Dipyridamole myocardial infarction

The AHA/ASA guidelines recommend that antiplatelet therapy as the cornerstone of antithrombotic therapy for the secondary prevention of ischemic stroke and should be used in noncardioembolic strokes. Aspirin, dopidogrel, and extended-release dipyridamole plus aspirin are all considered first-line antiplatelet agents (see Table 13-1). The combination of aspirin and clopido-grel can only be recommended in patients with ischemic stroke and a recent history of myocardial infarction or coronary stent placement and then only with ultra-low-dose aspirin to minimize bleeding risk. 

Brown KA, Heller GV, Landin RS, Shaw LJ, Beller GA, Pasquale MJ et al. Early dipyridamole (99m)Tc-sestamibi single photon emission computed tomographic imaging 2 to 4 days after acute myocardial infarction predicts in-hospital and postdischarge cardiac events comparison with submaximal exercise imaging. Circulation 1999 100 2060-2066... 

The antiplatelet/antithrombotic activity of dipyridamole has been demonstrated in laboratory and in animal models, and has been shown to inhibit platelet aggregation and vessel-wall thrombogenesis [9-11]. Dipyridamole has been given either alone or with aspirin in the management of myocardial infarction and stroke. For the secondary prevention of stroke or transient ischemic attack, the drug may be given as a modified-release preparation in a dose of 200 mg twice daily. Dipyridamole administered intravenously results in a marked coronary vasodilation and is used in stress testing in patients with ischemic heart disease [5]. 

The incidence of major adverse reactions to dipyridamole was determined in a multicenter retrospective study, involving 73 806 patients who underwent intravenous dipjridamole stress imaging in 59 hospitals and 19 countries (4). The main conclusion was that the risk of serious dipjridamole-induced adverse effects is very low, a conclusion that is in line with other reports (5), and comparable to that reported for exercise testing in a similar patient population. Combined major adverse events among the entire patient population included 7 cardiac deaths (0.95 per 10000), 13 non-fatal myocardial infarctions (1.76 per 10000), 6 non-fatal sustained ventricular dysrhythmias (0.81 per 10000) (ventricular tachycardia in 2 and ventricular fibrillation in 4), 9 transient cerebral ischemic attacks (1.22 per 10000), 1 stroke, and 9 severe cases of bronch-ospasm (1.22 per 10000). Minor non-cardiac adverse effects were less frequent among the elderly and more frequent in women and patients taking maintenance aspirin. 

A 43-year-old man had an acute myocardial infarction immediately after exercise and pharmacological stress echocardiography with dipyridamole + atropine 1 month after successful stent implantation (9). 

Nedeljkovic MA, Ostojic M, Beleslin B, Nedeljkovic IP, Stankovic G, Stojkovic S, Saponjski J, Babic R, Vukcevic V, Ristic AD, Orlic D. Dipyridamole-atropine-induced myocardial infarction in a patient with patent epicardial coronary arteries. Herz 2001 26(7) 485-8. 

Dipyridamole testing has been shown to be safe and effective in the elderly and in those with unstable angina immediately after MI (within days). It also may be used to assess the status of revascularization procedures. As a prognostic test, dipyridamole testing is very useful. In several studies, abnormal scans have shown about a 10-fold increase in event rates over 1 to 2 years of follow-up. Abnormal scans also have been shown to be an independent risk factor for myocardial infarction and death with a relative risk of 3.1. Reversible defects correlate best with events, with one study demonstrating a 4.41 relative risk for cardiac events. 

Regadenoson has an improved side effect profile in comparison to adenosine and dipyridamole. However, it may also precipitate myocardial infarction. This adverse effect is secondary to coronary steal phenomenon induced by regadenoson administration. Most likely, in this mechanism A2A vasodilatation causes intercoronary and transmxual steal phenomenon which in the presence of a preexisting stenotic lesion results in myocardial infarction [6]. 

A number of studies have been conducted which confirm earlier reports that dipyridamole promotes the development of collateral vessels in animals with experimentally-produced myocardial infarction. " In man, dipyridamole decreases arterial levels of lactic acid, pyruvate, glucose, and free fatty acids. A recent dotible blind study failed to substantiate earlier claims that any beneficial effects of dipyridamole would be related to the development of intercoronary collateral vessels, and that such changes would be observed only after long term treatment. There was no statistical difference in the effects of dipyridamole and placebo on... 

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