Pericardial Disease

Pericardial Effusion

Pericardial effusion is the most frequent complication in HIV-infected patients. Before the introduction of HAART therapy, its frequency varied from 5 to 46% with an incidence of 11 to 17%/year and was associ­ated with a high mortality rate [5].

In the pre-HAART era, pericardial effu­sion was more common in patients with HIV advanced disease. Clinical manifestation of pericardial disease varies from asympto­matic pericardial effusion to cardiac tam­ponade.

Echocardiography is the non-invasive ref­erence and accurate tool for the diagnosis of pericardial disease and tamponade. The echocardiographic diagnosis of pericardial effusions is usually based on visualization of a sonolucent circumcardiac space of vary­ing width with or without hemodynamic compromise (Fig. 1).

Heidenreich et al. [6] described the inci­dence of pericardial effusion and its relation

Fig. 1 Apical four-chamber view in an HIV infected patient showing a large and circumferential pericar­dial effusion

to mortality in HIV-positive subjects. In this study including outpatients, the prevalence of effusion in AIDS subjects was around 5%. The vast majority (80%) were small asympto­matic effusions, without any hemodynamic compromise. Survival of AIDS subjects with pericardial effusions was significantly short­er than AIDS subjects without (36 vs. 93% at 6 months, p32 mm/m² in diastole) associated with impaired ventricular systolic function, assessed by impaired left ventricular ejec­tion fraction (LVEF stage and no LV systolic dysfunc­tion [21].

In sub-Saharan Africa, dilated cardiomy­opathy remains an important issue. Out of 416 HIV-infected patients not receiving HAART, dilated cardiomyopathy was docu­mented by echocardiography in 17.7% of patients. Low socio-economic status, esti­mated duration of HIV-1 infection, CD4 count, HIV-1 viral load, CDC stage B and C of HIV disease and low plasmatic level of selenium were significant predictors of LV systolic dysfunction [24].

Cardiomyopathy could also be secondary to drug toxicity such as zidovudine, ampho­tericin B or foscarnet [25]. The exact mech­anism and pathogenesis of dilated car­diomyopathy in HIV patients is not unique. Nutritional disorders, direct effect of HIV on the heart, toxic effect of antiretroviral drugs, increased cytokine activity, oppor­tunistic infection, illicit drug abuse, autoim­mune reaction have been associated with dilated cardiomyopathy in HIV patients [21]. HAART has significantly decreased the incidence of dilated cardiomyopathy from 8.1 to 1.8% [8].