**5. HIV-associated pulmonary arterial hypertension**

Primary pulmonary arterial hypertension is rare in HIV infected persons, with a prevalence of 0.5% [57]. The use of ART has not impacted on the epidemiology of HIV-associated pulmonary arterial hypertension [58]. There is no correlation between HIV-associated pulmonary arterial hypertension and CD4 cell count, HIV viremia, or duration since HIV diagnosis [47]. The pathogenesis of HIV-associated pulmonary arterial hypertension is poorly understood, with inflammatory and genetic factors both implicated [59]. Pulmonary hypertension in HIV occurs without documented thromboembolic disease, intravenous drug use or pulmonary infections [57, 58]. In a study of 47 patients in the Swiss Cohort Study, patients receiving ART had a significantly decreased median right ventricular systolic pressure over right atrial pressure gradient compared to patients who did not receive ART [60]. ART has also been reported to improve the 6 minute walk test in HIV infected patients with pulmonary hypertension, but with no effect on haemodynamic parameters [61]. Histologically, HIV-associated pulmonary arterial hypertension manifests most commonly as a plexogenic pulmonary arteriopathy, but thrombotic pulmonary arteriopathy and pulmonary veno-occlusive disease also described [62].

## **6. Pericardial disease in HIV**

**3. Myocardial fibrosis in HIV**

dysfunction with CMR.

190 Advances in HIV and AIDS Control

found to be elevated in HIV infected individuals [56].

view and in the lateral wall in (B) short-axis (white arrows depict the fibrosis).

Myocardial fibrosis an important reason of development and progression systolic and diastolic cardiac failure [55]. There is histological evidence of interstitial fibrosis at autopsy in 40% of subjects with HIV infection [29]. CMR studies have demonstrated a prevalence of focal fibrosis in asymptomatic HIV infected individuals of close to 80% (**Figure 5**) [22, 23, 25, 56]. Diffuse myocardial fibrosis estimated by extracellular volume (ECV) calculation was also

**Figure 4.** CMR cine tagging using spatial modulation of magnetisation in a short axis image through the mid left ventricle at end-diastole (a) and at end-systole (B) in a patient infected with HIV. Tagging for strain and strain rate imaging in circumferential, longitudinal and radial directions is one of the main techniques for assessment of diastolic

**Figure 5.** Late post gadolinium images showing mid-wall focal fibrosis in the basal inferolateral wall in (a) 3-chamber

Pericardial effusion and pericarditis are encountered frequently in patients with HIV infection. The prevalence of symptomatic pericardial effusions before the advent of ART was up to 11% of patients with AIDS [63]. However, in the ART era, the incidence of pericardial effusions in HIV is much less: in a multicentre cohort study of treated HIV patients, only 2 of 872 HIV infected patients had pericardial effusions, neither clinically important [64]. Using CMR with greater resolution, our group has demonstrated the prevalence of small, asymptomatic pericardial effusions to be much higher [23]. While generally nonspecific, pericardial effusions may indicate active inflammation and may be associated with subclinical myocarditis or disseminated tuberculosis, particularly in patients with low CD4 cell counts. In patients with large pericardial effusions, *Mycobacterium tuberculosis* is likely pathogen, especially in tuberculosis endemic regions [65]. In prospective study of patients with a large pericardial effusion, tuberculosis was identified as cause in 85% of cases [66]. In HIV, tuberculous pericarditis is commonly associated with heart failure [67]. HIV is associated with reduced incidence of pericardial constriction [68].

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 sarcoma and lymphoma [71, 72].

patients presented with large thrombus burden than atherosclerotic plaques suggesting *de novo* arteriothrombosis and thrombophilia as possible causes of CAD events [87, 88].

HIV-Associated Cardiovascular Disease http://dx.doi.org/10.5772/intechopen.80483 193

Cardiac malignancy usually manifests late in HIV disease. Kaposi's sarcoma and cardiac lymphoma are the main malignancies associated with HIV [89]. Non-Hodgkin lymphoma occurs 25–60 times more in HIV infected patients [90]. Cardiac lymphoma can infiltrate the myocardium, the subendocardial layer or be located within pericardial effusion [90]. Clinical features include dyspnoea, right-sided heart failure, heart failure, chest pain and arrhythmia. Presentations range from asymptomatic to cardiac tamponade, myocardial infarction, heart

In the pre-ART era, the prevalence of Kaposi's sarcoma from autopsy studies ranged from 12 to 28%, however, cardiac sarcomas were rare [6, 62]. In Kaposi's sarcoma, the coronary arteries are not affected. The incidence of non-Hodgkin lymphoma is not related to the level

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 manuscript is not funded. Dr. Ntusi gratefully acknowledges support from the American Heart Association, the National Institutes of Health/National Heart, Lung, and Blood Institute,

**9. Cardiovascular malignancy in HIV**

failure or conduction abnormalities [91].

**10. Conclusion**

this field.

None.

**Funding**

**Conflicts of interest**

of immunosuppression and has not changed with ART use [92].
