Hemodynamic and reflex sympathetic control of transmural activation and rate of ventricular tachycardia in ischemic and hypertrophic ventricular myocardium of the dog.

Abstract

Background. A previous study found that the electrophysiological response to ischemia is altered in hypertrophic myocardium, resulting in prolonged transmural activation time (TAT) associated with induction of sustained monomorphic ventricular tachycardia. This study investigated the role of hemodynamics in modulating TAT and the cycle length of induced ventricular tachycardia (VT) in dogs with left ventricular hypertrophy (LVH).Methods and Resuts. Anesthetized open-chest dogs underwent 3 hours of uninterrupted circumflex coronary occlusion. During atrial drive, TAT was recorded between endocardial and epicardial bipolar pairs on the same multipolar plunge needle placed in nonischemic and ischemic zones, documented by triphenyltetrazolium chloride staining. TAT and VT induced by up to three extrastimuli were studied during hypertension (control), during normotension produced most frequently by nitroprusside infusion (3-6 ag/kg/min), and during further hypertension most frequently produced by phenylephrine infusion (1-5 jLg/kg/min). Twenty-five dogs with chronic hypertension and LVH (group 1) produced by a

Myocardial ischemia-reperfusion damage impacts occurrence of ventricular fibrillation in dogs

“…The effective refractory period (ERP) was determined by applying premature stimuli after eight regular-drive stimuli (at a 300-ms cycle length) at four times the threshold to the ventricular myocardium at the normal, ischemic, and IRD sites with a programmable cardiac electrophysiological stimulator. ERP was defined as the longest premature coupling interval without ventricular capture (12).…”