QRS alterations in body surface potential distributions during percutaneous transluminal coronary angioplasty in single-vessel disease

Abstract

Body surface QRS potentials were recorded with 63 chest leads in 20 patients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary artery (n = 6), or the left circumflex coronary artery (n = 4) before, during, and after percutaneous transluminal coronary angioplasty. In each case, three consecutive inflations of relatively short duration (37 ± 14 seconds) were carried out. Electrical activity was displayed as unipolar electrograms and body surface potential maps. The total QRS complex duration decreased in 14 of the 20 patients. Focal conduction disturbances were observed in six cases; all six had left anterior descending coronary artery occlusion and two were also accompanied by a clear shortening of the right epicardial breakthrough time. In these two cases, an initial activation loss seemed to be characteristic, whereas in the other four cases, a rather diffuse slowing of intraventricular conduction, especially during the terminal portion of the QRS, could be observed. Individual and group mean isointegral difference body surface potential maps (during-minus-before dilation) were considered valuable for the interpretation of localized changes in intraventricular conduction during percutaneous transluminal coronary angioplasty, and their individual variations could, at least partly, be explained by the presence or absence of collateral circulation. Two different hypotheses are suggested to account for the QRS complex shortening observed during short-term myocardial ischemic injury: (1) coronary artery occlusion delayed activation of the portion of the septal region that is normally activated early during the QRS, and/or (2) coronary artery occlusion increased the speed of propagation within the ventricles. Both of these hypotheses are discussed in light of earlier clinical and experimental results.