Do endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studies

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Μικρογραφία εικόνας

Ημερομηνία

Συγγραφείς

Oikonomidis, D. L.
Baltogiannis, G. G.
Kolettis, T. M.

Τίτλος Εφημερίδας

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Εκδότης

Περίληψη

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Είδος δημοσίευσης σε συνέδριο

Είδος περιοδικού

peer-reviewed

Είδος εκπαιδευτικού υλικού

Όνομα συνεδρίου

Όνομα περιοδικού

J Interv Card Electrophysiol

Όνομα βιβλίου

Σειρά βιβλίου

Έκδοση βιβλίου

Συμπληρωματικός/δευτερεύων τίτλος

Περιγραφή

Sudden cardiac death constitutes a major health-related problem. In the majority of cases, sudden cardiac death is due to ventricular tachyarrhythmias secondary to acute myocardial infarction. The pathophysiologic chain of events leading to ventricular tachyarrhythmias after acute coronary occlusion is complex and incompletely understood. Experimental and clinical studies have indicated that endothelin-1 production rises markedly very early in the course of myocardial infarction. Endothelin-1 exerts significant electrophysiologic actions on ventricular cardiomyocytes and participates in the genesis of ischemic ventricular tachyarrhythmias. Endothelin-1, acting via two G-protein-coupled receptors (ETA and ETB), prolongs the action potential duration and increases the occurrence of spontaneous calcium transients, resulting in early afterdepolarizations and ventricular tachyarrhythmias via triggered activity. Moreover, endothelin-1 enhances sympathetic stimulation, a well established contributor to ventricular arrhythmogenesis during acute myocardial infarction. Despite these considerations, the therapeutic potential of endothelin receptor antagonists as antiarrhythmic drugs during myocardial ischemia/infarction is still under investigation. To date, a number of endothelin-1 receptor antagonists are available, presenting different degrees of selectivity for ETA and ETB receptors. The arrhythmogenic effects of endothelin-1 are exerted mainly via stimulation of the ETA receptors, but the role of ETB receptors remains controversial, as previous studies have produced conflicting results. This review summarizes the current state-of-the-art on the role of endothelin-1 in the genesis of ventricular arrhythmias during acute myocardial infarction and raises some hypotheses that could be explored in future studies.

Περιγραφή

Λέξεις-κλειδιά

Animals, Coronary Occlusion/complications/physiopathology, Endothelin-1/blood/physiology, Humans, Myocardial Infarction/blood/*complications/etiology/pathology/physiopathology, Receptor, Endothelin A/drug effects/physiology, Receptor, Endothelin B/drug effects/physiology, Receptors, Endothelin/*drug effects, Signal Transduction/physiology, Sympathetic Nervous System/physiopathology, Tachycardia, Ventricular/physiopathology/prevention & control

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Σύνδεσμος

http://www.ncbi.nlm.nih.gov/pubmed/20532602
http://www.springerlink.com/content/2068701781834252/fulltext.pdf

Γλώσσα

en

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Εξεταστική επιτροπή

Γενική Περιγραφή / Σχόλια

Ίδρυμα και Σχολή/Τμήμα του υποβάλλοντος

Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής

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