Objectives: The purpose of the study was to evaluate the relationship between elevated lung/heart ratio (LHR) and transient ischemic dilation (TID) after stress thallium-201 myocardial perfusion imaging and to provide further insight into the mechanism of cavity dilation.
Background: Because both LHR and TID have been identified as adjunctive markers of severe coronary disease they should be found in the same patients. Although the mechanism of LHR has been defined, that of transient dilation has not.
Methods: We identified 4,618 consecutive patients undergoing maximal exercise perfusion imaging with thallium-201. Lung/heart ratio and a dilation index were derived and compared to each other and to relevant clinical parameters.
Results: There was a very weak relationship between the LHR and dilation index (r = 0.15, p < 0.001). Defining a dilation index > or =1.10 and LHR > or =50% as abnormal revealed that 322 of the patients (7%) had TID only, 351 (7.8%) had LHR only and 40 (0.9%) had both. When compared to patients without these findings both TID and LHR had higher thallium stress defect and redistribution scores. When comparing subjects who had elevated LHR uptake to those who had TID, it was found that those with LHR were more likely to have had prior myocardial infarction (MI) (29% vs. 9%), coronary artery bypass grafting (22% vs. 8%), lower ejection fraction (34+/-17% vs. 55+/-11%) and had more evidence of ischemia based on thallium stress defect and redistribution scores. However, patients with cavity dilation had a higher frequency of positive electrocardiographic response (31% vs. 19%) despite lower scintigraphic markers.
Conclusions: Although pulmonary uptake and transient cavity dilation have both been associated with severe coronary disease, they have a very weak correlation, which, in combination with the different clinical parameters associated with each, suggests that they represent different pathophysiologic responses to exercise-induced ischemia. Our data support the hypothesis that TID represents transient subendocardial ischemia rather than physical dilation from increased end-diastolic pressure.