Dipyridamole Nuclear Stress Test

A nuclear stress test is a relatively non-invasive diagnostic procedure that involves the injection of a small quantity of radioactive tracer into the bloodstream, administered in conjunction with myocardial perfusion imaging and a stress test, which challenges the functional capacity of the heart.[1] As blood containing the radioactive tracer flows through the heart, its energy is detected by a gamma camera or scanner that produces images of the heart’s vascular network after a stress test and/or at rest.[1][2] The stress test increases myocardial blood perfusion and creates a disparity in blood flow between normal and stenosed arteries,[3] allowing clinicians to see more clearly than if the patient were at rest if there are regions of the heart muscle that are ischemic. Indeed, this allows the clinician to determine the presence and progression of any suspected or known coronary heart disease, or if there is a history of myocardial infarction.[4] Additionally, a nuclear stress test can determine the potential or realized effectiveness of interventions or procedures (e.g., by-pass surgery or the installation of a coronary stent) that can be implemented to improve myocardial blood perfusion in the treatment of such cardiac complications.[2] One of the most commonly performed stress tests, which accompanies nuclear-based perfusion imaging, is exercise-based.[5] However, in certain circumstances, there may be contraindications for performing an exercise, and it is, subsequently, more appropriate to use a pharmacologically-based stress test involving the administration dipyridamole, adenosine, or regadenoson.[2][5][6] Indeed, these vasodilators can emulate the cardiac response to exercise,[7] increasing myocardial perfusion to reveal ischemic regions, while the patient remains physically passive throughout the test. Dipyridamole may not be the most potent vasodilator,[8] but it is associated with a lower frequency of side effects (although longer lasting) than adenosine, and it is far more cost-effective than regadenoson.[2][9][10] Mechanism of Action Dipyridamole is a phosphodiesterase enzyme inhibitor. It indirectly increases myocardial perfusion by inhibiting the degradation of cyclic adenosine monophosphate and by blocking the cellular reuptake of endogenous adenosine. Subsequently, the concentration of circulating adenosine increases by 3- to 4-fold.[2][3] Adenosine then acts on the A receptor, which upregulates the production of cyclic adenosine monophosphate.[2] Cyclic adenosine monophosphate then relaxes the vascular smooth muscle,[11] inducing vasodilation and increasing myocardial perfusion by 3.8- to 7-fold. Peak vasodilation after dipyridamole administration occurs on average 6.5 minutes after the start of the infusion.[2] The hyperemic effect of dipyridamole can last for more than 50 minutes, with the half-life of dipyridamole being 30 to 45 minutes.[2] The circulating adenosine may also act on the A, A and A receptors, which has the potential to induce several complications described further below.[2] It is metabolized in the liver to the glucuronic acid conjugate and excreted in the bile.