Electrophysiologic consequences of chronic experimentally induced left ventricular pressure overload.
Cardiac electrophysiologic alterations were evaluated 1 to 8 months after partial supracoronary aortic constriction in cats. This procedure induced left ventricular systolic hypertension and hypertrophy with marked connective tissue infiltration. In situ, premature ventricular complexes were observed during or after vagal slowing of sinus rate in 8 (26%) of the 31 experimental animals, while an additional 3 of the 31 developed ventricular fibrillation. No arrhythmias were recorded in 31 normal or 7 sham-operated cats. In vitro, 29% of the left ventricular preparations from cats with pressure overload and 5% from control cats showed spontaneous ectopic activity. During stimulation at cycle lengths of 800 to 1,000 ms, multiple site impalements of subendocardial muscle cells within fibrotic regions revealed heterogeneous electrical abnormalities. These included short action potential duration, low amplitude action potentials generated from low resting potentials, split upstrokes and electrically silent areas. Impalements in nonfibrotic areas of the left ventricle showed prolongation of muscle action potential duration. Long-term disturbances in cellular electrophysiologic properties may favor the development of arrhythmias and thereby contribute to sudden cardiac death in left ventricular hypertension and hypertrophy.
D000818:Animals; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology*; D002415:Cats; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000473:pathology*; D014693:Ventricular Fibrillation / Q000503:physiopathology