BACKGROUND: Diabetes and left ventricular hypertrophy (LVH) can cause coronary flow reserve abnormalities in the absence of coronary artery disease (CAD). We sought to evaluate the impact of LVH and diabetes on the relationship between ischemia, severe CAD, and transient ischemic dilation (TID) on adenosine myocardial perfusion imaging (MPI). METHODS AND RESULTS: We prospectively recruited 157 patients referred for routine single-day adenosine technetium 99m MPI. LVH was assessed by use of transthoracic echocardiography. A ratio of 1.19 or greater on MPI defined TID in men and 1.31 or greater in women. Summed difference scores were determined by use of a 17-segment 5-point scoring system. TID was present in 22 of 157 patients (14%), diabetes in 54 of 157 (34%), and LVH in 42 of 157 (27%). By multivariate logistic regression, LVH, ischemia (summed difference score >2), and diabetes were independently predictive of TID. The incidence of TID was stratified by the presence or absence of diabetes and/or LVH in those with ischemia on MPI (8/8 [100%] vs 0/11 [0%], P < .002) or severe CAD on angiography (5/7 [71%] vs 0/8 [0%], P < .01). All those with TID (22/22 [100%]) had either diabetes or LVH (or both). CONCLUSION: Although this study confirms the association between TID and both ischemia and severe CAD, all patients with TID had diabetes, LVH, or frequently, both, suggesting that the pathophysiology of these disease processes may play an integral role in the manifestation of TID on adenosine MPI.
BACKGROUND:Diabetes and left ventricular hypertrophy (LVH) can cause coronary flow reserve abnormalities in the absence of coronary artery disease (CAD). We sought to evaluate the impact of LVH and diabetes on the relationship between ischemia, severe CAD, and transient ischemic dilation (TID) on adenosine myocardial perfusion imaging (MPI). METHODS AND RESULTS: We prospectively recruited 157 patients referred for routine single-day adenosine technetium 99m MPI. LVH was assessed by use of transthoracic echocardiography. A ratio of 1.19 or greater on MPI defined TID in men and 1.31 or greater in women. Summed difference scores were determined by use of a 17-segment 5-point scoring system. TID was present in 22 of 157 patients (14%), diabetes in 54 of 157 (34%), and LVH in 42 of 157 (27%). By multivariate logistic regression, LVH, ischemia (summed difference score >2), and diabetes were independently predictive of TID. The incidence of TID was stratified by the presence or absence of diabetes and/or LVH in those with ischemia on MPI (8/8 [100%] vs 0/11 [0%], P < .002) or severe CAD on angiography (5/7 [71%] vs 0/8 [0%], P < .01). All those with TID (22/22 [100%]) had either diabetes or LVH (or both). CONCLUSION: Although this study confirms the association between TID and both ischemia and severe CAD, all patients with TID had diabetes, LVH, or frequently, both, suggesting that the pathophysiology of these disease processes may play an integral role in the manifestation of TID on adenosine MPI.
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