The right ventricle is the most difficult portion of the heart to evaluate due to its asymmetric geometry and its relatively thin wall. An important cause of sudden death in young patients is arrhythmogenic right ventricular dysplasia (ARVD). Cardiac MRI (CMR) provides a diagnostic approach that appears to be the most useful for diagnosing ARVD. Several findings on CMR imaging are useful in the diagnosis of ARVD: 1) demonstration of fatty infiltration involving the right ventricular (RV) free wall [1]; as an isolated finding, intramyocardial fat is not specific for the diagnosis of ARVD and may be a source of false-positive diagnosis [2]; 2) two morphologic features of ARVD are RV dilatation and variable size aneurysms involving the RV outflow tract; 3) demonstration of both global and regional RV systolic dysfunction; and 4) the presence of RV diastolic dysfunction as an early marker of disease has been considered by some investigators as an additional criterion for ARVD, even when systolic function is normal [3]. Until recently, no study has explored the use of RV delayed enhancement (DE) imaging after the intravenous administration of the CMR contrast agent gadolinium diethyltriaminepentaacetic acid (Gd-DTPA).It is widely accepted that DE in the proper location and given the appropriate clinical setting represents myocardial infarction (MI). Disruption of cell membrane integrity increases the size of interstitial space and provides an expansion of extracellular space for the distribution of contrast agents such as Gd-DTPA. The resulting contrast enhancement correlates with histology, serum myocardial enzymes, and troponin, and predicts the functional recovery in reperfused acute MI [4]. However, passive diffusion of Gd-DTPA into an expanded interstitial space is by no means specific for MI and has been described in scarred or inflamed myocardium.Although 59% of patients with dilated cardiomyopathy had no DE, and 13% had subendocardial DE similar to that observed in those with myocardial ischemia, up to 28% of patients with a nonischemic origin of their cardiomyopathy demonstrated midwall DE [5]. In familial hypertrophic cardiomyopathy, DE showed plexiform depots in hypertrophied regions predominantly in the junction of the septum and the RV free wall [6]. Furthermore, a positive correlation has been described between the magnitude of septal hypertrophy and the extent of DE-demonstrated scarring in young patients with hypertrophic cardiomyopathy experiencing ventricular tachycardia and sudden death [7]. Also, CMR imaging with Gd-DTPA-induced contrast enhancement as a marker of inflammation has been successfully used as a diagnostic approach in myocarditis, showing that the inflammatory process spreads from a focal to a disseminated involvement of the myocardium within the first 2 weeks after the onset of symptoms [8]. It correlates with left ventricular function in the very early stages of the disease and to clinical status in the longer term because the presence of symptoms after 3 months seems to be accompani...
Evaluation of: Mahnken A, Koos R, Katoh M et al.: Assessment of myocardial viability in reperfused acute myocardial infarction using 16-slice computed tomography in comparison with magnetic resonance imaging. J. Am. Coll. Cardiol. 12, 2042-2047 (2005). Myocardial contrast-enhanced (CE) cardiovascular magnetic resonance (CMR) imaging is a relatively new and well-validated technique for imaging both cell damage and scar resulting from myocardial infarction. Multislice (16-slice) x-ray computed tomography (MSCT) has recently been suggested as a means for imaging acute myocardial infarction. Both CMR and MSCT are becoming increasingly available, are less invasive than catheter-based techniques and have high spatial three-dimensional resolution, allowing interrogation and sizing of acute myocardial infarction. The cell damage in acute myocardial infarction may be distinguished from normal myocardium by either technique. But while both CMR and MSCT show agreement for infarct localization and size determination, MSCT exposes the patient to substantial ionizing radiation and to possible kidney damage associated with the necessary administration of radio-opaque, iodinated, contrast medium. Furthermore MSCT does not demonstrate the presence of pathological consequences of myocardial infarction, myocardial scarring. These points must be considered when choosing the most appropriate approach for the imaging of acute and/or chronic myocardial infarction.
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