2006
DOI: 10.1016/j.jacc.2006.07.051
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Magnetic Resonance Imaging of Arrhythmogenic Right Ventricular Dysplasia

Abstract: Qualitative assessment of RV structure and function is highly reproducible for experienced observers. Among the qualitative parameters, fat infiltration is less reproducible and lacks specificity compared with RV kinetic abnormalities.

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Cited by 169 publications
(40 citation statements)
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“…MR imaging has evolved to a promising tool for evaluation of ARVD [11,12]. In addition to highly accurate functional information about the right ventricle it provides unique information about myocardial characteristics, especially in differentiation of fatty and muscular tissue [13] that has been reported to be strongly associated with ARVD [3]. On T1-weighted MR-images fat appears with high signal intensity, whereas myocardium appears with intermediate signal intensity.…”
Section: Discussionmentioning
confidence: 99%
“…MR imaging has evolved to a promising tool for evaluation of ARVD [11,12]. In addition to highly accurate functional information about the right ventricle it provides unique information about myocardial characteristics, especially in differentiation of fatty and muscular tissue [13] that has been reported to be strongly associated with ARVD [3]. On T1-weighted MR-images fat appears with high signal intensity, whereas myocardium appears with intermediate signal intensity.…”
Section: Discussionmentioning
confidence: 99%
“…Low voltage and/or flat T waves in left precordial leads can be also observed in case of severe right or biventricular involvement. The echocardiographic evaluation usually reveals normal LV, RV dilatation, RV wall thinning and in late stages RV and/or biventricular dysfunction [1][2][3][4].Cardiac histology in ND reveals the characteristic fibrofatty replacement of the RV myocardium with aneurysms' formation and possible LV involvement. Usually it starts from right ventricular subepicardial layers towards the endocardium.…”
mentioning
confidence: 99%
“…Usually it starts from right ventricular subepicardial layers towards the endocardium. Initial changes are in the "triangle of dysplasia" (outflow tract, inflow tract and apex), but it may be diffuse involvement of both ventricles [1,2].A two base-pair deletion in the plakoglobin (cell adhesion protein) gene (Pk2157del2TG), which maps to17q21, has been identified as the cause of ND and provided evidence that the pathogenesis might be related to a defect in myocardial mechanical coupling. Defects in the linking sites of these proteins can interrupt the contiguous chain of cell adhesion, particularly under conditions of increased mechanical stress or stretch, leading to cell death, progressive loss of myocardium and fibro-fatty replacement [1][2][3][4].…”
mentioning
confidence: 99%
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