Dipyridamole is a drug that inhibits platelet aggregation and causes vasodilation.

• It inhibits the cellular reuptake of adenosine into platelets, red blood cells and endothelial cells leading to increased extracellular concentrations of adenosine.
• It also inhibits the enzyme adenosine deaminase which normally breaks down adenosine into inosine. This inhibition leads to further increased levels of extracellular adenosine.
• Dipyridamole also inhibits the enzyme phosphodiesterase which normally breaks down cAMP.
• Adenosine interacts with the adenosine receptors to cause increased cAMP via adenylate cyclase.
• cAMP impairs platelet aggregation and also causes arteriolar smooth muscle relaxation.

Modified release dipyridamole is used in conjunction with aspirin (under the trade name Aggrenox®) in the secondary prevention of stroke and transient ischemic attack. This practice is now confirmed by the ESPRIT trial.

Dipyridamole is also used in nuclear cardiac stress testing as a coronary vasodilator.

• Via the mechanisms mentioned above, it increases the local concentration of adenosine in the coronary circulation which causes vasodilation.
• Vasodilation of healthy arteries is physiologic, whereas diseased arteries actually experience a drop in blood flow via "steal" phenomena which can be detected by electrocardiogram and echocardiography when it causes ischemia.
• Flow heterogeneity (a necessary precursor to ischemia) can de detected with gamma-cameras and SPECT using nuclear imaging agents such as Thallium-201 and Tc99m-Sestamibi.

Antiplatelet drugs

Dipyridamol