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Effects of the dipyridamole test on left ventricular function in coronary artery disease
H O Klein1, R Ninio, S Eliyahu
1Department of Cardiology, Meir General Hospital, Sapir Medical Center, Kfar-Saba, Israel.
Insights
Dipyridamole stress testing in coronary artery disease (CAD) causes true ischemia and left ventricular dysfunction. Aminophylline can promptly reverse these dipyridamole-induced effects, suggesting its routine use in patients.
Area of Science:
- Cardiology
- Nuclear Cardiology
- Diagnostic Imaging
Background:
- Dipyridamole stress testing with thallium-201 is used to detect coronary artery disease (CAD).
- Uncertainty exists regarding dipyridamole's effect on myocardial perfusion and left ventricular function.
Purpose of the Study:
- To investigate whether dipyridamole induces true ischemia or only perfusion inhomogeneity.
- To assess dipyridamole's impact on global and segmental left ventricular function in CAD patients.
Main Methods:
- Ejection fraction, segmental wall motion, and ventricular volumes were measured before and after dipyridamole administration.
- 113 patients with suspected CAD and 32 normal subjects were studied.
- The effects were compared and the duration of dipyridamole's impact was noted.
Main Results:
- Dipyridamole significantly decreased ejection fraction in 87% of CAD patients, unlike in normal subjects.
- Left ventricular wall motion worsened in 66% of patients, and pressure/volume ratio deteriorated in 72%.
- Aminophylline rapidly reversed dipyridamole's effects, which lasted 10-25 minutes.
Conclusions:
- Dipyridamole stress testing generally induces true myocardial ischemia in patients with CAD.
- The severity of left ventricular dysfunction correlates with the angiographic severity of CAD.
- Routine administration of aminophylline is recommended to counteract dipyridamole-induced left ventricular dysfunction.
Abstract:
The dipyridamole stress test is used with thallium-201 to detect areas of inhomogeneity of blood flow that point to coronary artery disease (CAD). It is unclear whether dipyridamole produces inhomogeneous perfusion only or whether it actually decreases net flow in the obstructed vessels and produces true ischemia. It is also unclear what effect dipyridamole has on global and segmental left ventricular function. Therefore, ejection fraction, segmental wall motion and ventricular volume equivalents were measured before and after dipyridamole in 113 patients and 32 normal subjects. Ejection fraction responded in an abnormal fashion in 98 patients (87%), decreasing from 49 +/- 11% to 43 +/- 13% (p less than 0.0001), whereas it increased in 29 normal subjects (90%) from 57 +/- 6% to 64 +/- 10% (p less than 0.0001). Wall motion worsened distinctly in 75 patients (66%), and pressure/volume ratio deteriorated in 72%. The effect of dipyridamole lasted between 10 and 25 minutes, but was promptly reversed by aminophylline. These findings indicate that dipyridamole generally induces true ischemia in CAD. Furthermore, the degree of dysfunction is related to the angiographically assessed severity of CAD. The shortness of breath (seen in 10% of patients) may be partially explained by the findings, and it seems advisable to give aminophylline to every patient in order to promptly correct left ventricular dysfunction.