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Dipyridamole-Induced Angina Pectoris During Sestamibi Stress Test in Patients with Significant Coronary Artery Disease: Clinical, Angiographic, and Nuclear Determinants

P. Dendale

C. De Sadeleer

D. Schoors

P. Block

P.R. Franken

M. Rosseel, MD

Regelsbruggestraat 45 B-9300 Aalst Belgium

Intravenous dipyridamole induces angina pectoris (AP) in some patients with significant coronary artery disease (CAD). The aim of this prospective study was to identify the angiographic, nuclear, and clinical determinants. The authors examined 50 patients consecutively with significant CAD on coronary angiography. All antiischemic medica tions were stopped twenty-four hours (nitrates only 6 hours) before injection of dipyri damole (0.84 mg/kg). ECGs were taken before, during, and after this injection. The regional myocardial activity of Tc-99m-Sestamibi at rest and after dipyridamole injection was measured with single-photon emission computed tomography (SPECT).

During dipyridamole injection 20 patients had AP, of whom 15 had ST segment depression on ECG (P < 0.001). The only significant difference on coronary angiography between patients with dipyridamole-induced AP and those without AP was the presence of collaterals (P < 0.05). In patients with AP and collaterals, ECG and SPECT changes were always noted in the collateralized territory. Subgroup analysis showed that patients without previous myocardial infarction (MI, n=17, P < 0.05) or nontransmural MI (n=17, P < 0.05) had a good correlation between collaterals and AP, whereas patients with a history of transmural MI (n=16) did not. No further significant variables could be found as a predictor of AP after dipyridamole injection.

These findings suggest that AP during dipyridamole stress test is due to ischemia, which is not related to the severity of CAD. Ischemia is probably due to coronary steal to the collateralized territory in patients without transmural MI. Dipyridamole-induced angina pectoris is predictive for collaterals and may indicate viability in patients with MI.

Angiology, Vol. 48, No. 4, 301-307 (1997)
DOI: 10.1177/000331979704800403


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