Nutritional Deficiencies as a Factor in Left Ventricular Dysfunction

Nutritional deficiencies are common in HIV infection and may contribute to ventricular dysfunction independently of HAART. Mal­absorption and diarrhea can both lead to trace-element deficiencies which have been directly or indirectly associated with car­diomyopathy [34-36].

Fig. 6 The possible pathogenic mechanisms involved in the development of HIV-associated cardiomyopa­thy and encephalopathy and their relationship. The infection of dendritic cells, of CD4 lymphocytes, and of myocardial or neuronal cells by HIV-1 or by other viruses may be responsible for the release of specif­ic cytokines (TNF-α, IL-1, IL-6, IL-10) that activate the inducible form of nitric oxide synthase (iNOS). The interaction between cytotoxic T lymphocytes and the receptoral complex Fas/Fas ligand located on the sur­face of the target cell may cause mitochondrial damage with release of mitochondrial pro-apoptosis factors-cytochrome c, apoptosis inducing factor (AIF). Similar mitochondrial damage may be caused by reactive oxygen species (ROS) released by activated lymphomonocytes.The interaction between autoanti­gens and major histocompatibility complex (MHC) molecules on the surface of dendritic cells/macrophages, of myocardial cells (MHC-I), and of B lymphocytes (MHC-II) determines the production of autoantibodies (e.g., alpha-antimyosin) that are responsible for direct cellular damage. The neuronal damage, specifical­ly the impairment of the autonomic system, may enhance the functional damage to myocardial cells be­cause of increased adrenergic activity and down-regulation of beta-adrenergic receptors. CVB3, coxsack­ievirus B3; CMV, cytomegalovirus; EBV, Epstein-Barr virus; ADV, adenovirus; Ca++, calcium; cGMP, cyclic guanine monophosphate; Bid, a protein of the bcl 2 family involved in apoptosis. (From the Lancet [20], with permission from Elsevier)