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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