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Angiographic findings in patients exhibiting ischemia after oral dipyridamole
K S Virtanen1, S Mattila, A Järvinen
1First Department of Medicine, University Central Hospital, Helsinki, Finland.
Insights
Dipyridamole can cause ischemic responses in patients with severe coronary artery disease. These responses are linked to compromised collateral blood flow, suggesting a myocardial steal phenomenon.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Severe coronary arterial disease (CAD) necessitates understanding drug responses.
- Dipyridamole is used in cardiac stress testing, but its ischemic effects need clarification.
Purpose of the Study:
- To assess angiographic features in patients experiencing ischemic responses to dipyridamole.
- To investigate the relationship between dipyridamole-induced ischemia and coronary collateral circulation.
Main Methods:
- A randomized, placebo-controlled study of 74 patients with severe CAD prior to bypass surgery.
- Patients received either oral dipyridamole or a matching placebo.
- Angiographic features, including collateral vessel compromise, were evaluated.
Main Results:
- 16% of patients on dipyridamole experienced angina, and 35% showed electrocardiographic changes.
- Dipyridamole responders with angina or ECG changes had significantly more compromised collaterals.
- No significant differences were found in disease severity, symptoms, or cardiac function between responders and non-responders.
Conclusions:
- Ischemic responses to dipyridamole in severe CAD are associated with compromised collateral flow.
- The findings suggest a myocardial steal mechanism, exacerbated by poor collateral circulation.
- Dipyridamole-induced ischemia is primarily related to collateral vessel status rather than overall disease severity.
Abstract:
We have assessed the angiographic features of a group of 37 patients given oral dipyridamole and 37 patients given matching placebo. Both groups represented severe coronary arterial disease and were studied prior to bypass surgery. Six patients (16%) had angina and 13 patients (35%) had electrocardiographic changes after dipyridamole. All the patients in the control group were nonresponders. In the group given dipyridamole the patients responding with angina had significantly more compromised collaterals than the patients without chest pain (P = 0.021). The same applied to the patients with electrocardiographic changes versus those with no electrocardiographic changes (P = 0.034). No differences between responders and nonresponders could be found in terms of the severity of coronary arterial disease, severity of anginal symptoms, exercise tolerance, antianginal medication, number of past myocardial infarctions, and left ventricular ejection fraction. In conclusion, the data strongly suggest that ischaemic responses to dipyridamole originate from myocardial steal accentuated by compromised flow in collateral vessels.