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Dilated Cardiomyopathy (DCM)

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Dilated Cardiomyopathy
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Dilated Cardiomyopathy (DCM) is a type of heart disease in which the chambers of the heart increase in size and the muscle walls thin; the relative thinness of the heart’s walls, compared to the dilated size of the heart, leads to a weakened ability to pump blood to the rest of the body (3). DCM affects one out of 2500 people each year (4) and is one of the leading causes of heart failure in young adults (5). Diagnosis of this disease is difficult because its symptoms are not severe or debilitating, and diagnosis – taking a biopsy of the heart – is often invasive and risky (2); not as many people are being diagnosed with it as the number of those who have it. This limited sample size inhibits the study of …show more content…

Fewer muscles in the heart walls lead to weaker contractions, which results in an impaired ability to pump blood to the rest of the body; this tends to lead to heart failure (3). It is a type of systolic failure since DCM occurs during systole, the process in which the heart contracts to pump blood to the rest of the body. There are various treatments for DCM. The first option is to provide people with medicine, such as ACE inhibitors and beta-blockers (4). However, should their condition worsen, patients can receive ventricular assist devices to help them pump blood to the rest of their body. In extreme cases, heart transplants may be necessary …show more content…

Cihakova of Johns Hopkins University is working with her laboratory to investigate the auto-immune causes of DCM, particularly with eosinophils, a type of white blood cell. In one study, their lab had two study groups of mice, one lacking eosinophils and one with a normal amount thereof. They induced myocarditis in both of these groups; while both groups’ hearts had a similar amount of scar tissue and inflammation, the hearts of the mice lacking eosinophils were able to pump blood normally, whereas the mice with a normal level of eosinophils in their hearts developed heart failure (2). The protein IL5 tells the body to create more eosinophils, so in order to test if DCM is caused by an excess of IL5 (thus creating excess eosinophils) or eosinophils themselves, Cihakova and her team compared IL5-deficient mice to normal mice. In terms of inflammation and how severe DCM affected the mice, there was no difference between these two mice groups tested. This suggests that IL5 has no effect on the progression of DCM in mice hearts (5). In order to further confirm their findings, the team modified eosinophil-deficient mice to have an excess of IL5 proteins; they then compared them to normal mice. There was no difference in the heart’s systolic function for the former, and they appeared to show no signs of DCM or inflammation related thereof. As a result, because the mice lacking eosinophils and having excess IL5 proteins showed the same symptoms as mice only lacking

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