**10. Conclusion**

Mortality of pericardial effusions in HIV-infected patients is based on the severity and aetiology of the disease, especially if associated with tuberculosis [69]. We have demonstrated more frequent myocardial fibrosis in HIV-associated pericardial constriction when compared to those without HIV infection [35]. Prednisone does not reduce mortality in tuberculous pericarditis, but has been shown to be associated with reduced hospitalisation and constriction, but with increased risk of malignancies in those with HIV infection [70]. Other causes of pericarditis and pericardial effusions in HIV include HIV itself, bacterial infections, Kaposi's

The epidemiology and clinical profile of infective endocarditis in HIV infection are the same as in uninfected individuals [73]. The one setting where HIV is associated with increased risk of infective endocarditis is intravenous drug abuse. *Staphylococcus aureus, Streptococcus viridans* and Salmonella species are the most common organisms and the tricuspid valve is most involved in intravenous drug users developing infective endocarditis [74, 75]. Nonbacterial (marantic) endocarditis has been described in HIV, usually clinically silent and manifests with large, friable, sterile vegetations on the cardiac valves, which can lead to pulmonary embolization [75]. Patients with low CD4 counts have a poorer prognosis when they develop infective endocarditis [76]. Rates of infective endocarditis have decreased with the advent of ARV therapy [76]. When intravenous drug use is excluded, HIV infection has not been shown

HIV-infected patients are known to be at risk for premature coronary artery disease (CAD) [78]. Different factors related to HIV can lead to development atherosclerosis, including immune dysfunction, proliferation of T-cells, inflammation, endothelial dysfunction, and lipid abnormalities [79, 80]. During atherogenesis, HIV promotes monocyte penetration of the vascular intima to promote secretion of cytokines and expression of endothelial cell adhesion molecules [81]. The process of endothelial dysfunction in HIV patients may be driven by HIV transcription factors [82]. Increased risk of CVD in HIV infected patients is directly related to lower CD4 T-cell counts [83]. Higher number of activated CD8 T-cells is observed in relation to increased rates of coronary artery plaque and carotid artery

In the early stage of HIV infection both total cholesterol and high-density lipoprotein cholesterol are decreased [85]. Lower levels of apolipoprotein B and smaller low-density lipoprotein cholesterol have been reported in more advanced stages of HIV infection [86]. In addition, deleterious metabolic effects such as dyslipidaemia and insulin resistance after exposure to certain ART treatments have been reported [79]. Recent studies observed that HIV infected

sarcoma and lymphoma [71, 72].

192 Advances in HIV and AIDS Control

**7. Infective endocarditis in HIV**

to be a risk factor for infective endocarditis [77].

**8. Coronary artery disease in HIV**

stiffness [84].

Two third of those infected with HIV reside in SSA. Currently, 17 million people globally receive ART for HIV infection. This widespread use of ART has been associated with a dramatic reduction in HIV-related mortality. CVD and heart failure are on the increase in HIV: the mechanisms responsible for HIV-associated CVD are manifold and incompletely understood. Diastolic dysfunction has emerged as the dominant form of HIV-associated CVD in the era of ART. HIV-associated CVD encompasses heterogeneous disorders and has the propensity to involve every segment of the cardiovascular axis. We have described important recent developments and perspectives based on a systematic analysis of the important advances in this field.

## **Conflicts of interest**

None.
