Abstract
Myocardial infarction remains a major health-related problem with significant acute and long-term consequences. Acute coronary occlusion results in marked electrophysiologic alterations that can induce ventricular tachyarrhythmias such as ventricular tachycardia or ventricular fibrillation, often heralding sudden cardiac death. During the infarct-healing stage, hemodynamic and structural changes can lead to left ventricular dilatation and dysfunction, whereas the accompanying fibrosis forms the substrate for re-entrant circuits that can sustain ventricular tachyarrhythmias. A substantial proportion of such patients present clinically with overt heart failure, a common disease-entity associated with high morbidity and mortality. Several lines of evidence point toward a key role of the growth hormone/insulin-like growth factor-1 axis in the pathophysiology of post-infarction structural and electrophysiologic remodeling. Based on this rationale, experimental studies in animal models have demonstrated attenuated dilatation and improved systolic function after growth hormone administration. In addition to ameliorating wall-stress and preserving the peri-infarct myocardium, antiarrhythmic actions were also evident after such treatment, but the precise underlying mechanisms remain poorly understood. The present article summarizes the acute and chronic actions of systemic and local growth hormone administration in the post-infarction setting, placing emphasis on the electrophysiologic effects. Experimental and clinical data are reviewed, and hypotheses on potential mechanisms of action are discussed. Such information may prove useful in formulating new research questions and designing new studies that are expected to increase the translational value of growth hormone therapy after acute myocardial infarction.
Highlights
Myocardial infarction (MI) remains a major health-related problem worldwide, despite major treatment advances such as the widespread use of prompt reperfusion strategies [1]
The incidence of ventricular tachyarrhythmias (VTs) during the subsequent phase of evolving myocardial necrosis has decreased in the present era of primary percutaneous interventions, which are widely applied as first-line treatment of acute MI [1]
We found that phase-I VTs were unaffected, but we observed lower arrhythmogenesis in rats pre-treated with Growth hormone (GH) during phase-II (Figure 2), resulting in lower arrhythmic and total mortality 24 h post-MI
Summary
Myocardial infarction (MI) remains a major health-related problem worldwide, despite major treatment advances such as the widespread use of prompt reperfusion strategies [1]. Most patients with progressive LV enlargement and dysfunction present clinically with overt heart failure, an ominous disease-entity associated with high morbidity and mortality, including sudden cardiac death secondary to VTs. Driven by the high prevalence of coronary artery disease, ample research efforts have been devoted toward the prevention of acute-phase and long-term complications of MI. Growth hormone (GH), a 191-amino-acid single-chain peptide extracted from human pituitary glands, is abundantly expressed in the body, including the ventricular myocardium [3]. The present article reviews the current state-of-the-art on the effects of GH on the LV myocardium during the acute, healing, and chronic phases of MI, placing emphasis on the electrophysiologic actions and the presumed underlying mechanisms. The GH-effects will be examined separately for acute MI, the subsequent remodeling period, and chronic MI
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
