Ntobeko Ntusi1, Eoin O'Dwyer1, Lucy Dorrell1, Emma Wainwright1, Stefan Piechnik1, Genevieve Clutton1, Gemma Hancock1, Vanessa Ferreira1, Pete Cox1, Motasim Badri1, Theodoros Karamitsos1, Sam Emmanuel1, Kieran Clarke1, Stefan Neubauer1, Cameron Holloway2. 1. From the Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford Centre for Clinical Magnetic Resonance Research, Oxford, United Kingdom (N.N., S.P., V.F., T.K., S.N., C.H.); Division of Cardiology, Department of Medicine, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa (N.N., M.B.); Department of Cardiology, St.Vincent's Hospital, Darlinghurst, New South Wales, Australia (E.O., S.E., C.H.); Department of Medicine, University of New South Wales, Sydney, New South Wales, Australia (E.O., S.E., C.H.); Nuffield Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford and John Radcliffe Hospital, Oxford, United Kingdom (L.D., E.W., G.C., G.H.); Department of Physiology, Anatomy and Genetics (P.C., K.C., C.H.) and Oxford NIHR Biomedical Research Centre (S.N., C.H.), University of Oxford, Oxford, United Kingdom; and 1st Department of Cardiology, AHEPA Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece (T.K.). 2. From the Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford Centre for Clinical Magnetic Resonance Research, Oxford, United Kingdom (N.N., S.P., V.F., T.K., S.N., C.H.); Division of Cardiology, Department of Medicine, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa (N.N., M.B.); Department of Cardiology, St.Vincent's Hospital, Darlinghurst, New South Wales, Australia (E.O., S.E., C.H.); Department of Medicine, University of New South Wales, Sydney, New South Wales, Australia (E.O., S.E., C.H.); Nuffield Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford and John Radcliffe Hospital, Oxford, United Kingdom (L.D., E.W., G.C., G.H.); Department of Physiology, Anatomy and Genetics (P.C., K.C., C.H.) and Oxford NIHR Biomedical Research Centre (S.N., C.H.), University of Oxford, Oxford, United Kingdom; and 1st Department of Cardiology, AHEPA Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece (T.K.). cholloway@stvincents.com.au.
Abstract
BACKGROUND: Patients with treated HIV infection have clear survival benefits although with increased cardiac morbidity and mortality. Mechanisms of heart disease may be partly related to untreated chronic inflammation. Cardiovascular magnetic resonance imaging allows a comprehensive assessment of myocardial structure, function, and tissue characterization. We investigated, using cardiovascular magnetic resonance, subclinical inflammation and myocardial disease in asymptomatic HIV-infected individuals. METHODS AND RESULTS: Myocardial structure and function were assessed using cardiovascular magnetic resonance at 1.5-T in treated HIV-infected individuals without known cardiovascular disease (n=103; mean age, 45±10 years) compared with healthy controls (n=92; mean age, 44±10 years). Assessments included left ventricular volumes, ejection fraction, strain, regional systolic, diastolic function, native T1 mapping, edema, and gadolinium enhancement. Compared with controls, subjects with HIV infection had 6% lower left ventricular ejection fraction (P<0.001), 7% higher myocardial mass (P=0.02), 29% lower peak diastolic strain rate (P<0.001), 4% higher short-tau inversion recovery values (P=0.02), and higher native T1 values (969 versus 956 ms in controls; P=0.01). Pericardial effusions and myocardial fibrosis were 3 and 4× more common, respectively, in subjects with HIV infection (both P<0.001). CONCLUSIONS: Treated HIV infection is associated with changes in myocardial structure and function in addition to higher rates of subclinical myocardial edema and fibrosis and frequent pericardial effusions. Chronic systemic inflammation in HIV, which involves the myocardium and pericardium, may explain the high rate of myocardial fibrosis and increased cardiac dysfunction in people living with HIV.
BACKGROUND:Patients with treated HIV infection have clear survival benefits although with increased cardiac morbidity and mortality. Mechanisms of heart disease may be partly related to untreated chronic inflammation. Cardiovascular magnetic resonance imaging allows a comprehensive assessment of myocardial structure, function, and tissue characterization. We investigated, using cardiovascular magnetic resonance, subclinical inflammation and myocardial disease in asymptomatic HIV-infected individuals. METHODS AND RESULTS: Myocardial structure and function were assessed using cardiovascular magnetic resonance at 1.5-T in treated HIV-infected individuals without known cardiovascular disease (n=103; mean age, 45±10 years) compared with healthy controls (n=92; mean age, 44±10 years). Assessments included left ventricular volumes, ejection fraction, strain, regional systolic, diastolic function, native T1 mapping, edema, and gadolinium enhancement. Compared with controls, subjects with HIV infection had 6% lower left ventricular ejection fraction (P<0.001), 7% higher myocardial mass (P=0.02), 29% lower peak diastolic strain rate (P<0.001), 4% higher short-tau inversion recovery values (P=0.02), and higher native T1 values (969 versus 956 ms in controls; P=0.01). Pericardial effusions and myocardial fibrosis were 3 and 4× more common, respectively, in subjects with HIV infection (both P<0.001). CONCLUSIONS: Treated HIV infection is associated with changes in myocardial structure and function in addition to higher rates of subclinical myocardial edema and fibrosis and frequent pericardial effusions. Chronic systemic inflammation in HIV, which involves the myocardium and pericardium, may explain the high rate of myocardial fibrosis and increased cardiac dysfunction in people living with HIV.
Authors: James D Wilkinson; Paige L Williams; Wendy Yu; Steven D Colan; Armando Mendez; Justin P V Zachariah; Russell B Van Dyke; William T Shearer; Renee E Margossian; Steven E Lipshultz Journal: AIDS Date: 2018-06-19 Impact factor: 4.177
Authors: Javed Butler; Stephen J Greene; Svati H Shah; Sanjiv J Shah; Kevin J Anstrom; Raymond J Kim; Andreas P Kalogeropoulos; Eric J Velazquez; Adrian F Hernandez; Patrice Desvigne-Nickens; Rebecca Scherzer; Priscilla Y Hsue; Eugene Braunwald Journal: J Card Fail Date: 2019-11-02 Impact factor: 5.712
Authors: Nadine Kawel-Boehm; Scott J Hetzel; Bharath Ambale-Venkatesh; Gabriella Captur; Christopher J Francois; Michael Jerosch-Herold; Michael Salerno; Shawn D Teague; Emanuela Valsangiacomo-Buechel; Rob J van der Geest; David A Bluemke Journal: J Cardiovasc Magn Reson Date: 2020-12-14 Impact factor: 5.364
Authors: Javed Butler; Andreas P Kalogeropoulos; Kevin J Anstrom; Priscilla Y Hsue; Raymond J Kim; Rebecca Scherzer; Sanjiv J Shah; Svati H Shah; Eric J Velazquez; Adrian F Hernandez; Patrice Desvigne-Nickens; Eugene Braunwald Journal: J Card Fail Date: 2018-03-02 Impact factor: 5.712