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Why Not Dipyridamole: a Review of Current Guidelines and Re-evaluation of Utility in the Modern Era.Cardiovascular Drugs and Therapy Jun 2022Dipyridamole is an old anti-platelet and coronary vasodilator agent that inhibits platelet phosphodiesterase and increases interstitial adenosine levels. Its use in... (Review)
Review
Dipyridamole is an old anti-platelet and coronary vasodilator agent that inhibits platelet phosphodiesterase and increases interstitial adenosine levels. Its use in coronary artery disease (CAD) has fallen out of practice in the modern era with the advent of new anti-platelet agents, and most modern guidelines on the management of CAD either neglect to comment on its utility or outright recommend against it. The majority of the studies used in these guidelines are outdated and took place in an era when high doses of aspirin were used and statins were not widely utilized. There is growing evidence in rat models of dipyridamole's synergy with statins through adenosine modulation resulting in significant myocardial protection against ischemia-reperfusion injury and limitation of infract size. The data in human studies are limited but show a similar potential synergy between dipyridamole and statins. It would thus be prudent to reconsider the recommendations against the use of dipyridamole in CAD and to re-evaluate its possible role and potential benefits through well-designed randomized trials combining it with statins, low-dose aspirin, and/or other anti-platelet agents.
Topics: Adenosine; Animals; Aspirin; Dipyridamole; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Rats; Vasodilator Agents
PubMed: 34245446
DOI: 10.1007/s10557-021-07224-9 -
The New England Journal of Medicine May 1987
Review
Topics: Blood Platelets; Dipyridamole; Fibrinolytic Agents; Humans; In Vitro Techniques
PubMed: 3553945
DOI: 10.1056/NEJM198705143162005 -
The American Journal of Cardiology May 1991Dipyridamole cardiac imaging is a useful alternative to exercise stress testing in the evaluation of patients with ischemic heart disease. Intravenous dipyridamole has... (Review)
Review
Dipyridamole cardiac imaging is a useful alternative to exercise stress testing in the evaluation of patients with ischemic heart disease. Intravenous dipyridamole has been approved recently for clinical use. Oral dipyridamole is widely available. The hemodynamic effects of dipyridamole include an increase in coronary blood flow in excess of the increase in myocardial oxygen consumption and cardiac output. The quality of the thallium images is better or similar to that of exercise thallium images. The optimal dose of intravenous dipyridamole is 0.56 mg/kg and the optimal oral dose is 300-375 mg, although higher doses may be necessary in some patients. The sensitivity and specificity of dipyridamole-thallium imaging, whether intravenous or oral, have been shown in a number of studies to be quite adequate and comparable to that achieved during exercise thallium imaging. Dipyridamole-thallium imaging has also been useful in identifying high-risk patients undergoing major elective vascular surgery. The relative merits of dipyridamole imaging versus exercise testing after acute myocardial infarction require further studies.
Topics: Coronary Vessels; Dipyridamole; Exercise Test; Heart; Hemodynamics; Humans; Radionuclide Imaging; Thallium Radioisotopes; Vasodilation
PubMed: 2035431
DOI: 10.1016/s0002-9149(05)80004-9 -
Advances in Cardiology 2012The antithrombotic activity of dipyridamole was initially discovered in an in vivo experiment about half a century ago. At that time science had not appreciated the... (Review)
Review
The antithrombotic activity of dipyridamole was initially discovered in an in vivo experiment about half a century ago. At that time science had not appreciated the complexity of the regulation of local thrombus formation. Inhibition of platelets has been the main focus for the prevention of arterial thrombus formation. Unfortunately, established in vitro test systems have to take away several important components of the hemostatic system. Rather than directly inhibiting platelet aggregation, dipyridamole amplifies endogenous antithrombotic systems and modulates or downregulates prothrombotic processes. While for many years the main focus had been on preventing acute thrombus formation in the case of a rupture of an atherosclerotic plaque in large coronary arteries, it now has been appreciated that perfusion of tissue and patency of small vessels and capillaries is equally important for preventing further damage to the tissue. Here dipyridamole was experimentally shown to improve perfusion and function in chronic hypoperfused tissue unrelated to its vasodilatory properties. Recently, several clinical trials have shown the benefit of dipyridamole when given in a formulation that assures a sufficient plasma concentration. Its potential to scavenge particularly peroxy radicals, its direct reduction of innate inflammation, and a chronic elevation of interstitial adenosine seems to be of more importance for the prevention of vascular and tissue damage than its adenosine- and prostacyclin-mediated antithrombotic effect. In its extended-release preparation with the tartaric acid nucleus, not only does it not seem to add significantly to the risk of bleeding, but seems to hold potential for protecting tissue from oxidative and metabolic stress.
