[dahy-pir-i-duh-mohl, -puh-rid-uh-]
{{drugbox | IUPAC_name = 2-{[9-(bis(2-hydroxyethyl)amino)-2,7-bis(1-piperidyl)-
4-yl]-(2-hydroxyethyl)amino}ethanol | image = Dipyridamole.svg | CAS_number = 58-32-2 | ATC_prefix = B01 | ATC_suffix = AC07 | PubChem = 3108 | DrugBank = APRD00360 | C = 24 |H = 40 |N = 8 |O = 4 | molecular_weight = 504.626 g/mol | bioavailability = | protein_bound = 99% | metabolism = Hepatic | elimination_half-life = Alpha (40 mins), Beta (10 Hours) | pregnancy_category = B | legal_status = | routes_of_administration = PO, IV }} Dipyridamole is a drug that inhibits thrombus formation when given chronically and causes vasodilation when given at high doses over short time.

Mechanism and effects


  • Dipyridamole has shown to lower pulmonary hypertension without significant drop of systemic blood pressure
  • Dipyridamole inhibits formation of pro-inflammatory cytokines (MCP-1, MMP-9) in vitro and results in reduction of hsCRP in patients.
  • Dipyridamole inhibits proliferation of smooth muscle cells in vivo and has shown to prevent AV-shunt failure in dialysis patients.
  • Dipyridamole increases release of t-PA from brain microvascular endothelial cells
  • Dipyridamole treatment in vivo results in increase of 13 - HODE and decrease of 12 - HETE in the subendothelial matrix (SEM) and reduced thrombogenicity of the SEM.
  • Dipyridamole pretreatment reduced reperfusion injury in volunteers.
  • Dipyridamole treatment has shown to increase myocardial perfusion and left ventricular function in patients with ischemic cardiomyopathy.
  • Dipyridamole treatment resulted in reduction of the number of thrombin and PECAM-1 receptors on platelets in stroke patients.
  • cAMP impairs platelet aggregation and also causes arteriolar smooth muscle relaxation. Chronic therapy did not show significant drop of systemic blood pressure.
  • Dipyridamole inhibits the replication of mengovirus RNA.

Use in individuals with a history of stroke

Modified release dipyridamole is used in conjunction with aspirin (under the trade names Aggrenox in the USA or Asasantin Retard in the UK) in the secondary prevention of stroke and transient ischaemic attack. Dipyridamole absorption is pH-dependent and concomitant treatment with gastric acid suppressors (such as a proton pump inhibitor) will inhibit uptake significantly. This practice was now confirmed by the ESPRIT trial.

It is not, however, licensed as monotherapy for stroke prophylaxis, although a Cochrane Review has suggested that dipyridamole may reduce the risk of further vascular events in patients presenting after cerebral ischaemia.

A triple therapy of aspirin, clopidogrel and dipyridamole has been investigated, but this combination led to an increase in adverse bleeding events.

Use in nuclear stress testing

Dipyridamole (Persantine) is also used in pharmacological cardiac stress testing mediating coronary vasodilation.

  • Via the mechanisms mentioned above, when given as 3 to 5 min infusion it rapidly increases the local concentration of adenosine in the coronary circulation which causes vasodilation .
  • Vasodilation occurs in healthy arteries, whereas stenosed arteries remain narrowed. This creates a "steal" phenomenon where the coronary blood supply will increase to the dilated healthy vessels compared to the stenosed arteries which can then be detected by clinical symptoms of chest pain, electrocardiogram and echocardiography when it causes ischemia.
  • Flow heterogeneity (a necessary precursor to ischemia) can be detected with gamma cameras and SPECT using nuclear imaging agents such as Thallium-201 and Tc99m-Sestamibi. However relative differences in perfusion not necessarily imply absolute decrease in blood supply in the tissue supplied by a stenosed artery.

Other uses of dipyridamole

Dipyridamole also has non-medicinal uses in a laboratory context, such as the inhibition of cardiovirus growth in cell culture.


Dipyridamole overdose can be treated with aminophylline and reverses its hemodynamic effects (vasodilation).


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