Ventricular dyssynchrony as a cause of structural disease in the heart of Dorper sheep

J Ker,C.F Van Der Merwe,E.C Webb

doi:10.4102/ojvr.v71i3.260

Abstract

Ventricular dyssynchrony is a disturbance of the normal, organized electromechanical coupling of the two ventricles. This condition has many causes, such as left bundle branch block, ventricular preexcitation, right ventricular pacing and right ventricular premature ventricular complexes (PVCs). Ventricular dyssynchrony has many adverse haemodynamic effects on the left ventricle and we wanted to know whether these adverse haemodynamic effects might have any structural consequences on the left ventricles of such hearts. Six healthy Dorper wethers were subjected to numerous right ventricular PVCs to induce ventricular dyssynchrony in order to determine whether any structural consequences will occur in the left ventricles of these hearts. Myocarditis in the musculature of the left ventricles of all six these hearts was seen.

Highlights

In 1925 Wiggers observed that, if ventricular activation proceeds from the ventricular epicardium instead of from the atrium, the consequence will be a lower peak left ventricular pressure as well as a lower dP/dt
No sheep in this study showed any signs of infection as a result of the spring-wire guide during the entire study period
Relation between the premature ventricular complexes (PVCs) load and number of abnormal left ventricular segments We found no relation between the PVC load, as well as the number of days subjected to PVCs, and the number of abnormal left ventricular segments (Table 2)

Summary

Introduction

In 1925 Wiggers observed that, if ventricular activation proceeds from the ventricular epicardium instead of from the atrium, the consequence will be a lower peak left ventricular pressure as well as a lower dP/dt. Cardiac activation is initiated in the atria and proceeds to the ventricles via the specialized conduction system (SCS) This SCS consists of the His bundle, the left and right bundle branches with their major fascicles and the peripheral Purkinje network (Van Dam 1989). The terminal ramifications of this Purkinje network merge into the ventricular myocardium at sites of Purkinje-myocardial coupling Proximal to these sites the SCS has no functional connections with the myocardium because of a thin, collagenous sheath (Van Dam 1989)

Methods

Results

Conclusion