In this study, investigators plan to test two potential mechanisms contributing to diastolic dysfunction among asymptomatic persons with HIV who are on cART. The first proposed mechanism is that heightened systemic immune activation/inflammation in HIV contributes to myocardial inflammation, which in turn promotes myocardial fibrosis. The second mechanism is that ectopic fat deposition (increased visceral adiposity) in HIV relates to increased intramyocardial lipid content, which in turn contributes to diastolic dysfunction. Both HIV positive and HIV-negative participants will undergo cardiac MRI/ MRS imaging studies for evaluation of myocardial fibrosis, myocardial inflammation, and intramyocardial lipid content. Traditional markers of CVD risk, inflammatory markers/immune, hormonal markers, and markers of myocardial stretch/injury will be assessed in relation to cardiac MRI/MRS outcomes. Additionally, a small subset of participants with HIV will undergo longitudinal evaluations to assess effects of a clinically prescribed hormonal therapy on myocardial structure and function.
Study Type
OBSERVATIONAL
Enrollment
48
Massachusetts General Hospital
Boston, Massachusetts, United States
Extracellular Volume (ECV), a measure of myocardial fibrosis on Cardiac MRI
Time frame: 3 weeks
Myocardial Inflammation on Cardiac MRI
Time frame: 3 weeks
Intramyocardial fat on Cardiac MRI/MRS
Time frame: 3 weeks
Diastolic function on Cardiac MRI
Time frame: 3 weeks
Visceral Adiposity on MRI
Time frame: 3 weeks
Inflammation/ immune markers
Time frame: 3 weeks
Hormonal markers
Time frame: 3 weeks
Markers of myocardial stretch
Time frame: 3 weeks
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.