Coronary CT angiography offers further risk stratification in the management of patients with normal SPECT results

Risk stratification strategies used in the diagnosis and management of coronary artery disease (CAD) aim to identify patients with intermediate to high likelihood of significant CAD that might benefit from coronary revascularizations and/or aggressive medical therapy. Myocardial perfusion imaging (MPI) has been an integral part of the traditional risk stratification algorithm for more than two decades. While the presence of significant ischemia on MPI usually necessitates further evaluation with coronary catheterization, patients with normal or low risk scans are mostly managed medically. Even though a normal MPI result generally indicates a benign prognosis, the ‘‘warranty period’’ of such result could be substantially shorter in patients with certain clinical risk factors such as adenosine stress (due to inability to exercise), increasing age, diabetes, female gender in diabetics, and history of known CAD indicating a lower negative predictive value for MPI in this subset of high risk patients. Imaging modalities such as coronary artery calcium scanning (CACS) and coronary CT angiography (CTA) provide information about the coronary anatomy and histology rather than the coronary function. Coronary artery calcium is a marker of vascular injury and its amount (CACS) correlates closely with atherosclerotic burden. Along its comparable diagnostic accuracy in prediction of significant CAD, CACS has also been shown to have significant incremental prognostic value over MPI in several recent studies suggesting a strong potential for its complementary use with MPI. On the other hand, CTA has proven to provide highly accurate diagnosis of obstructive coronary plaques significantly outperforming MPI in all of the studies. CTA also presents more definitive information about the stage of atherosclerotic process by further characterizing the plaques as non-calcified (soft), mixed or calcified, which may also add more value in the prognostication of CAD. There is already some early evidence to support this independent incremental prognostic value for CTA over MPI. It also seems that traditional clinical risk assessment tools of Framingham Risk Score and Adult Treatment Panel III (ATP III) alone cannot accurately predict the atherosclerotic plaque burden as determined by CTA. This indicates CTA can identify a distinct subset of patients who would have been misdiagnosed as low risk for CAD by simply relying on their normal MPI result or on their traditional cardiac risk factors taking a further step in the risk stratification and optimal management of these patients. The prospective study of Choudhary et al which is published in the current issue of the Journal addressed exactly the above-mentioned issue of further risk stratification of patients with normal MPI scans who might benefit from aggressive medical therapy using CACS and CTA. The patient population included 81 mostly symptomatic (81%) patients (only three of them women) with mean age of 60.4 ± 9.6 years and without prior history of CAD or abnormal stress test who had normal results on stress MPI [either by exercise (48 patients) or dobutamine (33 patients) stress protocols]. All of the patients underwent CACS and 16-slice CTA within 2 to 4 weeks of the MPI. Cardiac risk estimates by ATP III criteria and post-MPI probability of CAD were also calculated for each patient. As a result of the study, 43 patients (53% of all patients) were identified as candidates for aggressive medical therapy using a post-test risk stratification model which classified patients as having a high risk, when at least one the following three conditions was present: either diabetes or ATP III 10 year-risk estimate of [20%; CACS [ 400; or coronary stenosis of[50% on CTA. While only one of these criteria was met in 29 patients, 7 patients shared all of From the Division of Cardiology, Department of Medicine, HarborUCLA Medical Center, Torrance, CA. Reprint requests: Matthew J. Budoff, Division of Cardiology, Department of Medicine, LA BioMed Research Institute at HarborUCLA Medical Center, 1124 Carson St, E5, Torrance, CA 90502; [email protected]. J Nucl Cardiol 2010;17:13–5. 1071-3581/$34.00 Copyright 2009 The Author(s). This article is published with open access at Springerlink.com doi:10.1007/s12350-009-9176-8