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Coronary artery disease (CAD) is a leading cause of global mortality. It results from atherosclerosis, which is a systemic and progressive disease involving the intimal layer of large- and medium-sized arteries. Atherothrombosis, defined as atherosclerotic plaque disruption (predominantly plaque rupture) with superimposed thrombosis, can lead to arterial occlusion and subsequent life-threatening conditions such as acute myocardial infarction (MI) or ischemic stroke. The concept of a “vulnerable plaque” was first introduced to distinguish unstable, rupture-prone plaques from plaques with a stable phenotype. Analyses of human coronary plaque have demonstrated that plaque rupture occurs at a higher frequency than clinical events, suggesting that prothrombotic conditions are also necessary for plaque rupture to trigger acute coronary syndromes. As such, effective risk stratification algorithms need to include both local and systemic factors that confer increased risk of cardiovascular events. At present, clinical risk scoring systems are largely based on the assessment of traditional risk factors with the addition of noninvasive imaging or functional (“stress”) testing for investigation of symptoms that are potentially ischemic in origin. A limitation of this approach includes failure to detect specific features of coronary plaque that confer increased risk of rupture. The identification of high-risk patients might be further improved through the direct assessment of coronary plaque burden, high-risk characteristics, or disease activity, allowing for targeted administration of therapies that are likely to result in prognostic benefits.
Subclinical atherosclerosis can precede the development of clinical disease by many years or even decades, providing an opportunity to identify high-risk patients for targeted primary prevention therapies and ongoing clinical surveillance. At present, multidetector computed tomography (MDCT) coronary angiography is often used for the assessment of low–intermediate risk patients with chest pain where its high negative predictive value allows for the exclusion of coronary artery disease in many individuals. MDCT also allows for the quantification of the overall atherosclerotic plaque burden and the identification of some vulnerable plaque characteristics, through patterns of positive remodeling, low x-ray attenuation, and spotty calcification. Cardiovascular magnetic resonance (CMR) imaging is a noninvasive modality with excellent contrast of soft tissues and the blood/vessel wall interface that has significant potential to assess coronary lumen integrity, plaque burden, and composition without the requirement for ionizing radiation. Advances in CMR data acquisition and gating techniques have improved image quality, which to date has been constrained by limited spatial and temporal resolution. As such, CMR is emerging as a promising modality for coronary artery imaging where its selective use in conjunction with myocardial perfusion imaging, viability, and ventricular function assessments, where CMR is the clinical reference standard, may allow for the complete assessment of suspected CAD with a single imaging modality. Furthermore, evolving molecular imaging techniques may allow for the assessment of disease activity, delineation of vulnerable plaque phenotypes and identification of novel therapeutic targets.
Studies have shown that coronary magnetic resonance angiography (CMRA) can identify significant coronary artery plaque (>50% stenosis) with a diagnostic accuracy comparable with MDCT. Multiple single center studies have compared the accuracy of CMRA against invasive angiography culminating in a meta-analysis that showed a sensitivity of 87% and specificity of 70% for detection of >50% stenoses. However, technical improvements in coil design, image acquisition/reconstruction, and motion compensation have allowed for a reduction in total imaging time for whole heart CMR coronary angiography to approximately 5 minutes with improved diagnostic accuracy (see Chapter 24 ). Another study has demonstrated that noncontrast, free breathing, three-dimensional (3D) balanced steady-state free precession (bSSFP) whole heart imaging has a sensitivity of 91% and a specificity of 86%, with an area under the receiver operator curve (ROC) of 0.92 when compared with quantitative invasive angiography for the detection of hemodynamically significant plaque. Furthermore, 3D cross-sectional imaging of the coronary vessel wall at 3 T has been able to achieve an in-plane resolution of 0.5 × 0.5 mm, which is comparable with MDCT ( Fig. 28.1 ).
Imaging of the coronary vessel wall and lumen is more challenging and technically demanding than imaging of other vascular beds because of the following :
Motion: myocardial contraction/relaxation and respiration
Small and tortuous vessels
Close proximity to epicardial fat, coronary blood, and myocardium
Requirement for high spatial resolution
In both noncontrast and contrast-enhanced CMR, the main limiting factor is imaging time. For coronary artery imaging, a compromise has to be made between imaging time, the spatial resolution achieved, and arterial coverage.
Because a high spatial resolution is paramount for diagnostic coronary artery imaging, longer scan times are necessary, which in turn results in greater susceptibility to motion-related artifacts such as ghosting and blurring. Adequately compensating for motion-induced artifacts is an unsolved problem and one of the technical challenges in CMR that remains an active area of current research.
Cardiac motion compensation involves synchronizing image acquisition to the electrocardiogram (ECG) to allow for imaging during a motion-free period in the cardiac cycle. The preferred time is the mid diastolic coronary rest period (100–150 ms, approximately 10% of the cardiac cycle), and the exact duration of this interval is heart rate dependent. ECG gating can be performed prospectively (image acquisition limited to mid diastole) or retrospectively, where data are acquired throughout the cardiac cycle but only data from mid diastole are used to generate images ( Fig. 28.2 ). These measures are essential to avoid cardiac-motion induced artifacts but reduce scan efficiency.
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