Topics: Blood Platelets; Dipyridamole; Humans; Phosphodiesterase 5 Inhibitors; Platelet Aggregation Inhibitors; Receptor, PAR-1; Thrombin; Thrombosis
PubMed: 22906904
DOI: 10.1159/000338053 -
Current Topics in Medicinal Chemistry 2015Dipyridamole was introduced on the market as coronary vasodilator drug more than half a century ago and is still used as antithrombotic and vasodilator. Among cellular... (Review)
Review
Dipyridamole was introduced on the market as coronary vasodilator drug more than half a century ago and is still used as antithrombotic and vasodilator. Among cellular targets, it inhibits phosphodiesterases and raises extracellular levels of adenosine through inhibition of adenosine reuptake by red blood cells. As a consequence, endocellular levels of cyclic nucleotides are upregulated. The rise of cGMP in vascular smooth muscle cells and of cAMP in platelets provide the mechanism of vasodilation and antithrombosis, which are further potentiated by the release of PGI2 consequent on the increase in endothelial cell cAMP. These effects support the use of dipyridamole in cardiovascular diseases in which the drug is approved for the secondary prevention of cerebrovascular events. On the other hand, dipyridamole has been shown to possess a potent, little perceived, antioxidant activity of potential use in the several fields where pathophysiological pathways are dependent on oxidative stress, including those occurring in atherosclerosis, thrombosis, CNS-related diseases, and cancer.
Topics: Animals; Antioxidants; Cardiovascular Diseases; Central Nervous System Diseases; Dipyridamole; Drug Discovery; Humans; Neoplasms; Oxidative Stress; Vasodilator Agents
PubMed: 25697566
DOI: 10.2174/1568026615666150220111942 -
Drug Intelligence & Clinical Pharmacy Nov 1984Dipyridamol is a vasodilator that is used primarily in clinical practice as an antiplatelet agent. It increases coronary blood flow and was originally introduced as an... (Clinical Trial)
Clinical Trial Review
Dipyridamol is a vasodilator that is used primarily in clinical practice as an antiplatelet agent. It increases coronary blood flow and was originally introduced as an antianginal agent. An ability to prolong a shortened platelet survival has been used to justify its value in preventing thromboembolic complications. Conditions characterized by a reduction in platelet survival and where dipyridamole has been used include heart valve replacement, arterial grafting, cerebrovascular disorders, and disorders of peripheral circulation. The in vivo effect of dipyridamole on platelet aggregation has not been well defined and may depend on additional factors. Prostaglandins appear to have important roles in platelet homeostasis; their relationships to the action of dipyridamole are discussed. Dipyridamole usually is combined with aspirin for synergistic anti-aggregatory purposes. However, the nature of the interaction has not been elucidated and benefit from the addition of dipyridamole has not been demonstrated in clinical studies. A review of clinical studies using dipyridamole indicates that it currently has limited value.
Topics: Angina Pectoris; Aspirin; Blood Platelets; Cerebrovascular Disorders; Clinical Trials as Topic; Coronary Artery Bypass; Dipyridamole; Graft Occlusion, Vascular; Heart Valve Prosthesis; Hemodynamics; Humans; Kinetics; Myocardial Infarction; Platelet Aggregation; Postoperative Complications; Vascular Diseases
PubMed: 6389068
DOI: 10.1177/106002808401801103 -
European Heart Journal Apr 1989Dipyridamole was first introduced as an antianginal, coronary vasodilator agent. It was soon found that this drug could not prevent effort ischaemia; on the contrary,... (Review)
Review
Dipyridamole was first introduced as an antianginal, coronary vasodilator agent. It was soon found that this drug could not prevent effort ischaemia; on the contrary, given intravenously, it could frequently induce ischaemia in the presence of coronary artery stenosis. This property was exploited for the diagnosis of coronary artery disease. The dipyridamole-induced ischaemia was detected by different techniques: ST-segment depression, thallium 201 scintigraphy and echocardiography. This review article describes the mechanisms underlying dipyridamole-induced ischaemia and discusses the value of this pharmacologic stress test for the detection of coronary artery disease.
Topics: Coronary Disease; Dipyridamole; Echocardiography; Exercise Test; Humans; Ischemia
PubMed: 2656267
DOI: 10.1093/oxfordjournals.eurheartj.a059494 -
Lancet (London, England) May 1992
Topics: Dipyridamole; Humans; Platelet Aggregation Inhibitors
PubMed: 1349956
DOI: 10.1016/0140-6736(92)91166-6 -
Harefuah Nov 1986
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DICP : the Annals of Pharmacotherapy 1991
Review
Topics: Angioplasty, Balloon, Coronary; Dipyridamole; Humans
PubMed: 1949933
DOI: No ID Found