ligation, left ventricular end-diastolic diameter and volume increased progressively above control, reached a peak and plateau at 120-130 seconds after ligation and did not return to control levels until more than 5 minutes after release of the occlusion. In contrast, the R-wave amplitude showed a biphasic response to acute ischemia, reaching a nadir (IR = 18.2% below control) at 30 seconds after coronary ligation and only subsequently increased to reach a peak ( =R 52% above control) at 150 seconds after ligation. In addition, R-wave amplitude returned immediately to control levels within 10 seconds after reperfusion. In six other dogs, both venae cavae were occluded for a 30-second period, beginning 180 seconds after coronary ligation. Although intracardiac volume decreased markedly, R-wave amplitudes increased even more. Thus, the demonstration of discordance between alterations in intracardiac volume and R-wave amplitude in these studies suggests that factors other than intracardiac volume determine R-wave amplitude changes in the course of acute myocardial ischemia.THE IMPORTANCE of intracardiac blood volume to the magnitude of scaler ECG potentials was first postulated by Brody.1 Brody suggested that an increase in intracardiac blood volume decreases tangentially oriented electrical vectors, whereas the radially oriented vectors are increased. The initial QRS vectors that generate the R wave on the surface ECG are radially oriented, so increases in intracardiac volume could thereby result in increases in R-wave amplitude -the Brody effect.' These theoretical considerations were later corroborated by a series of experiments in laboratory animals with normal myocardium2 8 and in other studies using biophysical and computer models.9'-1 Clinical studies have shown an increase in R-wave amplitude during maximal exercise in patients with proved coronary artery disease.12"17 Assuming that the increases in R-wave amplitude in these patients are directly related to ischemia-induced increases in intracardiac volume by the Brody effect, some authors have advocated using R-wave changes as a sensitive and specific indicator of coronary artery disease.12 Moreover, exercise-induced increases in R-wave amplitude have been suggested as a diagnostic marker to identify The present study was designed to determine, under controlled experimental conditions, the relationship between intracardiac volume changes and surface electrocardiographic R-wave amplitude variations during the immediate phase of acute myocardial ischemia. A canine model of acute coronary ligation was used. Materials and Methods Twenty

Intramyocardial conduction: a major determinant of R-wave amplitude during acute myocardial ischemia.

“…Subsequently, 2RWA increased significantly, peaking 20-30 seconds after the maximal increase in left ventricular dimensions. These findings and our previous work"' 10 challenge the hypothesis that the Brody effect is the major determinant of R-wave amplitude changes during acute myocardial ischemia. Therefore, other factors, including changes in myocardial con-(continued on next page) duction patterns, may have a role.…”

Dissociation between Alterations in Myocardial Perfusion and R-Wave Amplitude after Hemodialysis

“…This discordance between changes in LV performance and R-wave response excludes myocardial ischemia as the sole determinant of R-wave increase after dialysis. Since the role of left ventri cular volume in determining R-wave change (Brody effect) has been challenged [3][4][5][6], other factors could have an important influence on R-wave amplitude variations, in cluding abnormal myocardial conduction patterns, altered depolarization and repolarization patterns [3].…”

Geometric determinants of electrocardiographic left ventricular hypertrophy.

“…7 In support of this theory, a positive relationship has been found between LV volume and ECG voltage in several experimental studies8'-1 and has been inferred in man on the basis of voltage changes during exercise. However, other studies in patients with chronic heart disease,"2 13 as well as experimental studies of acute changes in LV volume, 14,15 suggest that ECG voltage for any given LV mass (LVM) may decrease with LV enlargement.…”