American Heart Journal
Volume 148, Issue 5 , Page e2, November 2004

Regarding: Right ventricular cardiac dysfunction in HIV-infected patients studied with radionuclide ventriculography

Department of Medical Pathophysiology, University of Rome “La Sapienza,” Viale Anicio Gallo 63, Rome, Italy

Article Outline

 

To the editor: I read with great interest the article by Lebech et al on the increased prevalence of right ventricular cardiac dysfuction in HIV-infected subjects by radionuclide ventrilography.1

The effects of highly active antiretroviral therapy (HAART) regimens on the clinical course of HIV-associated pulmonary hypertension are still being debated.The histopathology of HIV-associated pulmonary hypertension is similar to that of primary pulmonary hypertension.2 The most common alteration in HIV-associated pulmonary hypertension is the plexogenic pulmonary arteriopathy, while thrombotic pulmonary arteriopathy and pulmonary veno-occlusive disease are more rare histologic findings. This observation may suggest that similar etiopathogenetic mechanisms are at the basis of both HIV-associated pulmonary hypertension and primary pulmonary hypertension.2

A key role in HIV-associated pulmonary hypertension may be played by reservoir cells (interstitial cells, macrophages), which may hold HIV-1 on their surfaces for extended time periods and may chronically release cytotoxic cytokines (eg, TNF-α,IL-6,ET-1) thereby contributing to progressive tissue damage. HIV-1 may persist in alveolar macrophages, where it has been identified.3 These macrophages may release cytokines, oxide anions, and proteolytic enzymes in response to HIV infection, independently of HAART, determing vascular plexogenic lesions as consequence of reduced NO synthesis, proliferation and vasoconstriction of endothelial cells and proliferation and migration of smooth muscle cells.4 This may justify the increased prevalence of right ventricular dysfunction described by the authors in their study population independently of opportunistic infections, stage of HIV disease and HAART regimens.

However, a close collaboration between cardiologists and infectious disease specialists is warrented for an early detection and management of HIV-associated pulmonary hypertension because the prevalence of this condition is increasing in HIV-infected patients independently of HAART. Treatment with vasodilator agents such as PGI2 analogue (beraprost) or calcium-channel blockers may improve the adherence to a long-lasting antiretroviral therapy compared to continuous intravenous infusion of epoprostenol.2 The use of cGMP-specific phosphodiesterase inhibitors is promising, but long-term, controlled clinical trials are needed in this specific subset of patients.2

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References 

  1. Lebech AM, Gerstoft J, Hesse B, et al.  Right and left ventricular cardiac function in a developed world population with human immunodeficiency virus studied with radionuclide ventriculography. Am Heart J. 2004;147:482–488
  2. Pellicelli A, Barbaro G, Palmieri F, et al.  Primary pulmonary hypertension in HIV disease (a systematic review). Angiology. 2001;52:31–41
  3. Pellicelli AM, Palmieri F, D'Ambrosio C, et al.  Role of human immunodeficiency virus in primary pulmonary hypertension (case reports). Angiology. 1998;49:1005–1011
  4. Barbaro G. Pathogenesis of HIV-associated heart disease. AIDS. 2003;17:S12–20

PII: S0002-8703(04)00439-9

doi:10.1016/j.ahj.2004.06.016

American Heart Journal
Volume 148, Issue 5 , Page e2, November 2004

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