Comparison of pulmonary uptake with transient cavity dilation after dipyridamole Tl-201 perfusion imaging

Abstract

Background

Elevated lung-heart ratio (LHR) and transient ischemic dilation (TID) have been identified as markers of severe coronary artery disease after both exercise and pharmacologic stress testing. We have previously demonstrated a very weak correlation between elevated LHR and TID after exercise, which suggests that they reflect different pathophysiologic manifestations of coronary disease. Because the physiology of pharmacologic vasodilation with dipyridamole is significantly different than that of physical exercise, we undertook this study to evaluate the relationship between elevated LHR and TID after pharmacologic stress testing with dipyridamole.

Methods and Results

We identified 1129 consecutive patients who underwent pharmacologic stress imaging with dipyridamole and thallium 201. LHR and a dilation index were calculated and compared with each other and with relevant clinical parameters. Echocardiographic parameters were also compared in a subset of 475 patients who had echocardiography within 2 weeks of pharmacologic stress testing. There was no significant correlation between elevated LHR and TID despite the fact that both were associated with more severe thallium stress and redistribution scores. Patients with elevated LHR were more likely to have a history of myocardial infarction and coronary artery bypass grafting and to have lower ejection fraction. Patients with TID were more likely to have a positive electrocardiographic response (15% vs 7%, P = .0003), which was not seen in patients with elevated LHR (11% vs 8%, P = .23).

Conclusions

Although both elevated LHR and TID were associated with more severe coronary disease, they have no significant correlation. Patients with elevated LHR are more likely to have a history of myocardial infarction or coronary artery bypass grafting, a larger left ventricle, and lower ejection fraction. Our results support the hypothesis that TID is due to diffuse subendocardial hypoperfusion and represents a different pathophysiologic response to ischemia than elevated LHR.