Myocardial and microvascular inflammation/infection in patients with HIV-associated pulmonary artery hypertension

Andrea Frustaci, Nicola Petrosillo, Dario Vizza, Marco Francone, Roberto Badagliacca, Romina Verardo, Francesco Fedele, Giuseppe Ippolito, Cristina Chimenti

Research output: Contribution to journalArticlepeer-review


Background: Right ventricle compromise affects survival of patients with HIV-associated pulmonary artery hypertension (PAH).

Design: Myocardial histology with viral assessment may clarify the mechanism of right ventricular deterioration and provide clues on PAH origin.

Methods: Fifteen patients with HIV infection, PAH and right ventricular dysfunction underwent cardiac magnetic resonance, catheterization, coronary with ventricular angiography and biventricular endomyocardial biopsy. Endothelial expression of HLA-DR, ICAM-1, E-selectin and VCAM-1 was semi-quantitatively evaluated. PCR for HIV, hepatitis C virus, human herpes virus-6, human herpes virus-8, Epstein-Barr virus, adenovirus, cytomegalovirus, enterovirus, influenza A/B and parvovirus B19 was performed. In PCR-positive hearts, viral protein adenovirus-1 and TORDJI-22 were assessed by immunohistology.

Results: New York Heart Association class was 2.4±0.5, mean pulmonary artery pressure 49.93±10.15mmHg and wedge pressure 9.5±2.19mmHg. Coronaries were normal with slow flow. Left ventricular and/or right ventricular micro-aneurysms were seen in eight patients. Cardiac magnetic resonance documented increased right ventricular end-diastolic volume with reduced ejection fraction, normal left ventricular end-diastolic volume and left ventricular ejection fraction. Subepicardial/mesocardial oedema and delayed enhancement in the inter-ventricular junction and/or left ventricular inferolateral wall was detected in eight patients. Histology showed active lymphocytic myocarditis in 12 patients, with microvasculitis in three. Endothelial adhesion molecules were over-expressed in all patients. PCR was positive in four patients for hepatitis C virus and in two for adenovirus, and viruses localized both in cardiomyocytes and endothelial cells.

Conclusions: Inflammation/infection of myocardium and intramural vessels is detectable in patients with HIV-associated PAH. It may adversely affect right ventricular function and have a role in the compromised pulmonary circulation.

Original languageEnglish
Pages (from-to)2541-2549
Number of pages9
JournalAIDS (London, England)
Issue number17
Publication statusPublished - 2014


  • HIV
  • Myocarditis
  • Pulmonary artery hypertension
  • Viruses

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases
  • Medicine(all)


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