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Conclusion

Pulmonary hypertension associated with HIV infection is a cardiovascular complica­tion that has been recognized with increas­ing frequency in the last few years. The eti­ology of HIV-associated pulmonary hyper­tension is unknown.

At present, a multifac­torial pathogenesis of HIV-associated pul­monary hypertension has been hypothesi­zed. In this clinical condition, the endothelial

Fig. 6 a-d Transthoracic echocardiographic findings in HIV-associated pulmonary hypertension. It is pos­sible to observe a systolic flattening of the interventricular septum and right atrial (RA) and right ven­tricular enlargement (RV). LV, left ventricle. (From [28], with permission from Wiley-Blackwell)

Fig. 7 Transthoracic echocardiographic findings in HIV-associated pulmonary hypertension. A systolic flattening of the interventricular septum and right atrial (RA) and right ventricular enlargement can be observed (RV). LV, left ventricle; LA, left atrial

Fig. 8 Transthoracic echocardiographic findings in HIV-associated pulmonary hypertension. A signif­icant tricuspid regurgitation is observed

Fig. 9 a-d Transthoracic echocardiographic findings in HIV-associated pulmonary hypertension. The pul­monary arterial systolic pressure can be estimated by measuring the Doppler flow through the tricuspid valve according to Bernulli’s modified formula: P=4V2 (where P is pressure gradient and V is peak retro­grade velocity). The right atrial pressure (PRA) is nominally estimated at 10 mmHg.

LV, left ventricle; LA, left atrium

Fig. 10 Pulmonary angiography in a patient with HIV-associated pulmonary hypertension. It is possible to observe a “pruning” aspect with enlargement of the left pulmonary artery and decrease in peripheral vessels

dysfunction, the deregulation of circulat­ing cytokines, and genetic factors seem to be implicated in the pathogenesis of this disease. In particular, as in primary pul­monary hypertension, an increase in the plasma concentrations of ET-1, IL-6, and TNF-α has been found in patients with HIV-associated pulmonary hypertension. The role of antiretroviral therapy is still being debated. Vasodilator agents such as prostaglandin I2 analog (beraprost), and ET-1 receptor antagonists such as bosen- tan, seem to be interesting therapeutic alternatives in the treatment of HIV-associ­ated pulmonary hypertension compared to continuous intravenous infusion of epoprostenol. The use of cGMP-specific phosphodiesterase inhibitors such as silde­nafil, is promising, but long-term con­trolled clinical trials are needed in this specific subset of patients.

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Source: Barbaro Giuseppe, Boccara Franc (eds.). Cardiovascular Disease in AIDS. 2nd edition. — Springer,2009. — 169 p.. 2009
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