Original Article
Transient ischemic dilation for coronary artery disease in quantitative analysis of same-day sestamibi myocardial perfusion SPECT

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Abstract

Background

Transient ischemic dilation (TID) of the left ventricle in myocardial perfusion SPECT (MPS) has been shown to be a clinically useful marker of severe coronary artery disease (CAD). However, TID has not been evaluated for 99mTc-sestamibi rest/stress protocols (Mibi-Mibi). We aimed to develop normal limits and evaluate diagnostic power of TID ratio for Mibi-Mibi scans.

Methods

TID ratios were automatically derived from static rest/stress MPS (TID) and gated rest/stress MPS from the end-diastolic phase (TIDed) in 547 patients who underwent Mibi-Mibi scans [215 patients with correlating coronary angiography and 332 patients with low likelihood (LLk) of CAD]. Scans were classified as severe (≥70% stenosis in proximal left anterior descending (pLAD) artery or left main (LM), or ≥90% in ≥2 vessels), mild to moderate (≥90% stenosis in 1 vessel or ≥70%-90% in ≥1 vessel except pLAD or LM), and normal (<70% stenosis or LLk group). Another classification based on the angiographic Duke prognostic CAD index (DI) was also applied: DI ≥ 50, 30 ≤ DI < 50 and DI < 30 or LLk group.

Results

The upper normal limits were 1.19 for TID and 1.23 for TIDed as established in 259 LLk patients. Both ratios increased with disease severity (P < .0001). Incidence of abnormal TID increased from 2% in normal patients to >36% in patients with severe CAD. Similarly, when DI was used to classify disease severity, the average ratios showed significant increasing trend with DI increase (P < .003); incidence of abnormal TID also increased with increasing DI. The incidence of abnormal TID in the group with high perfusion scores significantly increased compared to the group with low perfusion scores (stress total perfusion deficit, TPD < 3%) (P < .0001). The sensitivity for detecting severe CAD improved for TID when added to mild to moderate perfusion abnormality (3% ≤ TPD < 10%): 71% vs 64%, P < .05; and trended to improve for TIDed/TIDes: 69% vs 64%, P = .08, while the accuracy remained consistent if abnormal TID was considered as a marker in addition to stress TPD. Similar results were obtained when DI was used for the definition of severe CAD (sensitivity: 76% vs 66%, P < .05 when TID was combined with stress TPD).

Conclusion

TID ratios obtained from gated or ungated Mibi-Mibi MPS and are useful markers of severe CAD.

Introduction

Transient ischemic dilation (TID) ratio has been clinically acknowledged as a measurement that provides clinically relevant information for the management of patients with coronary artery disease (CAD).1, 2, 3, 4, 5, 6, 7, 8, 9 The change in left ventricular (LV) volume as quantified by TID is probably related to a combination of myocardial and endocardial ischemia,10 although the exact mechanism remains unclear. When incorporated into stress/rest SPECT screening protocols, TID could provide additional information for severe CAD.4,8 Although the exact significance of quantitatively elevated TID in patients with normal or minimal perfusion abnormality remains unclear and some studies showed that TID had a low prevalence and poor predictive value in the otherwise normal MPI,11,12 the presence of TID in patients with abnormal myocardial perfusion abnormality, such as those in our study, has previously been shown to be associated with extensive and severe CAD,1,4,7,13,14 as well as a strong independent predictor of future cardiac events.15,16

Different scanning protocols may have different normal limits for TID ratios,8,9 and these have not been well established. To avoid averaging errors from static images, this study establishes the normal limits not only for ungated SPECT but also for gated SPECT without attenuation correction using a single isotope 99mTc-sestamibi tracer. This study also evaluates the Mibi-Mibi TID ratios’ incremental diagnostic value in detection of severe and extensive CAD in patients with suspected CAD by fully quantitative analysis.

Section snippets

Patients

The subjects who were referred to the Nuclear Medicine Department, Sacred Heart Medical Center, Eugene, Oregon, from March 1, 2003 to December 31, 2006 for rest and stress electrocardiography (ECG)-gated myocardial perfusion SPECT (MPS) were consecutively selected.17 All patients with a prior history of CAD, cardiomyopathy, significant valve disease, left bundle branch block, paced rhythm, and pharmacologic stress testing were excluded. Since the primary goal of this project is to show the

Normal Limits

The upper normal limit of each TID ratio was defined as the term of its mean plus two SDs generated from 259 stress and rest MPS patients with LLk of CAD randomly selected from our LLk patients on the basis of the random number generator results. The small differences of mean TID ratios between small hearts and regular hearts (0.98 ± 0.12 vs 0.98 ± 0.09 for TID, 1.05 ± 0.09 vs 1.07 ± 0.08 for TIDed, and 0.99 ± 0.27 vs 1.03 ± 0.15 for TIDes) were not significant (P > .05). We also obtained TID

Discussion

TID ratio of the LV are an important marker of severe and extensive CAD.4,8 In this study, we subsequently extended these observations to patients with suspected CAD undergoing single isotope 99mTc-sestamibi tracer. Both gated and ungated Mibi-Mibi MPS images were used to derive TID ratios. The normal limits of TID ratios were 1.19, 1.23, and 1.46 for static and gated MPS on the end-diastolic and end-systolic phase, respectively. The evaluation of incremental diagnostic value of TID ratios

Conclusion

We have established the normal limits for the ungated or gated 1-day Mibi-Mibi MPS and evaluated performance of TID for the detection of severe CAD. The results suggest that the TID ratios could provide incremental diagnostic information to standard perfusion analysis in fully automated quantitative analysis for the identification of severe and extensive disease in patients with suspected CAD.

Acknowledgments

This research was supported in part by Grant R0HL089765 from the National Heart, Lung, and Blood Institute/National Institutes of Health (NHLBI/NIH) (PI: Piotr Slomka). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NHLBI. We would like to thank Arpine Oganyan for editing and proof-reading the text.

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This research was supported in part by Grant R0HL089765 from the National Heart, Lung, and Blood Institute/National Institutes of Health (NHLBI/NIH).

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