LEFT-VENTRICULAR DILATATION AND PULMONARY THALLIUM UPTAKE AFTER SINGLE-PHOTON EMISSION COMPUTER-TOMOGRAPHY USING TL-201 DURING ADENOSINE-INDUCED CORONARY HYPEREMIA

This study examined the implications of left ventricular (LV) dilatation and increased pulmonary thallium uptake during adenosine-induced coronary hyperemia. The lung-to-heart thallium ratio in the initial images was significantly higher in patients with coronary artery disease (CAD) than normal subjects; 0.48 ± 0.16 in 3-vessel disease (n = 16), 0.43 ± 0.10 in 2-vessel disease (n = 20), 0.43 ± 0.08 in 1-vessel disease (n = 16) and 0.36 ± 0.05 in normal subjects (n = 7) (p < 0.001, 0.09 and 0.06, respectively). There was a significant correlation between the severity and the extent of the perfusion abnormality (determined from the polar maps) and the lung-to-heart thallium ratio (r = 0.51 and 0.52, respectively, p < 0.0002). There was also a significant correlation between lung thallium washout and lung-to-heart thallium ratio (r = 0.42, p = 0.0009) and peak heart rate (r = -0.49, p < 0.0001). The LV dilatation was mostly due to an increase in cavity dimension (30% increase) and to a lesser extent (6% increase) due to increase in LV size. (The cavity dimensions were measured from the short-axis slices at the midventricular level in the initial and delayed images.) The dilation was seen in patients with CAD but not in the normal subjects. These changes correlated with the extent and severity of the thallium perfusion abnormality. Thus, adenosine-induced coronary hyperemia may cause LV dilation and increased lung thallium uptake on the basis of subendocardial ischemia. © 1990.