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

J R Hopson and J B Martins
Circulation (New York, N.Y.), Vol.86(2), pp.618-627
08/1992
DOI: 10.1161/01.CIR.86.2.618
PMID: 1353421
url
https://doi.org/10.1161/01.CIR.86.2.618View
Published (Version of record) Open Access

Abstract

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). 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 micrograms/kg/min), and during further hypertension most frequently produced by phenylephrine infusion (1-5 micrograms/kg/min). Twenty-five dogs with chronic hypertension and LVH (group 1) produced by a single-kidney renal clamp mechanism and 15 control dogs were studied. In the latter, neither intervention altered TAT, and no VT was inducible. In group 1, however, nitroprusside reversibly prolonged TAT within the ischemic zone (mean +/- SEM, 31 +/- 3 to 34 +/- 3 msec, p less than 0.005) and cycle length of induced VT (204 +/- 19 to 240 +/- 17 msec, p less than 0.01). Phenylephrine reversibly shortened both TAT in the ischemic zone (33 +/- 2 to 28 +/- 2 msec, p less than 0.05) and cycle length of VT (219 +/- 17 to 165 +/- 11 msec, p less than 0.025). Cycle length of VT and TAT were dissociated from blood pressure elevation in two dogs with LVH; when blood pressure was elevated by sympathetic nerve stimulation, cycle length of VT and TAT were prolonged. In 11 dogs with LVH (group 2), prolongation of TAT with nitroprusside infusion was prevented by intravenous metoprolol (1.0 mg/kg). Of 12 dogs with LVH and inducible VT (group 3), seven still had VT inducible after metoprolol, but the cycle length of VT was still prolonged with nitroprusside infusion. These results suggest that 1) TAT in acutely ischemic LVH was uniquely responsive to hemodynamic influences, an effect prevented by beta-blockade with metoprolol, and 2) the cycle length of VT was also uniquely regulated by hemodynamic influences but not blocked by metoprolol.
 Adrenergic beta-Antagonists - pharmacology Animals Autonomic Nervous System - physiology Cardiac Pacing, Artificial Cardiomegaly - etiology Cardiomegaly - physiopathology Dogs Electrocardiography Heart Conduction System - physiopathology Hemodynamics - physiology Hypertension - complications Hypertension - physiopathology Metoprolol - pharmacology Tachycardia - etiology Tachycardia - physiopathology

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