The future of pharmacologic stress: selective a2a adenosine receptor agonists

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Abstract

Adenosine and dipyridamole, the currently available vasodilators for myocardial perfusion imaging, produce hyperemic coronary flow by stimulating A2A adenosine receptors on arteriolar vascular smooth muscle cells. However, both vasodilators nonselectively activate A1, A2B, and A3 adenosine receptors, which contributes to common undesirable effects. In the development of a novel pharmacologic stress agent, more selective agonism of the A2A receptor subtype would be desirable. Currently, 2 selective A2A adenosine receptor agonists are being evaluated in phase 3 studies as pharmacologic stress agents. The highly selective, potent, low-affinity A2A adenosine agonist regadenoson (also known as CVT-3146) holds significant potential as a pharmacologic stress agent, based on available results from experimental and clinical trials. Regadenoson produces maximal hyperemia quickly and maintains it for an optimal duration that is practical for radionuclide myocardial perfusion imaging. Regadenoson's simple rapid bolus administration and short duration of hyperemic effect point to an advantage of enhanced control for the clinician.

Section snippets

Ideal features of a novel pharmacologic stress agent

In SPECT myocardial perfusion imaging, the established pharmacologic stress agents adenosine and dipyridamole provide reproducible coronary vasodilation and significant clinical utility. However, as nonselective adenosine agonists, they are associated with a high incidence of side effects, are contraindicated in bronchospastic disease and high-grade AV nodal block, and require a controlled infusion. In theory, an ideal pharmacologic stress agent would be a selective A2A adenosine receptor

Selectivity, affinity, and clinical implications

The potency of an A2A agonist to induce coronary vasodilation depends primarily on 4 factors: (1) the affinity of the agonist for the target receptor (ie, agonist binding), (2) the density of the receptors at the targeted location, (3) the intrinsic efficacy of the bound agonist to activate the target receptor, and (4) the efficiency of receptor coupling to achieve a full functional response.1

In evaluating the selectivity, affinity, and duration of action of A2A agonists including regadenoson,

Clinical studies of regadenoson

In experimental studies, the A2A adenosine receptor agonist regadenoson has been shown to be a potent and selective coronary vasodilator and holds tremendous promise for use as a pharmacologic stress agent in myocardial perfusion imaging. Preclinical results demonstrate that regadenoson is a 10-fold more potent coronary vasodilator than adenosine (6 nmol/L versus 60 nmol/L, respectively).4 Regadenoson is functionally selective for the A2A adenosine receptor, with no AV block or

Regadenoson, binodenoson, and adenosine

Based on preclinical and early clinical studies reported in the literature, regadenoson is certainly promising as a pharmacologic stress agent. At the 400-μg dose using a rapid (≤10-second) bolus delivery, regadenoson produces a magnitude of maximal hyperemia comparable to adenosine that is rapid in onset (30 seconds) and short in duration (2.8 minutes),10 providing a favorable time frame to facilitate radionuclide imaging. In comparison, maximal hyperemia induced by binodenoson has been

Conclusion

Based on available results from experimental and clinical trials of selective A2A receptor agonists, regadenoson holds significant potential as a pharmacologic stress agent. As a highly selective, potent, low-affinity A2A adenosine agonist, regadenoson produces maximal hyperemia quickly and maintains it for an optimal duration that is practical for myocardial perfusion SPECT imaging. Regadenoson's simple rapid-bolus administration and short duration of hyperemic effect points to an advantage of

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