Echocardiographic assessment of pulmonary arterial stiffness in human immunodeficiency virus-infected patients.


Journal

Echocardiography (Mount Kisco, N.Y.)
ISSN: 1540-8175
Titre abrégé: Echocardiography
Pays: United States
ID NLM: 8511187

Informations de publication

Date de publication:
Jun 2019
Historique:
received: 06 01 2019
accepted: 30 03 2019
pubmed: 1 5 2019
medline: 28 1 2020
entrez: 1 5 2019
Statut: ppublish

Résumé

Pulmonary hypertension (PH) is one of the complications of human immunodeficiency virus (HIV) infection. Despite the emergence of effective therapies, pulmonary arterial hypertension is commonly seen, especially at advanced stages. At the time of diagnosis, a majority of patients are at New York Heart Association-Functional Class III or IV. Many of the current screening modalities are dependent on detecting a rise in pulmonary arterial pressure (PAP). However, high capacitance of the pulmonary circulation implies that early microcirculation loss is not accompanied by a change in resting PAP. Therefore, we aimed to demonstrate early changes in pulmonary vascular disease in HIV-infected patients with a new echocardiographic parameter, called as pulmonary arterial stiffness (PAS). Thirty-six HIV-infected patients and 36 age- and sex-matched healthy control subjects were enrolled in this study. PAS was calculated echocardiographically by using maximal frequency shift and acceleration time of the pulmonary artery flow trace. There was no significant difference in diastolic functions, right ventricular diameters, systolic PAP, inferior vena cava widths, right atrial area, and tricuspid annular plane systolic excursion values between the two groups. However, PAS was calculated as 24.3 ± 6.4 Hz/msn in HIV-infected patients and 19.3 ± 3.1 Hz/msn in healthy control group (P < 0.001). Increase in PAS was correlated with duration of HIV infection (P < 0.05). Our results suggest that HIV infection affects pulmonary vascular bed starting early onset of disease and this can be demonstrated by an easy-to-measure echocardiographic parameter.

Sections du résumé

BACKGROUND BACKGROUND
Pulmonary hypertension (PH) is one of the complications of human immunodeficiency virus (HIV) infection. Despite the emergence of effective therapies, pulmonary arterial hypertension is commonly seen, especially at advanced stages. At the time of diagnosis, a majority of patients are at New York Heart Association-Functional Class III or IV. Many of the current screening modalities are dependent on detecting a rise in pulmonary arterial pressure (PAP). However, high capacitance of the pulmonary circulation implies that early microcirculation loss is not accompanied by a change in resting PAP. Therefore, we aimed to demonstrate early changes in pulmonary vascular disease in HIV-infected patients with a new echocardiographic parameter, called as pulmonary arterial stiffness (PAS).
METHODS AND RESULTS RESULTS
Thirty-six HIV-infected patients and 36 age- and sex-matched healthy control subjects were enrolled in this study. PAS was calculated echocardiographically by using maximal frequency shift and acceleration time of the pulmonary artery flow trace. There was no significant difference in diastolic functions, right ventricular diameters, systolic PAP, inferior vena cava widths, right atrial area, and tricuspid annular plane systolic excursion values between the two groups. However, PAS was calculated as 24.3 ± 6.4 Hz/msn in HIV-infected patients and 19.3 ± 3.1 Hz/msn in healthy control group (P < 0.001). Increase in PAS was correlated with duration of HIV infection (P < 0.05).
CONCLUSION CONCLUSIONS
Our results suggest that HIV infection affects pulmonary vascular bed starting early onset of disease and this can be demonstrated by an easy-to-measure echocardiographic parameter.

Identifiants

pubmed: 31038789
doi: 10.1111/echo.14349
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1123-1131

Informations de copyright

© 2019 Wiley Periodicals, Inc.

Auteurs

Idris Bugra Cerik (IB)

Department of Cardiology, Igdir State Hospital, Igdir, Turkey.

Murat Meric (M)

Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

Okan Gulel (O)

Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

Hatun Ozturk Cerik (H)

Department of Infectious Diseases and Clinical Microbiology, Igdir State Hospital, Igdir, Turkey.

Metin Coksevim (M)

Department of Cardiology, Bulancak State Hospital, Giresun, Turkey.

Korhan Soylu (K)

Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

Aydin Deveci (A)

Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

Mahmut Sahin (M)

Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

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