Establishment of a canine model of cardiac memory using endocardial pacing via internal jugular vein

<p>Abstract</p> <p>Background</p> <p>Development of experimental animal models has played an important role in understanding the mechanisms of cardiac memory. The purpose of this study was to evaluate a new canine model of cardiac memory using endocardial ventricular pacing via internal jugular vein.</p> <p>Methods</p> <p>Twelve Beagle dogs underwent placement of a permanent ventricular pacemaker mimicking the use of pacemakers in humans and induction of cardiac memory by endocardial ventricular pacing.</p> <p>Results</p> <p>Cardiac memory was achieved in 11 of 12 attempts overall. Procedural mortality due to cardiac tamponade (n = 1) occurred in the first attempt. The T-wave memory persisted for 96 ± 17 minutes and 31 ± 6 days in the short-term and long-term cardiac memory groups, respectively. There were no significant differences in the heart rate, blood pressure and echocardiographic parameters in the animals between before and after ventricular pacing in the short-term and long-term cardiac memory groups. No significant pathologic changes with the light microscopy were found in the present study in all dogs.</p> <p>Conclusion</p> <p>The model does require surgery but is not as invasive as an open-chest model. This canine model can serve as a useful tool for studying mechanisms of cardiac memory.</p

Pacing-induced ventricular remodeling in the chick embryonic heart.

Chronic ectopic pacing in the adult heart induces myocardial hypotrophy close to the pacing site. We have recently described a similar localized decrease of compact myocardium thickness in the chick embryonic heart after 48 h of intermittent apical ventricular pacing. Here we analyze the cellular mechanisms underlying the response of the embryonic heart to pacing. Because the developing heart had been found to adjust its morphology according to functional demands by undergoing cellular hyperplasia or hypoplasia, we hypothesized that the stimulation should result in hypoplasia of the apical ventricular compartment. Morphologic analysis of hearts submitted to 18 h of effective pacing during 48 h showed a mild to moderate ventricular dilatation, a 28% decrease in the apical compact layer thickness with no changes in other ventricular locations, and atrial wall thickening. These modifications were caused by changes in the number of cell layers, whereas cell size was similar between paced and control hearts. Analysis of proliferative activity after 24 h of pacing showed a decrease of 32% in the rate of cell proliferation limited to the apical compact layer exposed to stimulation. No ultrastructural injury or increased cell death was found. These changes were accompanied by down-regulation of the myocardial growth factor fibroblast growth factor-2 but no differences were found in the expression of platelet-derived growth factor. Thus, chronic intermittent ventricular pacing induces myocardial remodeling in the chick embryonic heart, on the basis of locally regulated rates of cell proliferation