Dilated<unk>  can be due to pericardial effusion or infective endocarditis, especially in intravenous drug users which are common in the<unk>  population. However, the most researched cause of<unk>  is myocarditis (myocardial inflammation and infection) caused by<unk> -1, which the main subtype of<unk>  (the other being<unk> -2), with greater likelihood of transmission and shorter period between infection and illness.<unk> -1 virions infect cardiomyocytes in patches but there is no direct correlation between viral infection and dysfunction of cardiomyocytes.<unk> -related<unk>  is often not<unk>  with any specific opportunistic infection, and approximately 40% of patients have not experienced any opportunistic infection before the onset of cardiac symptoms. Myocarditis Myocarditis has been documented at autopsy in 40–52% of patients who died of AIDS before the introduction of HAART. Toxoplasma gondii is the most common opportunistic infectious agent<unk>  with myocarditis in AIDS occurring in 12% of deaths from AIDS 1987-1991 in one autopsy series. Myocardial toxoplasmosis causes an increase in the myocardial fraction of creatine kinase (CK-MB). In situ hybridization or polymerase chain reaction studies illustrate a high frequency of cytomegalovirus and<unk> -1 in AIDS patients with lymphocytic myocarditis and severe left ventricular dysfunction. Thus, it supports the hypothesis that<unk> -1 has a pathogenetic action and influences dilated<unk> . Coinfection with viruses (usually, coxsackievirus B3 and cytomegalovirus) seems to have an important effect as the GISCA autopsy records show that 83% of patients with myocarditis and 50% with dilated<unk>  were coinfected with viruses. Myocardial cytokine expression<unk> -1 invades the myocardium through endothelial cells by micropinocytosis infecting perivascular macrophages which produce additional virus and cytokines such as tumour necrosis factor-α (TNF-α). This induces cardiomyocyte apoptosis either by signalling through CCR3, CCR5 or CXCR4, by entry into cardiomyocytes (after binding to ganglioside GM1), or through TNF-α. In addition,<unk> -1-associated protein gp 120 may induce apoptosis through a mitochondrion-controlled pathway after activating inflammatory cytokines. TNF-α is produced by infected macrophages and the interaction between dendritic cells presenting the antigen to CD8 (T Killer cells). It causes a negative inotropic effect by interfering with the intracellular calcium ion concentrations perhaps by inducing the synthesis of nitric oxide (NO), also decreasing contractility. The intensity of the stains for TNF-α and inducible nitric oxide synthase (iNOS) of the myocardium was greater in patients with<unk>  (as opposed to idiopathic<unk> , myocardial viral infection and was inversely correlated with CD4 count with antiretroviral therapy having no effect. Autoimmune<unk>  Cardiac autoimmunity affects the pathogenesis of<unk> -related heart disease as<unk> -infected patients with dilated<unk>  are more likely to have cardiac-specific autoantibodies (anti-α-myosin autoantibodies) than<unk> -infected patients with healthy hearts and<unk> -negative controls. In addition, patients with echocardiographic evidence of left ventricular dysfunction had a higher chance of having cardiac autoantibodies. Furthermore, impaired myocardial growth and left ventricular dysfunction may be immunologically mediated as monthly intravenous immunoglobulins (IVIG) in<unk> -infected children reduces left ventricular dysfunction, increases left ventricular wall thickness, and reduces peak left ventricular wall stress. Perhaps this is because immunoglobulins inhibit the cardiac autoantibodies by competing for Fc receptors. Alternatively, the immunoglobulins can reduce the effects or secretions of cytokines and cellular growth factors. Encephalopathy<unk> -infected patients with encephalopathy are more likely to die of congestive heart failure than are those without encephalopathy; the hazard ratio is 3.4.<unk>  and encephalopathy are hypothesised to be linked by the<unk>  reservoir cells which are in the myocardium and cerebral cortex and keep<unk> -1 on their surfaces for long periods of time even after receiving HAART. They also secrete TNF-α, interleukin-6 (IL-6) and endothelin-1 which are cytotoxic cytokines causing tissue damage. Drug cardiotoxicity Zidovudine is an example of a nucleoside analogue and has been shown to cause: myocarditis and dilated<unk>  as well as an increase in total cholesterol, triglycerides, LDL, HDL and insulin resistance. Protease inhibitors are another group of drugs (e.g. ritonavir) and some of them can cause a range of problems such as: lipodystrophy, atherosclerosis, increase total cholesterol, triglyceride, HDL, LDL, and insulin resistance. Amphotericin B can cause dilated<unk> , hypertension and bradycardia whereas, Ganciclovir can cause ventricular tachycardia. Interferon-alpha can cause arrhythmia and myocardial infarction/ischemia.
HIV associated cardiomyopathy
Viral cardiomyopathy
Coxsackievirus-induced cardiomyopathy
Amyloid cardiomyopathy
Cardiac amyloidosis
Alcoholic cardiomyopathy
Eosinophilic myocarditis
Idiopathic giant-cell myocarditis