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• W2006768045 abstract "Cardiac magnetic resonance imaging (CMR) has long been recognized as an accurate and reliable means of evaluating cardiac anatomy and ventricular function. Considerable progress has been made in the field of CMR, providing accurate evaluation of myocardial ischemia and infarction [1–3]. Contrast-enhanced CMR can be used to visualize the transmural extent of myocardial infarction with high spatial resolution [4–6]. Infarcted myocardium appears hyperenhanced compared with normal myocardium when imaged by a late enhancement MRI technique with the use of T1-weighted sequence after injection of gadolinium chelates. Late gadolinium-enhanced CMR can clearly delineate subendocardial infarction and the transmural extent of delayed enhancement potentially predicts functional outcome after revascularization in acute myocardial infarction and chronic ischemic heart disease [7]. Stress first-pass contrast-enhanced myocardial perfusion CMR can be used to detect subendocardial ischemia and recent studies have demonstrated the high diagnostic accuracy of stress myocardial perfusion CMR for detecting significant coronary artery disease [8–10]. Magnetic resonance angiography (MRA) was recently introduced as a method that can provide visualization of all three major coronary arteries, coronary bypasses, and the aorta within a single three-dimensional acquisition [11, 12]. CMR has become the first choice imaging modality in complex congenital heart disease [13–16] and imaging great vessels [17, 18]. In recent years, late gadolinium enhancement CMR has also been used to visualize myocardial interstitial abnormalities. Previous studies have clearly shown late enhancement patterns in patients with different forms of cardiomyopathies, amyloidosis, myocarditis, and storage diseases [19–22]. Silva et al. [20] showed that late gadolinium enhancement can be demonstrated in cardiomyopathy patients, with a mean signal intensity of 390 ± 220% compared with normal regions. The affected areas included papillary muscles (sarcoid), the mid-myocardium (Anderson-Fabry disease, glycogen storage disease, myocarditis, Becker, and Duchenne muscular dystrophy) and the global subendocardium (systemic sclerosis, Loeffler’s endocarditis, amyloid, and ChurgStrauss). Focal myocardial late gadolinium enhancement is found in the specific cardiomyopathies, and the pattern is distinct from that seen in myocardial infarction, recent studies have demonstrated right ventricular late gadolinium enhancement in patients with congenital heart disease and right ventricular loading conditions [14, 23]. Myocardial preservation is likely a multifactorial process that may affect the right and left ventricles differently [24–28]. B. J. M. Mulder Cardiology Department, B2-240, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands" @default.
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• W2006768045 date "2008-10-01" @default.
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• W2006768045 title "Duchenne muscular dystrophy; a cardiomyopathy that can be prevented?" @default.
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• W2006768045 doi "https://doi.org/10.1007/s10554-008-9370-9" @default.
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