Effect of acute volume load on refractoriness and arrhythmia development in isolated, chronically infarcted canine hearts.
- 1 March 1989
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 79 (3) , 687-697
- https://doi.org/10.1161/01.cir.79.3.687
Abstract
In normal isolated, perfused canine ventricles, increased ventricular volume leads to shortening of refractoriness. To test the hypothesis that myocardium within an infarction zone is more susceptible to volume-induced changes in refractoriness than is normal myocardium, we measured strength-interval curves at low and high end-diastolic volumes at control and infarcted sites in 14 isolated, blood perfused, canine hearts with chronic (greater than 25 days) infarctions. In addition, the effect of volume load on inducing ventricular arrhythmias was studied at one to six sites in 11 hearts. Differences in refractoriness and inducibility at low (22 +/- 5 ml) and high (48 +/- 6 ml) end-diastolic volumes were compared. At control sites, volume load reduced the absolute refractory period from 178 +/- 16.5 to 175 +/- 16.7 msec (p less than 0.05), but no significant change in the relative refractory period occurred. At infarcted sites, the change in refractoriness with volume load was greater, and the absolute refractory period decreased from 171.5 +/- 21 to 160.6 +/- 26.3 msec (p less than 0.01), and the relative refractory period decreased from 180.1 +/- 22.1 to 169.9 +/- 26 msec (p = 0.05). This differential effect of volume load on refractoriness led to an increased dispersion of overall refractoriness at high volume. Infarcted sites showing the largest changes in refractoriness were characterized by patchy scars extending at least to the midmyocardium, whereas sites located within areas of transmural scar, endocardial scar, or rare microfoci of fibrosis showed no increased sensitivity to volume load. Of eight hearts in which no tachyarrhythmias were inducible during programmed electrical stimulation at low volume, four had tachyarrhythmias induced at high volume. Sites of stimulation associated with a conversion from noninducible to inducible tachyarrhythmias showed a larger degree of shortening of refractoriness (change in absolute refractory period: 24.7 +/- 16.5 vs. 3.9 +/- 6.5 msec, p less than 0.05). These data indicate that volume loading may have electrophysiologic significance and that it may be of greater functional importance under pathologic conditions.This publication has 34 references indexed in Scilit:
- Effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart FailureNew England Journal of Medicine, 1986
- Inducible sustained ventricular tachycardia and ventricuar fibrillation in conscious dogs with isolated right ventricular infarction: Relation to infarct structureJournal of the American College of Cardiology, 1986
- Effect of enalapril on ventricular arrhythmias in congestive heart failureThe American Journal of Cardiology, 1985
- Serial analysis of electrically induced ventricular arrhythmias in a canine model of myocardial infarctionJournal of the American College of Cardiology, 1985
- Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: Prediction of mortality by ambulatory electrocardiographyThe American Journal of Cardiology, 1985
- Functional Left Ventricular Aneurysm Formation after Acute Anterior Transmural Myocardial InfarctionNew England Journal of Medicine, 1984
- Localized reentry. Mechanism of induced sustained ventricular tachycardia in canine model of recent myocardial infarction.Journal of Clinical Investigation, 1984
- Natural and evoked atrial flutter due to circus movement in dogs: Role of abnormal atrial pathways, slow conduction, nonuniform refractory period distribution and premature beatsThe American Journal of Cardiology, 1980
- Electrophysiologic and anatomic correlates of sustained ventricular tachyarrhythmias in a model of chronic myocardial infarctionThe American Journal of Cardiology, 1980
- Mechanisms of ventricular arrhythmias associated with myocardial infarctionThe American Journal of Cardiology, 1969