Antiarrhythmic effects of growth hormone--in vivo evidence from small-animal models of acute myocardial infarction and invasive electrophysiology.

INTRODUCTION

A growing body of evidence suggests a possible role for growth hormone (GH) in the treatment of congestive heart failure (CHF) and myocardial infarction (MI). The aim of this study was to investigate in vivo the effects of GH treatment on incidence and severity of ventricular arrhythmias normal and MI rats.

METHODS

Male Sprague-Dawley rats weighing approximately 350 g were randomized into 3 groups. Growth hormone-treated rats (n = 6) received 6 mg/kg of human GH. The placebo group (n = 10) received 1 mL of saline. Amiodarone-treated rats (n = 10) were injected with 25 mg/kg and served as positive controls. All animals received a single intraperitoneal injection 6 hours before induction of MI. Myocardial infarction was induced by ligation of the left coronary artery, resulting in a large (approximately 40%) anterolateral MI. A computerized electrocardiographic tracing was obtained continuously before induction of MI and up to 1 hour postinfarction. Invasive hemodynamics including intraventricular and arterial pressure were registered for 60 minutes post-MI. Qualitative as well as quantitative variables of ventricular arrhythmias were analyzed. Invasive electrophysiology with pacing in right atrium and ventricle was performed in normal rats (control, n = 13; GH, n = 6; amiodarone, n = 6) to asses inducibility of supraventricular and ventricular arrhythmias.

RESULTS

Growth hormone- and amiodarone-treated rats had lower resting heart rate at baseline before induction of MI. The arrhythmia scores in the GH- (3.8 +/- 1) and amiodarone-treated (3.9 +/- 0.5) animals were significant lower than in the placebo group (5.9 +/- 0.5, P < .05). There was no significant difference in arrhythmia score between the GH and amiodarone groups. The incident of inducible ventricular arrhythmias was lower in the GH (2/6, 33%) and amiodarone (2/6, 33%) groups compared with controls (13/16, 81%; P = .05). There was no difference in inducibility of atrial fibrillation between the GH (5/6, 83%) and control (13/14, 93%) groups, whereas the inducibility of atrial fibrillation was significantly lower in the amiodarone group (2/6, 33%; P < .05).

CONCLUSIONS

Pretreatment with GH reduces the burden of ventricular arrhythmias in rats with postinfarction CHF due to acute MI. Growth hormone may be useful in the treatment of CHF and acute MI.