Dilated cardiomyopathy (DCM) is defined as left ventricular chamber dilation with decreased systolic function (FEVG <40%). There may also be right ventricular dysfunction. Causes are related to intrinsic myocardial damage.
There are dilated, thin-walled, poorly contracting ventricles +/- atria.
Although a variety of aetiologies can result in a dilated cardiomyopathy which are listed as below. Some are classified as separate entities. (See WHO 1995 classification of cardiomyopathies)
- ischaemic (coronary artery disease) - ischaemic cardiomyopathy
- infectious (myocarditis: virus, bacteria)
- infiltrative disease (sarcoid, amyloid)
- metabolic (uraemia, hypocalcemia, hypophosphataemia, thyrotoxicosis)
- toxic (alcohol, cocaine)
- chemotherapy (doxorubicin)
- others (peripartum, muscular dystrophies)
- autoimmune cross-reactivity (e.g. late-onset cardiomyopathy in Chagas disease)
- idiopathic: idiopathic dilated cardiomyopathy
- familial: familial dilated cardiomyopathy 7
Chest radiographs commonly show enlarged left ventricle and atria with pulmonary oedema +/- pleural effusions.
The degree of left ventricular dilatation is highly variable and depends on the stage of disease and severity of left ventricular dysfunction.
- acute phase
- the ventricle is just mildly dilated or may even be normal in size because compensatory dilatation has not yet developed.
- those with additional volume overload (mitral or aortic regurgitation) tend to have larger ventricles.
- chronic phase: with progressive dilatation the ventricle assumes a more spherical shape
The left ventricular wall is rather thin. However, as the left ventricle is enlarged, the total left ventricular mass may be increased.
In idiopathic dilated cardiomyopathy, the left heart is markedly dilated and thinned, and mid wall enhancement, especially in the septum, is present in more than 50% of patients 4.
Late-enhancement MR images may demonstrate areas of fibrosis within the myocardium, characteristically in the mid- or subepicardial myocardium, allowing differentiation from ischaemic cardiomyopathy 6.
On plain radiographs consider:
- large pericardial effusion
- 1. Dähnert W. Radiology review manual. Lippincott Williams & Wilkins. (2007) ISBN:0781738954. Read it at Google Books - Find it at Amazon
- 2. Miller SW. Cardiac imaging, the requisites. Mosby Inc. (2005) ISBN:032301755X. Read it at Google Books - Find it at Amazon
- 3. Belloni E, De cobelli F, Esposito A et-al. MRI of cardiomyopathy. AJR Am J Roentgenol. 2008;191 (6): 1702-10. doi:10.2214/AJR.07.3997 - Pubmed citation
- 4. Bluemke DA. MRI of nonischemic cardiomyopathy. AJR Am J Roentgenol. 2010;195 (4): 935-40. doi:10.2214/AJR.10.4222 - Free text at pubmed - Pubmed citation
- 5.O'Donnell DH, Abbara S, Chaithiraphan V et-al. Cardiac MR imaging of nonischemic cardiomyopathies: imaging protocols and spectra of appearances. Radiology. 2012;262 (2): 403-22. Radiology (full text) - doi:10.1148/radiol.11100284 - Pubmed citation
- 6. François CJ, Schiebler ML, Reeder SB. Cardiac MRI evaluation of nonischemic cardiomyopathies. J Magn Reson Imaging. 2010;31 (3): 518-30. J Magn Reson Imaging (full text) - doi:10.1002/jmri.22030 - Pubmed citation
- 7. Koikkalainen JR, Antila M, Lötjönen JM et-al. Early familial dilated cardiomyopathy: identification with determination of disease state parameter from cine MR image data. Radiology. 2008;249 (1): 88-96. doi:10.1148/radiol.2491071584 - Pubmed citation