Electrophysiologic Effects of Growth Hormone Post-Myocardial Infarction
Autor: | Konstantinos V Stamatis, Evangelos P. Daskalopoulos, Theofilos M. Kolettis, Marianthi Kontonika |
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Přispěvatelé: | UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire |
Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Hemodynamics structural remodeling Review 030204 cardiovascular system & hematology Ventricular tachycardia Catalysis Sudden cardiac death lcsh:Chemistry Inorganic Chemistry 03 medical and health sciences 0302 clinical medicine Fibrosis Internal medicine medicine Animals Humans Myocardial infarction cardiovascular diseases Physical and Theoretical Chemistry ventricular tachyarrhythmias lcsh:QH301-705.5 Molecular Biology Spectroscopy Ventricular Remodeling business.industry Human Growth Hormone Organic Chemistry General Medicine medicine.disease Computer Science Applications Electrophysiological Phenomena 030104 developmental biology myocardial infarction lcsh:Biology (General) lcsh:QD1-999 Coronary occlusion Heart failure Ventricular fibrillation growth hormone Cardiology cardiovascular system electrophysiologic remodeling Tachycardia Ventricular business |
Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 21, Iss 3, p 918 (2020) International Journal of Molecular Sciences, Vol. 21, no. 3, p. 918 [1-16] (2020) |
ISSN: | 1422-0067 |
Popis: | 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. |
Databáze: | OpenAIRE |
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