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.

This article has been cited by other articles:

				E. Zakynthinos, Ch. Pierrutsakos, Z. Daniil, and D. Papadogiannis Losartan Controlled Blood Pressure and Reduced Left Ventricular Hypertrophy But Did Not Alter Arrhythmias in Hypertensive Men with Preserved Systolic Function Angiology, July 1, 2005; 56(4): 439 - 449. [Abstract] [PDF]

				D. G Katritsis and A.J. Camm Nonsustained ventricular tachycardia: where do we stand? Eur. Heart J., July 1, 2004; 25(13): 1093 - 1099. [Abstract] [Full Text] [PDF]

				S. S Chugh, S. Whitesel, M. Turner, C. T Roberts Jr., and S. R Nagalla Genetic basis for chamber-specific ventricular phenotypes in the rat infarct model Cardiovasc Res, February 1, 2003; 57(2): 477 - 485. [Abstract] [Full Text] [PDF]

				R. Berger, M. Huelsman, K. Strecker, A. Bojic, P. Moser, B. Stanek, and R. Pacher B-Type Natriuretic Peptide Predicts Sudden Death in Patients With Chronic Heart Failure Circulation, May 21, 2002; 105(20): 2392 - 2397. [Abstract] [Full Text] [PDF]

				M. A. Vos, S. H. M. de Groot, S. C. Verduyn, J. van der Zande, H. D. M. Leunissen, J. P. M. Cleutjens, M. van Bilsen, M. J. A. P. Daemen, J. J. Schreuder, M. A. Allessie, et al. Enhanced Susceptibility for Acquired Torsade de Pointes Arrhythmias in the Dog With Chronic, Complete AV Block Is Related to Cardiac Hypertrophy and Electrical Remodeling Circulation, September 15, 1998; 98(11): 1125 - 1135. [Abstract] [Full Text] [PDF]

				L. R. C. Dekker, H. Rademaker, J. T. Vermeulen, T. Opthof, R. Coronel, J. A. E. Spaan, and M. J. Janse Cellular Uncoupling During Ischemia in Hypertrophied and Failing Rabbit Ventricular Myocardium : Effects of Preconditioning Circulation, May 5, 1998; 97(17): 1724 - 1730. [Abstract] [Full Text] [PDF]

				A. M. Gillis, R. A. Geonzon, H. J. Mathison, E. Kulisz, W. M. Lester, and H. J. Duff The Effects of Barium, Dofetilide and 4-Aminopyridine (4-AP) on Ventricular Repolarization in Normal and Hypertrophied Rabbit Heart J. Pharmacol. Exp. Ther., April 1, 1998; 285(1): 262 - 270. [Abstract] [Full Text]

				G. Schillaci, P. Verdecchia, C. Borgioni, A. Ciucci, I. Zampi, M. Battistelli, R. Gattobigio, N. Sacchi, and C. Porcellati Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension Hypertension, August 1, 1996; 28(2): 284 - 289. [Abstract] [Full Text]

				J. Diez, C. Laviades, G. Mayor, M. J. Gil, and I. Monreal Increased Serum Concentrations of Procollagen Peptides in Essential Hypertension : Relation to Cardiac Alterations Circulation, March 1, 1995; 91(5): 1450 - 1456. [Abstract] [Full Text]