Myocardial deformation imaging unmasks subtle left ventricular systolic dysfunction in asymptomatic and treatment-naïve HIV patients
Background Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to stu...
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Published in | Clinical research in cardiology Vol. 104; no. 11; pp. 975 - 981 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.11.2015
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Background
Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients.
Methods
We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment.
Results
Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls,
p
= 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7,
p
= 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8,
p
= 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3,
p
= 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/−0.9 ± 0.3, 25.3 ± 1.7/−1.9 ± 0.2,
p
< 0.001), anterior (16.7 ± 3/−1.0 ± 0.1, 26.7 ± 1.7/−1.9 ± 0.2,
p
< 0.001), lateral (16.0 ± 6/−1.0 ± 0.1, 27.5 ± 1.8/−2.2 ± 0.3,
p
< 0.001) and posterior (15.2 ± 5.8/−1.0 ± 0.2, 26.2 ± 1.8/−2.2 ± 0.3,
p
< 0.001) left ventricular wall.
Conclusions
HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1861-0684 1861-0692 1861-0692 |
DOI: | 10.1007/s00392-015-0866-8 |