Regadenoson in the detection of coronary artery disease.
Myocardial perfusion studies use either physical exercise or pharmacologic vasodilator stress to induce maximum myocardial hyperemia. Adenosine and dipyridamole are the most commonly used agents to induce coronary arterial vasodilation for myocardial perfusion imaging. Both cause frequent undesirable side-effects. Because of its ultrashort half-life, adenosine must be administered by constant intravenous infusion during the examination. A key feature of an ideal A2A agonist for myocardial perfusion imaging studies would be an optimal level and duration of hyperemic response. Drugs with a longer half-time and more selective A2A adenosine receptor agonism, such as regadenoson, should theoretically result in a similar degree of coronary vasodilation with fewer or less severe side-effects than non-selective, ultrashort-lasting adenosine receptor stimulation. The available preclinical and clinical data suggest that regadenoson is a highly subtype-selective, potent, low-affinity A2A adenosine receptor agonist that holds promise for future use as a coronary vasodilator in myocardial perfusion imaging studies. Infusion of regadenoson achieves maximum coronary hyperemia that is equivalent to adenosine. After a single bolus infusion over 10 s, hyperemia is maintained significantly longer (approximately 2-5 min) than with adenosine, which should facilitate radionuclide distribution for myocardial perfusion imaging studies. In comparison with the clinically competitive A2A adenosine receptor agonist binodenoson, regadenoson has a several-fold shorter duration of action, although the magnitude of hyperemic response is comparable between the two. The more rapid termination of action of regadenoson points to an advantage of enhanced control for the clinical application. Regadenoson selectively causes vasodilation of the coronary circulation, whereas effects on systemic blood pressure are only mild. The clinical adverse effect profile of regadenoson appears to be favorable, particularly with respect to dreaded atrioventricular conduction disturbances and bronchospasm.
Department of Cardiology, West-German Heart Center Essen, University of Duisburg-Essen, Essen, Germany. christiane.buhr@uk-essen.de
Christiane
C
Buhr
Mario
M
Gössl
Raimund
R
Erbel
Holger
H
Eggebrecht
D058908:Adenosine A2 Receptor Agonists; D000818:Animals; D000075202:Contraindications; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000378:metabolism / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D006334:Heart Function Tests; D006801:Humans; D006940:Hyperemia / Q000378:metabolism / Q000503:physiopathology; D011687:Purines / Q000009:adverse effects; D011720:Pyrazoles / Q000009:adverse effects; D043705:Receptor, Adenosine A2A / Q000378:metabolism; D013329:Structure-Activity Relationship; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000009:adverse effects
D058908:Adenosine A2 Receptor Agonists; D011687:Purines; D011720:Pyrazoles; D043705:Receptor, Adenosine A2A; D014665:Vasodilator Agents; C430916:regadenoson