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Commentary |
1 Department of Radiology, Case Western Reserve University, MetroHealth Medical
Center, Cleveland, OH.
2 Present address: 2820 Broxton Rd., Shaker Heights, OH 44120.
Received May 20, 2008; accepted after revision May 30, 2008.
Address correspondence to A. J. Duerinckx
(andrejd{at}earthlink.net).
Keywords: coronary artery disease • coronary CT angiography • coronary lesion • nonculprit coronary lesion
Coronary plaque burden and plaque vulnerability are important for predicting future cardiac events and there is great interest in developing noninvasive tools to detect and quantify them. The article on the quantification of nonculprit coronary lesions using cardiac 64-MDCT angiography [1], published in this issue of the American Journal of Roentgenology, raises some interesting related questions. Is it worthwhile to quantify the nonculprit lesion severity or should coronary lesion detection and characterization be more important? And if lesion quantification is attempted, do we have reliable tools to do so?
Why the interest in nonculprit lesions? The importance of detection and characterization of multiple coronary lesions is well recognized in patients with coronary artery disease (CAD). In patients with acute myocardial infarction (AMI), the lesion, which causes the initial AMI, is called the "culprit" lesion and can be defined on the basis of the association of the angiographic lesion appearance with ECG changes or myocardial ischemia determined by stress testing [1]. During the year after myocardial infarction, among patients with AMI, the presence of multiple complex lesions and plaques has been associated with an increased incidence of recurrent acute coronary syndromes (ACS); repeated angioplasty (particularly of noninfarct-related lesions); and coronary artery bypass graft surgery [2]. Long-term cardiac events in patients with acute myocardial infarction after discharge are more likely to develop in patients with multiple complex plaques than in patients with single complex plaques [3]. These other lesions are referred to as the nonculprit lesions.
Stratifying Cardiac Risk
Should we look at lesion severity, coronary plaque burden, or coronary plaque characterization? There is a well-known evolution of atherosclerotic disease from positive vessel remodeling (without luminal narrowing) to severe luminal stenosis and occlusion. However, critical events (like hemodynamically significant luminal narrowing causing AMI) are mostly due to changes in the culprit and nonculprit lesions, with plaque erosions and ruptures and subsequent clot formation, causing vessel occlusion. This explains the great interest in the concepts of the vulnerable plaque, vulnerable blood, and vulnerable patient from the perspective of both detection [4, 5] and treatment [6]. It is therefore important to monitor the severity of isolated lesions, all areas of plaque formation in coronary vessels even if there is no significant luminal narrowing, as well as total plaque burden and plaque stability. The use of coronary calcium scoring, which reflects the calcific plaque burden, is relatively well established in stratifying cardiac risk. Coronary CT angiography (CCTA) allows us to go beyond plaque burden quantification by adding characterization of the plaque as noncalcific, calcific, and mixed, with implications for plaque stability. Early disease with positive vessel remodeling and lower CT attenuation plaque also has negative implications as to plaque stability [7]. Varnava et al. [8] showed that coronary artery plaques with positive remodeling have a higher lipid content and macrophage count, both markers of plaque vulnerability. Their results may explain why plaque rupture is often apparent at sites with only modest luminal stenoses (but marked positive remodeling).
Is it important to detect early coronary disease? And if it is important, how early can we actually detect and characterize it and will we be able to track changes? Early coronary disease detection may not be a bad thing, assuming there is no excessive associated harm or cost due to unproven premature therapy or interventions. Until the advent of CCTA we had no easy approach to coronary plaque detection or characterization, except for invasive coronary angiography (ICA) in combination with intravascular ultrasound (IVUS). Early disease can be difficult to detect on ICA alone as many vessel segments can appear normal on ICA, but show evidence of disease and positive vessel remodeling by CCTA or IVUS. In one study, up to 54% of coronary vessel segments negative for CAD by ICA were positively remodeled on CCTA [9]. In the same study, ICA only detected CAD in as little as 20%, 48%, and 46% of segments with noncalcified, calcified, and mixed plaques, respectively, seen by CCTA [9]. Lee et al. [3] showed that little angiographic change occurs during 6 months of follow-up in the nonculprit complex plaques. CCTA can probably do better because Hoffmann et al. [10], using cardiac 16-MDCT angiography, were already able to identify differences in lesion morphology and plaque composition between culprit lesions in patients with ACS and stable lesions in ACS or stable angina, consistent with previous IVUS studies. CCTA may some day be able to reliably track changes in plaque burden and morphology over time.
Value of 64-MDCT in ACS Assessment
Let us now review the finding in the article by Dodd et al. [1] in this issue of the AJR in view of the above discussions. The authors showed that in patients presenting with ACS, 64-MDCT can provide an accurate grade of stenosis for nonculprit lesions in proximal coronary artery segments (> 3 mm). They opted to focus on lesion quantification, and not lesion detection or characterization. This is very promising preliminary work in the field of CCTA, and it opens the door for future research. However, several shortcomings of this study are worth mentioning. The very important issue of vessel remodeling in early nonculprit lesions was not addressed. Also, only 12 of 46 (26%) analyzable coronary segments with nonculprit lesions fulfilled the size > 3 mm criterion, thus limiting where 64-MDCT can be applied. New 3D workstations are now available that allow us to quantify and track calcific, noncalcific, and total plaque burden. The authors showed that the software tools available on some of these workstations do not yet perform reliably for automated quantification of nonculprit lesions in the 30% to 70% range, and more work needs to be done to improve these semiquantitative coronary software tools. These are exciting times for CCTA as we improve our ability to detect, quantify, characterize, and track coronary artery disease. We look forward to the day when cardiac CTA and cardiac MRI will be better able to characterize coronary plaque and detect plaque vulnerability [4].
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