Identifying patterns of atherosclerotic disease manifestation with coronary computed tomography. Impact on clinical management and outcome?

Since its introduction as a tool for non-invasive coronary imaging, computed tomographic angiography (CTA) has undergone significant clinical validation. Its feasibility and diagnostic performance for the assessment of luminal stenosis have been evaluated against conventional angiography. In multiple comparative studies, it has been demonstrated that significant luminal stenosis can be excluded with high negative predictive value. The positive predictive value for the detection of stenotic lesions is reduced by stenosis overestimation due to artefact associated with advanced, calcified atherosclerotic lesions. At the same time, CTA has been validated for assessment of plaque burden and plaque characteristics. Several studies have demonstrated reliable identification and differentiation of calcified and non-calcified plaque in comparison with intravascular ultrasound (IVUS), but further characterization of non-calcified components based on the CT Hounsfield unit value is limited. The ultimate goal of atherosclerosis imaging is the identification of ‘the vulnerable plaque’, prior to their causing acute cardiovascular events. In post-mortem studies, these high-risk lesions, the so-called thin cap fibroatheromata (TCFA), are characterized by a necrotic core, separated from the lumen by a thin fibrous cap (,65 mm), which consists of smooth muscle cells and inflammatory cells in a proteoglycan-rich collagen matrix. While reliable in vivo identification is still not possible, invasive imaging modalities including IVUS and optical coherence tomography (OCT) allow identification of individual high-risk features. Grey-scale IVUS studies comparing lesion morphology in stable and unstable patients found low echodensity, positive remodelling, and small ‘spotty’ calcium deposits to be more prevalent in unstable patients. Advanced analysis of the IVUS backscatter information [IVUS radiofrequency analysis (RFA)] allows further plaque differentiation. Based on emerging data, the IVUS-derived fibroatheroma (ID TCFA) is defined as a plaque with significant plaque burden, a confluent necrotic core .10–20% of the total plaque volume, and no imaging evidence of a fibrous cap (i.e. minimal thickness of the cap below the resolution of IVUS). The amount of calcium is variable, .10%, with a speckled appearance. Pundziute et al. describe data comparing IVUS RFA plaque analysis with CTA in 50 patients presenting with acute coronary syndromes (ACS) or stable CAD. By CTA, plaques were classified as non-calcified, calcified, and mixed (non-calcified and calcified components within the same plaque). In ACS patients, 32% of plaques were non-calcified and 59% were mixed. In patients with stable CAD, predominantly calcified lesions were most prevalent (61%). The percentage of necrotic core was higher in the plaques of ACS patients (P 1⁄4 0.02), and ID TCFAs were more prevalent than in stable patients (32% vs 3%, P ,0.001). Importantly, ID TCFAs were most frequently observed in mixed plaques. Similar to previous IVUS and CTA studies, these results suggest that mixed calcified lesions with spotty calcification are related to plaque vulnerability. The overall risk of developing an acute cardiovascular event is probably related to the number of plaques and their individual level of vulnerability. This has diagnostic and therapeutic implications. On the one hand, focal identification of the most vulnerable lesions would allow evaluation of novel, plaque-stabilizing interventions, including prophylactic stenting or local drug delivery. It has been suggested that CTA could be used as a roadmap to identify hot spots for subsequent further evaluation with IVUS in