Health & Medicine: Dilated Cardiomyopathy

Dilated cardiomyopathy (DCM) is one of the non-ischemic disorders of the heart wall. It is characterized by the enlargement of the left ventricle (LV) due to reasons other than coronary artery disease and abnormal loading conditions. Consequently, DCM reduces the heart’s ability to pump blood. DCM may be caused by genetic mutation or various non-genetic factors, such as pathogen infections, autoimmune diseases, neuromuscular diseases, and toxin exposure (Schultheiss et al., 2019). The global prevalence of the disease was estimated at 2.5 million cases in 2015, marking a 27% increase in the last ten years (Schultheiss et al., 2019). The morbidity of dilated cardiomyopathy has significantly increased in recent years.

In addition to causes and prevalence, the article discusses the risk factors for and pathophysiology of DCM. Men and Black people are at a higher risk of contracting the disease. In terms of pathophysiology, the dilation of the LV results from fibrosis or remodeling (Schultheiss et al., 2019). DCM is characterized by scar tissue within the left ventricle. It also reduces the blood volume pumped at each contraction by the LV as well as the amount of blood pumped per minute by the heart. Other changes include an increase in cardiac preload and afterload and a decrease in end-systolic blood pressure.

The article includes information on the pathophysiology of dilated cardiomyopathy. It discusses the biological abnormalities within the heart due to DCM. This information is important because it shows how DCM impacts the body. Pathophysiology of disease is relevant since it gives healthcare professionals a cellular-level understanding of the body. It also directs them on what to test for when they detect changes in vital organs, such as the heart.


Schultheiss, H. P., Fairweather, D., Caforio, A. L., Escher, F., Hershberger, R. E., Lipshultz, S. E., Liu, P. P., Matsumori, A., Mazzanti, A., McMurray, J. & Priori, S. G. (2019). Dilated cardiomyopathy. Nature Reviews Disease Primers, 5(1), 1-19. Web.

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