Modification of Ventricular Fibrillation Activation Patterns Induced by Local Stretching

Abstract

Local stretching increases the electrophysiological heterogeneity of myocardium and accelerates and increases the complexity of VF in the stretched area, without significantly modifying the occurrences of the types of VF activation patterns in the nonstretched zone.

Pharmacological modifications of the stretch-induced effects on ventricular fibrillation in perfused rabbit hearts

“…Activation maps during VF were constructed every 100 ms in the 2-s time windows analyzed immediately before stretch and at the third minute of the stretching and poststretching periods. Isochrones were drawn, and, in each map, the wavefronts, conduction block lines, reentrant activations, and breakthrough patterns were analyzed as in previous studies (6,8) (Figs. 2 and 3).…”

“…In the propranolol series, the drug (at a concentration of 1 M) was added to the perfusion fluid from the beginning of the experiments to ensure its effects during the stretching stage of the experiments. Ten minutes after the induction of VF, stretching was applied and maintained for 10 min by displacing the stem of the L-shaped intraventricular device 6 mm, thus giving rise in the SZ to 12% longitudinal increments along the vertical and horizontal axes (8). After this period, local stretching was discontinued, and VF recording was continued for another 5 min.…”

“…An L-shaped device was introduced through the left atrium into the left ventricular cavity to induce local stretching of the left ventricular free wall (8,63). The device consisted of a hollow tube measuring 3.5 mm in diameter, through which a stem 1.5 mm in diameter could be advanced.…”

“…The present study analyzed and compared the acceleration of ventricular fibrillation (VF) activation frequency produced by acute stretch (8) under the influence of three substances: the Na ϩ /Ca 2ϩ exchanger blocker KB-R7943 (22,23,38,67), the ␤-blocker propranolol, and the adenosine A 2 receptor antagonist SCH-58261 (71). In relation to the first of these drugs, the inactivation of the Na ϩ /Ca 2ϩ exchanger results in a decrease in the slow force response to stretch and in the magnitude of Ca 2ϩ transients (69), although there is little information about its effects upon the electrophysiological modifications induced by stretch.…”

“…Adenosine A 2 receptor stimulation produces an increase in adenylyl cyclase activity and cAMP (12,50,53,54), with a positive inotropic response similar to that seen with an increase in extracellular Ca 2ϩ concentrations (49,52), although it is not known whether adenosine A 2 receptor block would modulate the electrophysiological effects of stretch. To clarify the modifications of the electrophysiological effects of stretching under the influence of these three substances, we used an isolated Langendorff-perfused rabbit heart model in which analysis of the dominant frequency (DF) and the activation patterns of VF allowed us to illustrate the electrophysiological modifications produced by acute stretch applied on the free wall of the left ventricle (8,63).…”