| pubmed-article:7616143 | pubmed:abstractText | This study was undertaken to investigate the activation patterns of spontaneous ventricular arrhythmias during acute myocardial ischemia in dogs. In 14 open-chest dogs, the left anterior descending coronary artery was occluded for 2 hours. Three-dimensional activation maps were derived from 240 bipolar sites by insertion of 60 plunge needle electrodes into both ventricles and the septum. Global ventricular activation sequences were displayed in five planes in 10 dogs, whereas the high density regional activation maps of the anterior wall were displayed in four layers in 4 dogs. Three-dimensional activation maps of 95 sinus beats, 82 premature ventricular complexes (PVCs), and 210 beats of ventricular tachycardia (VT) were analyzed. Sinus beats had a uniform activation pattern with total ventricular activation times measuring 42 +/- 4 ms and 67 +/- 8 ms during baseline and ischemia, respectively (P < .05). The PVCs and VTs originated from the subendocardial and intramural layers, and activation patterns invariably suggested focal excitation. Macroeentry was not operative because (1) the breakthrough sites were always remote from the latest activation areas; (2) there was no electrical activity bridging the gap between the termination of a beat and initiation of the subsequent beat; and (3) impulse conduction was not sufficiently delayed to reexcite the area of impulse origin even though functional conduction block was frequently present. In high-density regional activation maps, fragmented activity spanning the diastolic interval was never found. In conclusion, spontaneously occurring PVCs and VTs during acute myocardial ischemia in dogs display focal excitation with no evidence of macroreentry. | lld:pubmed |
