Assessment of left ventricular wall motion in angina pectoris by two-dimensional echocardiography and myocardial perfusion by technetium-99m sestamibi tomography during adenosine-induced coronary vasodilation and comparison with coronary angiography

Abstract

Myocardial perfusion and regional wall motion during adenosine-induced coronary vasodilation were assessed in 40 patients with angina pectoris by technetium-99m sestamibi single-photon emission computed tomography (SPECT) and simultaneous 2-dimensional echocardiography. Adenosine was infused intravenously at a dose of 140 μg/kg body weight per minute for 6 minutes, and technetium-99m sestamibi was injected at 3 minutes. Adenosine caused a significant decrease in systolic and diastolic blood pressure and a significant increase in heart rate and the heart rate-blood pressure product. Adverse effects were mild and transient and no patient required aminophylline. Completely or partially reversible defects on SPECT were present in 28 patients, a fixed defect was seen in 4 patients, and no defect was seen in 8 patients. Two-dimensional echocardiography revealed a new or worsening wall motion abnormality in 21 patients, a fixed abnormality in 4 patients and no abnormality in 15. Transient perfusion defects were associated with transient wall motion abnormalities in 71% of cases. The overall sensitivity, specificity and predictive accuracy of adenosine echocardiography in detecting significant coronary artery disease (>50% diameter stenosis) were 74,100 and 78%, respectively, whereas those of adenosine SPECT were 94, 100 and 95%, respectively (p <0.05, NS, and <0.05, respectively). Thus adenosine technetium-99m ses tamibi SPECT has a higher sensitivity and predictive accuracy than adenosine echocardiography, suggesting that adenosine-induced perfusion defects are not always associated with wall motion abnormality. Although the principal underlying mechanism of myocardial ischemia during adenosine infusion is a “coronary steal” phenomenon, the ischemia is also due to an enhanced myocardial oxygen demand, as indicated by an increased rate-pressure product.