Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Myocardial infarction related atrial fibrillation: role of endogenous adenosine.

Myocardial infarction related atrial fibrillation: role of endogenous adenosine. Exogenous administration of adenosine induces atrial fibrillation in up to 7.0% of patients. Animal studies affirm endogenous adenosine released in response to tissue hypoxia may play a mechanistic role in arrhythmias associated with myocardial ischaemia or hypoxia. Therefore, atrial fibrillation occurring early after the acute phase of myocardial infarction involving atrial tissue may be secondary to an excessive accumulation of adenosine that leads to a shortening of atrial refractory period. Early in the course of acute inferior myocardial infarction, two patients (males aged 45 and 68) suffered new onset sustained atrial fibrillation that was abrupt in onset and complicated their clinical management. They were administered 250 mg theophylline as a slow intravenous injection at a rate of 100 mg/min or until conversion to normal sinus rhythm occurred. Both patients converted to normal sinus rhythm within five minutes of the administration of theophylline. In up to 52 hours of continuous ECG monitoring after the theophylline administration the atrial fibrillation did not recur. Neither patient experienced any adverse outcome from theophylline administration. These observations are the first reported in humans or laboratory animals to suggest that atrial fibrillation, presumably due to elevated interstitial atrial concentration of adenosine caused by myocardial ischaemia, can be terminated with an adenosine receptor antagonist. However, the hypothesis that excessive accumulation of endogenous adenosine in atrial tissue may induce atrial fibrillation is well substantiated by other investigators. Thus, A1 adenosine receptor antagonists may prove to be valuable in the management of ischaemia related atrial fibrillation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Heart British Medical Journal

Myocardial infarction related atrial fibrillation: role of endogenous adenosine.

Myocardial infarction related atrial fibrillation: role of endogenous adenosine.

Heart , Volume 78 (1) – Jul 1, 1997

Abstract


Exogenous administration of adenosine induces atrial fibrillation in up to 7.0% of patients. Animal studies affirm endogenous adenosine released in response to tissue hypoxia may play a mechanistic role in arrhythmias associated with myocardial ischaemia or hypoxia. Therefore, atrial fibrillation occurring early after the acute phase of myocardial infarction involving atrial tissue may be secondary to an excessive accumulation of adenosine that leads to a shortening of atrial refractory period. Early in the course of acute inferior myocardial infarction, two patients (males aged 45 and 68) suffered new onset sustained atrial fibrillation that was abrupt in onset and complicated their clinical management. They were administered 250 mg theophylline as a slow intravenous injection at a rate of 100 mg/min or until conversion to normal sinus rhythm occurred. Both patients converted to normal sinus rhythm within five minutes of the administration of theophylline. In up to 52 hours of continuous ECG monitoring after the theophylline administration the atrial fibrillation did not recur. Neither patient experienced any adverse outcome from theophylline administration. These observations are the first reported in humans or laboratory animals to suggest that atrial fibrillation, presumably due to elevated interstitial atrial concentration of adenosine caused by myocardial ischaemia, can be terminated with an adenosine receptor antagonist. However, the hypothesis that excessive accumulation of endogenous adenosine in atrial tissue may induce atrial fibrillation is well substantiated by other investigators. Thus, A1 adenosine receptor antagonists may prove to be valuable in the management of ischaemia related atrial fibrillation.

Loading next page...
 
/lp/british-medical-journal/myocardial-infarction-related-atrial-fibrillation-role-of-endogenous-4m61MNR0yT

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
British Medical Journal
ISSN
1355-6037
eISSN
1468-201X
DOI
10.1136/hrt.78.1.88
Publisher site
See Article on Publisher Site

Abstract

Exogenous administration of adenosine induces atrial fibrillation in up to 7.0% of patients. Animal studies affirm endogenous adenosine released in response to tissue hypoxia may play a mechanistic role in arrhythmias associated with myocardial ischaemia or hypoxia. Therefore, atrial fibrillation occurring early after the acute phase of myocardial infarction involving atrial tissue may be secondary to an excessive accumulation of adenosine that leads to a shortening of atrial refractory period. Early in the course of acute inferior myocardial infarction, two patients (males aged 45 and 68) suffered new onset sustained atrial fibrillation that was abrupt in onset and complicated their clinical management. They were administered 250 mg theophylline as a slow intravenous injection at a rate of 100 mg/min or until conversion to normal sinus rhythm occurred. Both patients converted to normal sinus rhythm within five minutes of the administration of theophylline. In up to 52 hours of continuous ECG monitoring after the theophylline administration the atrial fibrillation did not recur. Neither patient experienced any adverse outcome from theophylline administration. These observations are the first reported in humans or laboratory animals to suggest that atrial fibrillation, presumably due to elevated interstitial atrial concentration of adenosine caused by myocardial ischaemia, can be terminated with an adenosine receptor antagonist. However, the hypothesis that excessive accumulation of endogenous adenosine in atrial tissue may induce atrial fibrillation is well substantiated by other investigators. Thus, A1 adenosine receptor antagonists may prove to be valuable in the management of ischaemia related atrial fibrillation.

Journal

HeartBritish Medical Journal

Published: Jul 1, 1997

There are no references for this article.