[In Process Citation]
Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role id ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhythmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrhythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recomendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)
IV. interna klinika Lekarskej fakulty Univerzity Komenskeho v Bratislave, Slovakia.
O
Jurkovicova
S
Cagan