Julian A Luetkens1, Jonas Doerner1, Carolynne Schwarze-Zander1, Jan-Christian Wasmuth1, Christoph Boesecke1, Alois M Sprinkart1, Frederic C Schmeel1, Rami Homsi1, Juergen Gieseke1, Hans H Schild1, Jürgen K Rockstroh1, Claas P Naehle2. 1. From the Department of Radiology (J.A.L., J.D., A.M.S., F.C.S., R.H., J.G., H.H.S., C.P.N.) and Department of Internal Medicine I (C.S.-Z., J.-C.W., C.B., J.K.R.), University of Bonn, Bonn, Germany; Department of Radiology, University Hospital Cologne, Germany (J.D.); and Philips Healthcare, Clinical Science, Hamburg, Germany (J.G.). 2. From the Department of Radiology (J.A.L., J.D., A.M.S., F.C.S., R.H., J.G., H.H.S., C.P.N.) and Department of Internal Medicine I (C.S.-Z., J.-C.W., C.B., J.K.R.), University of Bonn, Bonn, Germany; Department of Radiology, University Hospital Cologne, Germany (J.D.); and Philips Healthcare, Clinical Science, Hamburg, Germany (J.G.). cp@naehle.net.
Abstract
BACKGROUND: People living with chronic HIV infection are at an increased risk for cardiovascular disease. With this study, we aimed to determine the extent of cardiovascular involvement in asymptomatic HIV-infected patients by a comprehensive cardiac magnetic resonance (CMR) approach. METHODS AND RESULTS: Asymptomatic patients with chronic HIV infection undergoing combination antiretroviral therapy (n=28) and control subjects (n=22) underwent CMR. HIV-infected patients were successfully controlled for the disease with a consistent plasma viremia of <200 copies/mL (mean CD4(+)-cell count, 475.1±307.9 cells/μL). CMR protocol allowed for the determination of cardiac function, myocardial inflammation, myocardial fibrosis, aortic stiffness, and pericardial fat volume. When compared with healthy controls, HIV-infected patients showed alterations in left ventricular function as demonstrated by a lower ejection fraction (60.9±7.1% versus 65.2±5.5%; P=0.023) and lower global peak systolic longitudinal and circumferential strain values (longitudinal strain, -17.7±3.4% versus -20.2±3.2%, circumferential strain, -21.2±4.6% versus -24.7±5.1%; P<0.001, respectively). CMR parameters indicating myocardial inflammation were elevated in HIV-infected patients (native T1 relaxation times, 1128.3±53.4 ms versus 1086.5±54.5 ms; P=0.009; relative T2 signal intensity ratio, 1.6±0.3 versus 1.4±0.3; P=0.046; early gadolinium enhancement ratio, 3.1±1.2 versus 2.1±0.6; P=0.003). Myocardial fibrosis, predominantly at the subepicardium of the midventricular and basal inferolateral wall, was prevalent in 82.1% of HIV-infected patients, but only in 27.3% of healthy controls (P<0.001). CONCLUSIONS: Comprehensive CMR revealed a high burden of cardiovascular disease in asymptomatic HIV-infected patients. Subclinical myocardial inflammation as detected by CMR may be a potential precursor of the increased cardiovascular morbidity and mortality observed in patients with chronic HIV infection.
BACKGROUND:People living with chronic HIV infection are at an increased risk for cardiovascular disease. With this study, we aimed to determine the extent of cardiovascular involvement in asymptomatic HIV-infectedpatients by a comprehensive cardiac magnetic resonance (CMR) approach. METHODS AND RESULTS: Asymptomatic patients with chronic HIV infection undergoing combination antiretroviral therapy (n=28) and control subjects (n=22) underwent CMR. HIV-infectedpatients were successfully controlled for the disease with a consistent plasma viremia of <200 copies/mL (mean CD4(+)-cell count, 475.1±307.9 cells/μL). CMR protocol allowed for the determination of cardiac function, myocardial inflammation, myocardial fibrosis, aortic stiffness, and pericardial fat volume. When compared with healthy controls, HIV-infectedpatients showed alterations in left ventricular function as demonstrated by a lower ejection fraction (60.9±7.1% versus 65.2±5.5%; P=0.023) and lower global peak systolic longitudinal and circumferential strain values (longitudinal strain, -17.7±3.4% versus -20.2±3.2%, circumferential strain, -21.2±4.6% versus -24.7±5.1%; P<0.001, respectively). CMR parameters indicating myocardial inflammation were elevated in HIV-infectedpatients (native T1 relaxation times, 1128.3±53.4 ms versus 1086.5±54.5 ms; P=0.009; relative T2 signal intensity ratio, 1.6±0.3 versus 1.4±0.3; P=0.046; early gadolinium enhancement ratio, 3.1±1.2 versus 2.1±0.6; P=0.003). Myocardial fibrosis, predominantly at the subepicardium of the midventricular and basal inferolateral wall, was prevalent in 82.1% of HIV-infectedpatients, but only in 27.3% of healthy controls (P<0.001). CONCLUSIONS: Comprehensive CMR revealed a high burden of cardiovascular disease in asymptomatic HIV-infectedpatients. Subclinical myocardial inflammation as detected by CMR may be a potential precursor of the increased cardiovascular morbidity and mortality observed in patients with chronic HIV infection.
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