Subclinical myocyte injury, fibrosis and strain in relationship to coronary plaque in asymptomatic HIV-infected individuals.
Cardiovascular disease (CVD) rates are increased in HIV. The degree to which myocyte injury, strain, and fibrosis occur prior to clinical disease and relate to coronary plaque in HIV is unknown.



To investigate newer cardiac biomarkers of subclinical myocyte injury [high-sensitivity troponin T (hs-cTnT)], strain (amino terminal proB-type natriutretic peptide), fibrosis (soluble ST2, Galectin-3), and vascular inflammation (oxidized LDL, lipoprotein-associated phospholipase A2) in HIV-infected individuals and non-HIV controls and relate these to coronary plaque by cardiac computed tomography angiography.



Observational.



Markers were investigated in 155 HIV-infected and 70 non-HIV-infected participants without known CVD and with low traditional CVD risk and related to cardiac computed tomography angiography data.



Age, sex, and race did not differ between the groups. Hs-cTnT [3.1 (3.0, 6.4) vs. 3.0 (3.0, 4.0) ng/l, P = 0.03], Galectin-3 [13.5 (10.6, 18.1) vs. 11.6 (9.9, 14.5) ng/ml, P = 0.002], and soluble ST2 [31.5 (24.5, 41.5) vs. 28.3 (20.2, 33.5) ng/ml, P = 0.01] were significantly higher in HIV-infected participants vs.



Detectable hs-cTnT (seen in 50% of HIV participants) related to the overall presence of plaque [odds ratio (OR) 2.3, P = 0.01] and particularly to coronary calcium (OR for Agatston calcium score > 0, 3.3, P = 0.0008 and OR for calcified plaque 7.4, P = 0.01) in HIV, but not in non-HIV.



Subclinical myocyte injury is observed among young, asymptomatic HIV-infected individuals with low traditional cardiac risk factors. In the setting of HIV infection, the presence of detectable cardiac troponin is strongly associated with coronary plaque, particularly calcified plaque among an asymptomatic group. Future studies are needed to assess if early subclinical injury marked by hs-cTnT predicts plaque progression and cardiac events in HIV.
aProgram in Nutritional Metabolism, Mass General Hospital and Harvard Medical School, Boston, Massachusetts bCardiology Division, Inova Health System, Falls Church, Virginia cDepartment of Pathology, University of Maryland School of Medicine, Baltimore, Maryland dMGH Biostatistics Center eCardiac MR PET CT Program, Department of Radiology, Mass General Hospital and Harvard Medical School, Boston, Massachusetts, USA. *Kathleen V. Fitch and Christopher DeFilippi contributed equally to the article.
Kathleen V
KV
Fitch
Christopher
C
DeFilippi
Robert
R
Christenson
Suman
S
Srinivasa
Hang
H
Lee
Janet
J
Lo
Michael T
MT
Lu
Kimberly
K
Wong
Eva
E
Petrow
Laura
L
Sanchez
Sara E
SE
Looby
Udo
U
Hoffmann
Markella
M
Zanni
Steven K
SK
Grinspoon
D000293:Adolescent; D000328:Adult; D000792:Angiography; D058070:Asymptomatic Diseases; D015415:Biomarkers / Q000097:blood*; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000473:pathology*; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology*; D032342:Muscle Cells; D058226:Plaque, Atherosclerotic / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000473:pathology; D014056:Tomography, X-Ray; D014947:Wounds and Injuries; D055815:Young Adult
D015415:Biomarkers