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Dr Yusuf (November 2001 JRSM, p. 609), commenting on my review on cardiovascular manifestations of HIV infection1, raises the question of selenium deficiency. Nutritional deficiencies must certainly be considered as potential aetiologies in HIV-related heart disease, along with myocardial infection with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection and drug-related cardiotoxicity2. Nutritional deficiencies are common in late-stage disease and may contribute in inducing ventricular dysfunction independently of antiretroviral therapy2. The role of selenium in the development of HIV-associated cardiomyopathy is still controversial. The relation between selenium deficiency and cardiomyopathy has also been studied in selenium-deficient mice with contrasting results3. Selenium replacement may reverse cardiomyopathy and restore left ventricular function in nutritionally depleted patients, but the evidence is mainly based on case reports4; controlled prospective clinical trials are lacking. Levels of vitamin B12, carnitine, and growth and thyroid hormone may also be altered in HIV disease5; all have been associated with left ventricular dysfunction in relation to an impairment of the process of oxidative phosphorylation and increased production of free radicals5. Increased lipoperoxidation and reduced glutathione levels may be observed in plasma, in peripheral mononuclear cells and in T lymphocytes of HIV-infected patients6,7, especially those who are coinfected with hepatitis C virus8, independently of nutritional disorders. I agree with Dr Yusuf that nutritional disorders (including selenium deficiency) should be carefully checked in HIV-infected patients but HIV-associated cardiomyopathy should not be compared to Keshan disease because of its multifactorial pathogenesis2.