Prognostic impact of TID in regadenoson MPI: Some patients and certain events

Journal of Nuclear Cardiology, Oct 2015

Adrián I. Löffler, Jamieson M. Bourque

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Prognostic impact of TID in regadenoson MPI: Some patients and certain events

Received Sep Prognostic impact of TID in regadenoson MPI: Some patients and certain events Adria´n I. Lo¨ffler 0 2 Jamieson M. Bourque 0 MHS 0 1 2 0 Reprint requests: Adria ́n I. Lo ̈ffler, MD, Cardiovascular Division and the Cardiac Imaging Center, Department of Medicine, University of Virginia Health System , Box 800158, 1215 Lee Street, Charlottes- ville, VA 22908 1 Department of Radiology, University of Virginia Health System , Charlottesville, VA 2 Cardiovascular Division and the Cardiac Imaging Center, Department of Medicine, University of Virginia Health System , Charlottesville, VA Single-photon emission-computed tomographic (SPECT) myocardial perfusion imaging (MPI) has incremental diagnostic and prognostic value over exercise stress electrocardiography, and the assessment of transient ischemic dilation (TID) is a key contributor to its ability to detect higher risk patients. The diagnostic and prognostic role of TID has been evaluated extensively in those undergoing exercise MPI.1,2 However, approximately 50% of the *10 million MPI studies performed annually in the US undergo pharmacologic MPI,3 the majority receiving regadenoson for vasodilator stress due to its improved tolerability by patients, safety profile, and ease of administration.4 Given the high prevalence of this testing, the significance of TID in this population is of high importance. The diagnostic role of TID in regadenoson MPI has been assessed previously, but the prognostic impact has not determined. In this issue of the Journal, Lester et al provide the first analysis of the prognostic utility of TID with regadenoson MPI. In this well-performed study, Lester et al assessed the prognostic impact of an abnormal TID ratio of 1.33 on a composite of cardiac death, myocardial infarction (MI), or late coronary revascularization (CR) in 887 patients over a mean of 29 months; 75% of the cohort had an abnormal perfusion pattern. TID was found in 6% of this population. After multivariable adjustment, TID had a hazard ratio of 1.92 for predicting the composite endpoint. Although the predominant conclusion of the study is that TID has prognostic importance, there are two significant additional considerations. The first is that TID was only prognostic in this cohort in those with abnormal MPI. In those with normal perfusion, there was no association. The second is that the prognostic significance was driven by late CR, rather than the hard cardiac events of cardiac death and nonfatal MI. Given these findings, we will discuss the potential mechanism for TID in vasodilator MPI and its potential effect on specific cardiac events, the diagnostic and prognostic significance of TID with respect to concurrent MPI abnormalities, and future directions for research and clinical application of TID in vasodilator MPI. - TID: DEFINITION AND POTENTIAL MECHANISM IN VASODILATOR MPI TID refers to an enlarged left ventricular (LV) cavity measured in post-stress scintigraphy images relative to resting images. Lester et al appropriately highlight the importance of selecting an appropriate TID cut-off ratio. The cut-off ratio used to define TID has varied in the literature based on stress modality, nuclear tracer, imaging protocol, and other technical factors.5 The authors derived a cut-off ratio of 1.33 in this study, as this value encompassed 95% of the cohort population. TID has been shown to independently provide diagnostic utility in predicting severe and extensive coronary artery disease (CAD) and overall poor prognosis. However, there is a controversy regarding its appropriate application across varying clinical settings. Some of these inconsistent findings may be explained by the underlying mechanism of TID, which is still debated. One hypothesized pathophysiologic mechanism is diffuse subendocardial hypoperfusion resulting in reduced radiotracer uptake in the subendocardial zone, thus, making the appearance of an enlarged LV cavity.5 An alternative theory is ischemia resulting in reduced LV function with resultant elevated end-systolic volume. The true mechanism may combine these two theories.6,7 These potential mechanisms can explain why TID is not always associated with severe CAD on angiography or poor prognosis. Patients who have other causes of diffuse subendocardial ischemia, such as hypertensive heart disease and LV hypertrophy or hypertrophic cardiomyopathy, can have TID without obstructive CAD. Other potential mechanisms for falsely increased TID ratios include suboptimal technique, errors in slice selection for tomographic analysis, patients with small LV ventricles, different doses of administered radionuclide, or motion artifacts.5 Thus, it is important to appropriately identify these factors prior to assessing for TID. Regadenoson is a selective adenosine A2A receptor agonist which causes sinus tachycardia. It has been proposed that the mechanism for tachycardia is mainly due to sympathoexcitation rather than being baroreflex mediated (...truncated)


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Adrián I. Löffler, Jamieson M. Bourque. Prognostic impact of TID in regadenoson MPI: Some patients and certain events, Journal of Nuclear Cardiology, 2015, pp. 1156-1159, Volume 23, Issue 5, DOI: 10.1007/s12350-015-0299-9