Picano E, Masini M, Distante A, Simonetti I, Lattanzi F, Marzilli M, L'Abbate A
Am J Cardiol. 1986 Apr 1;57(10):765-8. doi: 10.1016/0002-9149(86)90610-7.
Fourteen consecutive patients with exercise-induced ST-segment elevation in the absence of previous infarction and basal left ventricular asynergy at rest performed a dipyridamole test (infusion of dipyridamole, 0.14 mg/kg/min intravenously for 4 minutes) during 12-lead electrocardiographic (ECG) and 2-dimensional echocardiographic monitoring. In 7 of the 14 patients, dipyridamole infusion consistently induced ST-segment elevation in the leads that showed ST elevation on effort; reversible asynergy (occurring in the region corresponding to the ECG leads with diagnostic changes) could always be documented by echocardiography. In 2 patients dipyridamole induced reversible asynergy in presence of ST-segment depression. In these 9 patients angiography invariably revealed a severe organic stenosis in the coronary artery feeding the region that became transiently asynergic after dipyridamole. In the other 5 patients (all of whom had either spontaneous or ergonovine-induced ST-segment elevation), the dipyridamole test yielded no significant echocardiographic or ECG change; coronary angiography showed absent (2 patients) or significant (3 patients) coronary artery disease. In conclusion, dipyridamole may induce transmural ischemia in humans, as detected by the electrical hallmark of ST elevation; this ECG pattern, in contrast to ST depression, reliably predicts the presence and site of transient regional asynergy. When dipyridamole induces ST-segment elevation, severe basal stenosis is invariably present in the coronary artery supplying the transiently asynergic myocardial region.
