QRS ALTERATIONS IN BODY-SURFACE POTENTIAL DISTRIBUTIONS DURING PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY IN SINGLE-VESSEL DISEASE

Citation
I. Preda et al., QRS ALTERATIONS IN BODY-SURFACE POTENTIAL DISTRIBUTIONS DURING PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY IN SINGLE-VESSEL DISEASE, Journal of electrocardiology, 27(4), 1994, pp. 311-322
Citations number
39
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00220736
Volume
27
Issue
4
Year of publication
1994
Pages
311 - 322
Database
ISI
SICI code
0022-0736(1994)27:4<311:QAIBPD>2.0.ZU;2-D
Abstract
Body surface QRS potentials were recorded with 63 chest leads in 20 pa tients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary arter y (n = 6), or the left circumflex coronary artery (n = 4) before, duri ng, 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 u nipolar electrograms and body surface potential maps. The total QRS co mplex duration decreased in 14 of the 20 patients. Focal conduction di sturbances were observed in six cases; all six had left anterior desce nding coronary artery occlusion and two were also accompanied by a cle ar 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 sur face potential maps (during-minus-before dilation) were considered val uable 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 th e presence or absence of collateral circulation. Two different hypothe ses are suggested to account for the QRS complex shortening observed d uring short-term myocardial ischemic injury: (1) coronary artery occlu sion delayed activation of the portion of the septal region that is no rmally activated early during the QRS, and/or (2) coronary artery occl usion increased the speed of propagation within the ventricles. Both o f these hypotheses are discussed in light of earlier clinical and expe rimental results.