Pharmacologic Stress Testing Medication
- Author: David Akinpelu, MD, FACP; Chief Editor: Eric H Yang, MD more...
Adenosine, dipyridamole (Persantine), and dobutamine are the most widely available pharmacologic agents for stress testing. Regadenoson, an adenosine analog, has a longer half-life than adenosine, and therefore a bolus versus continuous administration.
Adenosine, dipyridamole, and regadenosine are cardiac vasodilators. They dilate coronary vessels, which causes increased blood velocity and flow rate in normal vessels and less of a response in stenotic vessels. This difference in response leads to a steal of flow, and perfusion defects appear in cardiac nuclear scans or as ST-segment changes.
Dobutamine is a cardiac inotrope and chronotrope. The heart responds to dobutamine similarly to the way it responds to exercise.
Pharmacologic stress agents are used in myocardial perfusion for diagnostic purposes.
When used in myocardial perfusion scintigraphy reveals areas of insufficient blood flow. Adenosine increases blood flow and causes coronary vasodilation in normal coronary arteries while it causes little or no increase in stenotic coronary arteries. Adenosine is also a short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion.
Pharmacologically induces stress in patients unable to undergo adequate exercise-induced stress. Acts as low-affinity agonist for A2A adenosine receptor. Produces coronary vasodilation and increased coronary blood flow in normal nonstenotic arteries. Indicated for radionuclide myocardial perfusion imaging.
Antiplatelet Agents, Cardiovascular
Agents in this class inhibit the activation of factors responsible for platelet aggregation.
Platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased adenosine, adenine nucleotides, and cyclic-3', 5'-adenosine monophosphate within platelets. These mediators subsequently inhibit platelet aggregation and may cause vasodilation.
H3 Beta1/Beta2 Adrenergic Agonists
Agents in this class that stimulate beta1-adrenergic receptors and that have little effect on beta2 or alpha receptors are used. The agents cause increased contractility and heart rate.
Synthetic catecholamine and a direct inotropic agent that stimulates cardiac beta-receptors with minimal increase in systemic vascular resistance.
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