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[Sudden death (II). Myocardial ischemia and ventricular arrhythmias in experimental models: triggering mechanisms]. / Muerte súbita (II). Isquemia miocárdica y arritmias ventriculares en modelos experimentales: mecanismos desencadenantes.
Rodríguez-Sinovas, A; Cinca, J.
Affiliation
  • Rodríguez-Sinovas A; Laboratorio A de Cardiología Experimental, Hospitals Vall d'Hebron, Barcelona. ars@hg.vhebron.es
Rev Esp Cardiol ; 52(10): 851-9, 1999 Oct.
Article in Es | MEDLINE | ID: mdl-10563159
Metabolic and electrolytic alterations generated in the acute ischemic myocardium, such as an increase in extracellular potassium or acidosis, are responsible for the occurrence of ventricular arrhythmias. In the first 5-10 minutes following coronary occlusion, reentry seems to have an important role, although not in the next 15 minutes. If the patient survives, a subacute arrhythmia period appears, 6 to 72 hours after the onset of ischemia, probably due to abnormal automaticity in the surviving Purkinje fibers. Finally, reentry in the epicardial border zone is the most likely mechanism for chronic arrhythmias. In this review we focus on the studies dealing with the mechanisms of ischemia-induced arrhythmias, with special reference to those conducted in experimental models.
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Collection: 01-internacional Database: MEDLINE Main subject: Arrhythmias, Cardiac / Myocardial Ischemia Type of study: Etiology_studies Limits: Humans Language: Es Journal: Rev Esp Cardiol Year: 1999 Document type: Article Country of publication: Spain
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Collection: 01-internacional Database: MEDLINE Main subject: Arrhythmias, Cardiac / Myocardial Ischemia Type of study: Etiology_studies Limits: Humans Language: Es Journal: Rev Esp Cardiol Year: 1999 Document type: Article Country of publication: Spain