The definitions of DCM and ischemic cardiomyopathy, with the latter defined as a “dilated cardiomyopathy with impaired contractile performance not explained by the extent of the coronary artery disease or ischemic damage,” have been controversial in the past. In acute infarctions the contrast enters the damaged myocardial cells due to myocyte membrane disruption. Patients with ischemic cardiomyopathy are managed with β blockers, myocardial stenting, risk factor modification, or coronary artery bypass. MR findings in cardiac amyloidosis. Notice the dilated right ventricle with severe segmental dyskinesis resulting in small aneurysms. It is problematic that most MRI scanners cannot adequately image the right ventricle using T1-weighted turbo or fast spin-echo imaging [20, 21]. Dilated cardiomyopathy is defined as dilatation with an end diastolic diameter greater than 55mm measured on the left ventricular outflow image and an ejection fraction < 40%. Other MRI characteristics of importance are the imaging correlates of histologically identified fibrofatty infiltration. The arrow points to the hypertrophic basal septum. Because the most vulnerable zone of the myocardium is the subendocardial layer, the subendocardial layer is always involved by a myocardial infarction. On the left a long axis cine 6 days after revascularization of an acute inferior wall infarction. Female patients suffered more cardiac arrest than males (11% vs. 2%) and more adult females experienced ischemic stroke than males (9% vs. 3%). Functionally cine images are evaluated for RV dysfunction, microaneurysm formation, and focal areas of RV dyskinesia. Myocardial tagging in either a grid or line pattern is performed by applying pulses that eliminate the MRI signal along the tag lines. The left ventricle is also involved in at least 15% of patients. Thus, despite being somewhat rare, ARVD is a common reason for referral for MRI. Histologically, there is apoptosis of myocytes and replacement by fibrofatty tissue. Role of magnetic resonance imaging in arrhythmogenic right ventricular dysplasia: insights from the North American arrhythmogenic right ventricular dysplasia (ARVD/C) study. Since all infarctions start subendocardially and may progress to transmural, the subendocardial region is always involved. This phenomenon is highly significant clinically because it usually manifests itself in the setting of chronic ischemia, that is potentially reversible by revascularization. Using steady-state free precession imaging, a movie loop of a single slice of the heart is easily obtained in 5–6 seconds. MRI can show segmental hypokinesis, dilatation, fatty infiltration in the right ventricular myocardium, small aneurysms and late enhancement of the myocardium [5,27]. Noice the following: After PTCA there is improvement of the function of the anterior wall. The tag lines deform with the myocardium as it contracts or relaxes, allowing precise determination of myocardial contraction patterns Because several experimental medical treatments are now being studied for HCM, MRI will be used in future clinical trials to determine if subtle improvements in regional contraction or relaxation may occur after therapy. Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle (myocardium) becomes abnormally thick (hypertrophied). As a result, some patients are diagnosed as genotype positive but may be phenotype negative if they have not yet expressed the disease. When the cause of the myocardial dysfunction is unknown, a major benefit of MRI is to help separate an ischemic (atherosclerotic) cause from a nonischemic cause. The MRI features of other nonischemic cardiomyopathies are myriad but have been recently reviewed [2]. If a person is diagnosed to have early stage non-ischemic cardiomyopathy, then his life expectancy is much better because proper treatment begins earlier. The diagnosis appears more specific when these morphologic and functional changes have a predominant right-sided involvement. Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance. Other identifiable causes of cardiomyopathy are hyperthyroidism, malnutrition, cytotoxic drugs, such as anthr… There is an inverse relationship between the transmural extent of hyperenhancement, and the likelihood of wall motion recovery following revascularization. CT Angiography of Coronary Artery Aneurysms: Detection, Definition, Causes, and Treatment, Review. Circulation 2004; 109:1250-1258, Mahrholdt H, Wagner A, Deluigi CC, Kispert E, Hager S, Meinhardt G, Vogelsberg H, Fritz P, Dippon J, Bock CT, Klingel K, Kandolf R, Sechtem U. The ejection fraction was measured to be 28%. The ejection fraction improved from 17 to 49%. In about 25% of patients there is obstruction of the left ventricular outflow tract (LVOT) due to hypertrophy of the basal septum and a systolic anterior motion of the mitral valve (SAM). The pathogenesis is unknown, but it is probably caused by the release of catecholamines. On the left a 4-chamber view of a patient with idiopathic cardiomyopathy. The myocardium has a very limited response to cellular injury and can be replaced by either fibrosis or fat tissue. Circulation 2006; 114:1581-1590, by Srijita Sen-Chowdhry et al J Am Coll Cardiol, 2006; 48:2132-2140, by Heiko Mahrholdt et al On the left the late enhancement images of the same patient. No reflow phenomenon is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed. Cardiac Imaging: Part 1, MR Pulse Sequences, Imaging Planes, and Basic Anatomy, Review. In coronary artery disease myocardial dysfunction is a consequence of infarction, hibernation, stunning and secondary changes by remodelling. 4). Myocardial regions that demonstrate little or no evidence of hyperenhancement (i.e. MRI also possesses the unique ability to add information regarding tissue composition. On an end-systolic image the following findings can be depicted (figure): HOCM (2) Thus, whereas nonischemic myocardial disease usually can be distinguished from ischemic disease, determining the particular cause of nonischemic cardiomyopathy requires clinical correlation and often myocardial biopsy. Dilated Cardiomyopathy – it occurs due to progressive cardiac dilatation with concomitant hypertrophy. In nonischemic myocardial disease the delayed enhancement usually does not occur in a coronary artery distribution and is often midwall or epicardial rather than subendocardial or transmural. 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