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Cardiac magnetic resonance (CMR) imaging has become a powerful diagnostic tool in the assessment of cardiomyopathy. CMR not only provides a comprehensive evaluation of structure and function, but also allows for tissue characterization. CMR is the gold standard for quantification of cardiac volumes and function; it allows 3-dimensional visualization of the heart, as well as detailed flow evaluation with velocity encoded cine imaging. Tissue characterization has become the most exciting aspect of CMR in the field of heart failure (HF). The use of late gadolinium enhancement (LGE) allows for direct visualization of focal ischemic and nonischemic scar. Advances in T1 mapping now enable quantification of diffuse myocardial fibrosis by measuring the extent of interstitial expansion via extracellular volume (ECV) fraction. Further tissue characterization is performed with T2 mapping allowing for visualization of myocardial edema, while T2 star mapping directly quantifies myocardial iron content. The comprehensive nature of CMR not only yields high-quality diagnostic data, but also significant prognostic information, especially in patients with HF. This chapter will highlight the critical role of CMR in the assessment of cardiomyopathies.



A 50-year-old woman with a history of coronary artery disease (CAD) and coronary artery bypass grafting, prior myocardial infarction (MI), and ischemic cardiomyopathy presented with dyspnea and decompensated systolic HF. Her bypass grafts were found to be occluded, including her left internal mammary artery, and she was being evaluated for possible repeat bypass surgery. CMR was ordered to assess myocardial viability.

Assessment of cardiac function with electrocardiogram (ECG)-gated steady-state free precession (SSFP) cine imaging, a key element of the standard CMR cardiomyopathy protocol, demonstrated multiple regional wall motion abnormalities (Figure 23-1) and moderate to severe left ventricular (LV) systolic dysfunction. LGE imaging showed near transmural MI of the basal to mid inferolateral wall and the entire apex (Figure 23-2), consistent with nonviable myocardium. Subendocardial infarction involving 50% of myocardial wall thickness was present in the anteroseptal, anterior, and anterolateral segments (Figure 23-3), suggesting partial viability. Given multiple segments with limited to no viability, high risk of redo sternotomy, and concern for medication noncompliance with dual antiplatelet therapy, the patient was managed with aggressive goal-directed medical therapy.

Figure 23-1

Horizontal long-axis steady-state free precession (SSFP) cine at end diastole (A) and end systole (B) in a patient with severe ischemic cardiomyopathy.

Figure 23-2

Subendocardial to transmural hyperenhancement (blue arrows) in horizontal long-axis (A) and 3-chamber (B) views on late gadolinium enhancement images represents infarcted myocardium.

Figure 23-3

Subendocardial myocardial infarction (blue arrow), transmural myocardial infarction (red arrow), and papillary muscle infarction (yellow arrow) on late gadolinium enhancement short-axis image.


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