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Magnetic resonance imaging (MRI) is recognized as a useful tool for the noninvasive evaluation of the heart by providing clinicians with high quality diagnostic images, in any imaging plane, without interference from surrounding soft tissue or bone, using only a peripheral intravenous catheter, and administration of MRI contrast agents characterized by a favorable safety profile. Recent technological advances in gradient performance and surface coil design allow for short acquisition times, high signal-to-noise ratio and contrast-to-noise ratio, and improved spatial and temporal resolution.

Cardiomyopathy is a spectrum of diseases where the primary pathology directly involves the myocardium (nonischemic cardiomyopathy) or is the consequence of obstructive epicardial coronary artery disease (ischemic cardiomyopathy). Cardiovascular MRI provides unique insights into the etiology of cardiomyopathy in ways not available by other diagnostic tools.

Normal myocardium is comprised mainly of tightly compacted myocytes. The extracellular space consists of the capillary network of the coronary circulation and the interstitial space. The interstitial space is filled with interstitial fluid that bathes the myocytes and a small amount of collagen and proteoglycans that form a supporting framework. MRI contrast agents freely disperse though the extracellular space following an intravenous injection. Since the interstitial space of normal myocardium is small, contrast quickly washes out of normal myocardium though the capillaries. Cardiomyopathic processes often lead to interstitial expansion, whether from necrosis, fibrosis or paraprotein deposition, lymphocytic infiltration, edema accumulation, or granuloma formation. Therefore, in the presence of interstitial expansion, the clearance of MRI contrast agents from the interstitial space is prolonged resulting in a higher contrast concentration in affected myocardium.

Cardiovascular MRI takes advantage of the difference between the brisk washout of contrast from normal myocardium and the delayed washout from abnormal myocardium. By acquiring images 10-20 minutes following the injection of contrast, regions of late or delayed enhancement represent regions of myocardial histopathology. Thus, cardiovascular MRI has the potential to indentify the etiology of cardiomyopathy and characterize the extent of abnormal myocardium depending on the observed pattern of myocardial delayed enhancement (MDE).

In new-onset cardiomyopathy, determining whether left ventricular systolic dysfunction is secondary to an ischemic or nonischemic etiology is clinically important since ischemic heart disease often has a worse prognosis than nonischemic etiologies and left ventricular performance may improve following revascularization. Myocytes are replaced by collagenous fibrotic scar in regions of prior myocardial infarction. Accordingly, regions of subendocardial or transmural MDE that correspond to coronary artery territories are the result of the “wavefront” of myocardial necrosis that occurs with myocardial infarction. Figure 4A demonstrates the MDE pattern of transmural myocardial infarction (arrows) in the distribution of the left circumflex coronary artery. In this case, transmural MDE would predict a very low likelihood of improved contractility following revascularization since the scar tissue has replaced the full thickness of the basal and mid lateral wall of the left ventricle. Although there is a strong correlation between infarct size and outcome in patients with myocardial infarction, even patients with unrecognized “microinfarctions” (involving <2% of the left ventricular myocardial mass) detected by MRI experience >7-fold hazard increase for adverse outcomes. In contrast to subendocardial or transmural MDE, patients with idiopathic dilated cardiomyopathy often develop intramural MDE of the interventricular septum. Figure 4B demonstrates the so called “mid wall striae” pattern of MDE (arrows) in dilated cardiomyopathy that corresponds to bands of septal myocardial fibrosis found at autopsy. Another pattern of MDE that spares the subendocardium is the pattern of subepicardial MDE that has been described in active myocarditis that match regions of cellular infiltrate and edema. Figure 4C demonstrates skip regions of subepicardial MDE (arrows) associated with myocarditis in a 19 year-old patient presenting with chest pain, diffuse ST-segment elevation on the electrocardiogram, CPK 1900 U/L, and elevation in the cocksachie B type 3 viral titer. Regions of subepicardial MDE can decrease in size and even resolve during recovery from myocarditis. Finally, patchy regions of intramural MDE are detectable in patients with hypertrophic cardiomyopathy, often present in abnormally thickened myocardium. In the typical form of hypertrophic cardiomyopathy with asymmetric septal hypertrophy, patchy MDE can demonstrated in the septum as illustrated in Figure 4D. Septal MDE is more prominent at the insertion sites of the right ventricle (but can appear anywhere within the septum) and correlate with histological findings of myofibril disarray and fibrosis. Similarly, apical hypertrophs have MDE limited to the thickened apical myocardium. The extent of MDE correlates with the presence and number of the clinical risk factors for sudden cardiac death.

MRI contrast agents are gadolinium chealates that have no pharmacological or hemodynamic properties. The side effect profile is favorable with rare reports of allergic reactions (about 1:400,000). MRI contrast agents are not nephrotoxic. However, recent reports have linked MRI contrast agents to a condition known as nephrogenic systemic fibrosis or NSF (also called nephrogenic fibrosising dermopathy) which is a serious late complication of contrast exposure in patients with advanced renal disease. NSF primarily affects the skin resulting in fibrosis and presenting with thickened and retracted skin similar to scleroderma. While the skin is the organ principally affected, NSF may progress to a multisystem fibrosing disorder. Until more is learned about NSF, patients with low creatinine clearances (<30 ml/min) should not undergo contrast-enhanced MRI.

With the advent of MDE techniques, physicians can learn not only quantitative measures of left ventricular morphology and function for which MRI is well known (such as end-diastolic, end-systolic, and stroke volumes, left ventricular ejection fraction and mass) but also potentially learn the cause and treatability of cardiomyopathy. These features make cardiovascular MRI a comprehensive diagnostic tool which is virtually painless to the patient and can be completed during a single visit to the cardiovascular MRI suite.





References

Pennell DJ, et al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. Eur Heart J 2004;25:1940-1965

Mahrholdt H, et al. Delayed enhancement cardiovascular magnetic resonance assessment of non-ischemic cardiomyopathies. Eur Heart J 2005;26:1461-1474.

McCrohon JA, et al. Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance. Circulation 2003;108:54-59.

Kwong RY, et al. Impact of unrecognized myocardial scar detected by cardiac magnetic resonance imaging on event-free survival in patients presenting with signs and symptoms of coronary artery disease. Circulation 2006;113:2733-2743).

Moon JCC, et al. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol 2003;41:1561-1567.



Presented in Partnership by Nashville Medical News and Vanderbilt University Medical Center



August 2008

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