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)