Insights Into Left Ventricular Remodeling Through Noninvasive Measures of Myocardial Matrix Expansion With Cardiovascular Magnetic Resonance

Cardiovascular disease is the leading cause of morbidity and mortality in the United States. Although clinical assessment is the cornerstone of patient management, clinicians often demand additional laboratory or imaging studies (disease markers or biomarkers) to assess differential diagnosis and to help formulate a management plan.1 There are growing, consistent data supporting an important role for noninvasive cardiac imaging studies as clinically and cost-effective tools in the diagnosis and risk stratification of patients with known or suspected cardiovascular disease. The past decade has witnessed an accelerated evolution of cardiovascular imaging, not only in its growing body of evidence to support its use, but also the development of novel technologies (eg, cardiac magnetic resonance, multidetector computed tomography, positron emission tomography) that will likely expand our ability to see more (eg, atherosclerosis, plaque morphology, myocardial tissue characterization) and possibly extend our treatment options.Article see p 1206Cardiac magnetic resonance (CMR) imaging has emerged as a powerful imaging technique that allows precise tissue characterization in a wide range of myocardial disorders. Several CMR techniques have been described and used for diagnosis, risk stratification, and to guide patient management. One of the most widely used and validated approaches is the detection and quantification of late gadolinium enhancement (LGE) in myocardial tissue. Myocardial tissue characterization with LGE is one of the unique biomarkers of CMR, which reflects the relative differences in the volume of distribution of the gadolinium contrast between normal and abnormal myocardium. Gadolinium is normally confined to the extracellular space. Expansion of the extracellular space resulting from infiltrative processes, fibrosis, or edema increases the myocardial volume of distribution, thereby allowing a larger amount of gadolinium to leak and accumulate in the tissue. This excess gadolinium accumulation combined with its slower washout (compared with normal myocardium) leads to the characteristic bright signal …