Pharmacological stress with adenosine for myocardial perfusion imaging

Abstract

Adenosine is a ubiquitous purine base that has many physiological actions in the body, including arterial vasodilation in all vascular beds, with the exception of the kidneys. Myocardial ischemia causes an immediate breakdown of adenosine triphosphate and generates adenosine, thereby producing coronary vasodilation and restoring flow. Adenosine produces vasodilation by interacting with the adenosine receptors in the cell wall. Exogenously administered adenosine has a very short half-life (less than 10 seconds) and produces maximal or near-maximal coronary vasodilation in a dose-dependent fashion. The underlying mechanism for production of myocardial perfusion defects by adenosine thallium 201 scintigraphy is a greater coronary flow increase in the normal arteries and a lesser increase in the stenotic arteries. The ultra-short half-life of adenosine requires a continuous intravenous infusion for its use. Adenosine is often administered as a continuous intravenous infusion at a dose of 140 micrograms/kg per minute for 6 minutes, with the thallium injection given midway through the infusion. The safety of this regimen has been demonstrated in several thousand patients around the country. Side effects, due in great part to the potent vasodilatory effect of the drug, occur in most patients during adenosine infusion. Chest pain also occurs often and in some cases may be due to a true coronary steal phenomenon. First-degree atrioventricular (AV) block occurs in approximately 10% and second- or third-degree AV block in approximately 4% of patients due to the inhibitory effect of adenosine on the AV node conduction. The side effects are very short-lived and typically disappear within 1 or 2 minutes after discontinuing the adenosine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)