With a global prevalence of approximately 35.3 million people, human immunodeficiency virus (HIV) infection represents a major public health concern ¹. The introduction of antiretroviral therapy (ART) has distinctly reduced acquired immunodeficiency syndrome (AIDS)-related morbidity and mortality. However, due to the high prevalence of cardiovascular risk factors in HIV-infected patients and concurrent metabolic changes induced by ART, HIV-infected patients are at increased risk for cardiovascular disease ². In addition, chronic inflammatory processes can accelerate the development of atherosclerosis, eventually aggravating the incidence of cardiovascular disease in HIV-infected patients ³. Besides the association of HIV and atherosclerosis, a high prevalence of myocardial disease, especially dilated cardiomyopathy and myocarditis, has been reported frequently in the pre-ART era ⁴. The aim of this prospective study was therefore to investigate whether signs of cardiac involvement in HIV-infected patients without known cardiac disease receiving ART-therapy can be detected by the use of a comprehensive cardiovascular magnetic resonance (CMR) protocol.The institutional review committee approved this study and all subjects gave informed consent prior to CMR. This prospective study included subjects with HIV-infection undergoing ART-therapy and non-infected control subjects. HIV-infected patients were treated in accordance with national guidelines. All scans were performed on a 3 Tesla CMR system. CMR scans allowed for assessment of cardiac function (including global peak systolic longitudinal and circumferential strain values), myocardial inflammation and myocardial fibrosis. For functional analysis ECG-gated steady-state free precession cine images were obtained. Strain measurements were obtained using the feature tracking technique. In order to detect inflammatory changes of the myocardium T2 signal intensity ratio (T2-ratio), early gadolinium enhancement ratio (EGEr), and myocardial T1 relexation times were assessed. For myocardial T1 mapping a 3(3)3(3)5 MOLLI acquisition scheme was used. MOLLI sequences were performed in before as well as 10 and 20 minutes after contrast administration. The extracellular volume (ECV) was calculated from the T1 relexation times. For the assessment of myocardial fibrosis late gadolinium enhancement (LGE) imaging was performed. LGE images were analyzed using a qualitative and quantitative approach. Continuous variables were tested for normal contribution. The independent two-sample Student’s t-test (for normally distributed variables) or the Mann-Whitney U test (for not normally distributed variables) was used for comparison of continuous variables between two different groups. A P value <0.05 was considered indicative of a significant difference.A total of 50 subjects were included in this study (28 asymptomatic HIV-infected patients and 22 healthy controls). Mean age of HIV-infected patients was 49.0±9.3 years (range: 28–68). Mean age of healthy controls was 45.4±15.8 years (range: 20–71). Age (P=0.321), sex (P=0.084) and body mass index (P=0.672) did not differ significantly between both groups. 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). Left ventricular ejection fraction was significantly lower in HIV-infected patients when compared to healthy controls, but still within normal range (60.9±7.1% vs. 65.2±5.5%; P=0.023). Global peak systolic longitudinal and circumferential strain values were reduced in HIV-infected patients compared to healthy controls (longitudinal strain: -17.7±3.4% vs. -20.2±3.2%, circumferential strain: -21.2±4.6% vs. -24.7±5.1%; P=<0.001 respectively) (see Figure 1). T2-ratio (1.6±0.3 vs. 1.4±0.3; P=0.046) and EGEr (3.1±1.2 vs. 2.1±0.6; P=0.003) were elevated in HIV-infected subjects when compared to healthy controls (see Figure 1). Myocardial native T1 relaxation times were increased in HIV-infected patients when compared to healthy controls (1128.3±53.4ms vs. 1086.5±54.5ms; P=0.009) (see Figure 1 and 2). T1-derived ECV measures showed no differences between both groups at 10 minutes (27.4±4.1% vs. 26.5±3.7%; P=0.435) and 20 minutes (28.1±5.1% vs. 26.1±2.8%; P=0.123) after contrast injection. LGE imaging demonstrated that 23/28 (82.1%) of HIV-infected patients, but only 6/22 (27.3%) healthy controls had evidence of patchy or linear myocardial fibrosis on visual assessment (P<0.001). Enhanced areas were mostly visible at the subepicardium of the midventricular and basal inferolateral wall (in 64.3% of HIV-infected patients). This qualitative impression was confirmed in quantitative LGE analysis where enhanced areas were also more pronounced in HIV-infected patients (7.0±7.1% vs. 3.6±2.7%; P=0.043).In asymptomatic HIV-infected patients a comprehensive CMR approach revealed a high burden of subclinical cardiovascular disease, including structural and functional myocardial alterations. CMR parameters indicating myocardial inflammation were elevated in HIV-infected patients, which leads to the hypothesis that these findings are consistent with a subclinical myocardial inflammation in HIV-infected patients. Myocardial functional alteration might be a sequel of this higher inflammatory burden. Our findings therefore may help to explain the increased cardiac morbidity and mortality observed in patients with chronic HIV infection.