Stephen Gerard, MD, PhD

In his guest editorial [April 2007], David A. Dowe, MD, argued in support of coronary CTA in lieu of nuclear myocardial perfusion scintigraphy (MPS) for diagnosis of coronary artery disease (CAD).1 At the end of his article, Dr Dowe asked the question, “So why shouldn’t CCTA be as quickly accepted as CTA was for PE?” I would like to respond to the author’s question.

A very basic premise that Dr Dowe has ignored is that MPS is a functional test for CAD—CTA is not. As an anatomical imaging modality, CTA may indeed be evolving into a highly competitive diagnostic tool for CAD.2-4 However, assessments of structure and function are often complementary in the diagnostic armamentarium. Another perfect example of this premise is with renovascular hypertension. No one would question the ability of MRA and other interventional angiographic imaging methods to identify the presence of renovascular stenosis. However, captopril renal scintigraphy better identifies patients more likely to respond clinically to revascularization.5-6 Similarly, for patients with an intermediate pretest likelihood of underlying coronary disease, MPS adds specificity to the diagnostic assessment and therapeutic intervention, assuring against mere treatment of the patient’s diagnostic images, a liability known as the “oculostenotic reflex.”7

Although the evidence may be accruing in the literature in favor of using CTA for initial assessment of potential coronary disease, it does not compete with the consensus in the literature in support of MPS for risk stratification and for evaluation of potential benefit from revascularization.3,8-14 Apart from the unique contribution of functional assessment, there are potentially confounding effects on CTA by coronary calcium, which may be prevalent among at-risk patients, as well as potential for other technical artifacts, including patient motion, misalignment from heart rates >65-70, and respiratory motion.2 The prevalence of these confounding influences on CTA for assessment of CAD is largely unknown.

Dr Dowe cites the replacement of nuclear ventilation/perfusion imaging by CTA of the chest for pulmonary embolism (PE) diagnosis as an analogous example where “improvements and benefits were obvious.” I suggest that this might alternatively represent an example where clinical enthusiasm that encouraged this transition might have in fact been overzealous, with less certain cost/benefit to the patient in hindsight. Admittedly, the specificity of CTA for PE is superior to that of nuclear V/Q scanning. However, the largest multicenter evaluation to date of CTA for PE diagnosis recently reported in the PIOPED II study found only an 83% sensitivity,15 questionably adequate as a primary screening test with which to rule out disease. This is much less than the 100% sensitivity touted in one of the early reports of CTA for PE diagnosis.16 It should be further noted that an additional 6% (51/824) of CTA studies in PIOPED II were technically suboptimal and therefore excluded from the analysis.15 More recently, it has been reported that SPECT perfusion imaging improves both sensitivity and specificity compared to the conventional planar technique for V/Q scanning.17-20 In addition, concern has been raised about the estimated 20 mGy radiation dose per breast for female patients undergoing CTA of the chest, exceeding by ~7-fold the maximum recommended radiation dose for diagnostic mammography.21 This breast dose for CTA is approximately 30-fold larger than that from a standard V/Q scan performed with 148 MBq technetium 99m-MAA and 370 MBq xenon 133 gas.22 Moreover, the dosimetry to the lungs is likely to be somewhat higher from CTA than that from V/Q scans as well (17.6 mGy for CTA,23 versus 10.7 mGy for V/Q scanning with the same doses).22 A group from Yale more recently reported comparable definitive efficacy of V/Q scintigraphy for PE diagnosis among patients with a clear chest x-ray compared to that obtained using CTA for patients with an abnormal chest x-ray.24 With further consideration of the additional risks of IV contrast, the relative merits of nuclear lung scanning versus CTA for PE diagnosis may be open to reconsideration, at least for some patients. I would suggest that the evolution of these considerations in contrast to the initial glowing reports on CTA for PE diagnosis16 mitigates strongly in favor of caution before undertaking such comprehensive diagnostic paradigm shifts with CTA for coronary assessment as Dr Dowe has suggested.

Dr Dowe further mentioned that radiologists are best suited to assume responsibility for coronary CTA because they can evaluate “the entire study.” This alludes to the additional unordered diagnostic reading of the chest CT, which adds cost without any benefit to the assessment of CAD. That cost must also include all of the noninvasive and invasive follow-up testing for “positive” chest CT findings, including any associated morbidity, all of which is unknown.

Consideration of the importance of functional assessment, the potential confounding influence of several physiologic and technical factors, dosimetry to the patient, and the uncertain overall cost/benefit collectively mitigates against a rush to judgment to replace nuclear MPS by coronary CTA. In the reference cited by Dr Dowe in his editorial, evidence was presented in support of using CTA to follow up mildly abnormal nuclear stress tests.25 I suggest that such an incremental algorithm is more rational than the nihilistic approach suggested by Dr Dowe. To answer the question posed in the title of this editorial reply: The time is now for further ongoing careful evaluation of the appropriate place of coronary CTA in the diagnostic algorithm for assessment of CAD.

Stephen Gerard, MD, PhD, is chief of nuclear medicine for Seton Medical Center in Daly City, Calif.

References

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