Background— Patients with HIV have increased risk for cardiovascular disease, but the underlying mechanisms remain unknown. The purpose of this study was to determine the prevalence of echocardiographic abnormalities among asymptomatic HIV-infected individuals compared with HIV-uninfected individuals. Methods/Results— We performed echocardiography in 196 HIV-infected adults and 52 controls. Left ventricular ejection fraction, left ventricular mass indexed to the body surface area, and diastolic function were assessed according to American Society of Echocardiography standards. Left ventricular mass index was higher in HIV-infected patients (77.2 g/m 2 in patients with HIV versus 66.5 g/m 2 in controls, P <0.0001). Left ventricular ejection fraction was similar in both groups. Eight (4%) of the patients with HIV had evidence of left ventricular systolic dysfunction (defined as an EF <50%) versus none of the controls; 97 (50%) had mild diastolic dysfunction compared with 29% of the HIV-uninfected subjects ( P =0.008). After adjustment for hypertension and race, HIV-infected participants had a mean 8 g/m 2 larger left ventricular mass index compared with controls ( P =0.001). Higher left ventricular mass index was independently associated with lower nadir CD4 T-cell count, suggesting that immunodeficiency may play a role in this process. After adjustment for age and traditional risk factors, patients with HIV had a 2.4 greater odds of having diastolic dysfunction as compared with controls ( P =0.019). Conclusions— HIV-infected patients had a higher prevalence of diastolic dysfunction and higher left ventricular mass index compared with controls. These differences were not readily explained by differences in traditional risk factors and were independently associated with HIV infection. These results suggest that contemporary asymptomatic patients with HIV manifest mild functional and morphological cardiac abnormalities, which are independently associated with HIV infection.

HIV-infected persons have a high prevalence of elevated PASP, which is independent of other risk factors for PAH. This suggests a causal role of HIV in PAH and emphasizes the need to understand the natural history of PAH in this setting. A role for HHV-8 infection in PAH remains much less definitive.

Objective-To evaluate the eVects of one year's treatment with beraprost, an orally active prostacyclin analogue, in patients with severe pulmonary hypertension. Patients-13 patients with severe pulmonary hypertension. This was primary in nine, thromboembolic in three, and caused by Eisenmenger syndrome in one. Methods-All patients underwent right heart catheterisation. Mean (SD) right atrial pressure was 5 (3) mm Hg, mean pulmonary artery pressure was 48 (12) mm Hg, cardiac index was 2.6 (0.8) l/min/m 2 , and mixed venous oxygen saturation was 68 (7)%. Beraprost was started at the dose of 20 µg three to four times a day (1 µg/kg/day), increasing after one month to 40 µg three to four times a day (2 µg/kg/day), with further increases of 20 µg three to four times a day in case of clinical deterioration. Main outcome measures-New York Heart Association (NYHA) functional class, exercise capacity measured by distance walked in six minutes, and systolic pulmonary pressure (by echocardiography) were evaluated at baseline, after one month's treatment, and then every three months for a year. Results-After the first month of treatment, NYHA class decreased from 3.4 (0.7) to 2.9 (0.7) (p < 0.05), the six minute walking distance increased from 213 (64) to 276 (101) m (p < 0.05), and systolic pulmonary artery pressure decreased from 93 (15) to 85 (18) mm Hg (NS). One patient died after 40 days from refractory right heart failure, and another was lost for follow up at six months. The 11 remaining patients had persistent improvements in functional class and exercise capacity and a significant decrease in systolic pulmonary artery pressure in the period from 1-12 months. Side eVects were minor. Conclusions-Oral administration of beraprost may result in long lasting clinical and haemodynamic improvements in patients with severe pulmonary hypertension. (Heart 2001;86:661-665)

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