Quick Fire Session
SCMR 22nd Annual Scientific Sessions
Katia Menacho Medina, MD
Senior Cardiac Research Fellow
Institute of Cardiovascular Science - University College London
Sara Ramirez, MD
Imaging Cardiologist
Hospital Central FAP / Clinica Internacional - Sede San Borja
Liana Falcón, MD
Cardiac Imaging
Clínica Internacional. Lima .Peru
Jorge Alave, MD
Consultant Infectologist
Cayetano Heredia Hospital
Daniela Salazar, MD
Consultant Neumologist
Cayetano Heredia Hospital
Flavio Mosto, RT
Cardiac Specialist Technologist
International Clinic, Lima, Peru
Veronica Culotta, MD
Cardiac Research Fellow
Barts Heart Centre, St Bartholomew’s Hospital
Astrid Putri, MD
Researcher
University College London
Darwin Gonzales Zelada, RT
Cardiac Specialist Technologist
International Clinic, Lima, Peru
Julio Menacho Lopez, MD
Consultant Haematologist
Santiago Antunez de Mayolo University, Huaraz, Ancash
Malcolm Walker, MD
Clinical Director Consultant Cardiologist
University College Hospital London
James Moon, MD
Clinical Director, Imaging
Barts Heart Centre and UCL
Claudia Banda, MD
Consultant Infectologist
Cayetano Heredia Hospital and University
Fernando Mejia Cordero, MD
Consultant Infectologist
Cayetano Heredia Hospital and University
Background: Antiretroviral therapy (ART) in HIV reduces morbidity and mortality, but there is increased cardiovascular disease in survivors. The exact mechanism are unclear but appears related to the interaction of traditional risk factors, comorbidities, drugs and the virus causing changes in myocardial structure and function with myocardial oedema and fibrosis1. But research has been focused on treated HIV patients confounding full understanding. We explored early cardiac involvement in un-treated and treated HIV patients by deploying advanced CMR in the developed world (where untreated HIV remains prevalent).
Methods: A single centre cross-sectional study in Lima - Peru, 3T SIEMENS Prisma between 2016 – 2017. 62 participants: 26 patients with chronic HIV infection receiving ART, 25 HIV treatment naïve patients and 21 healthy controls selected by frequency matching age and sex. CD4 and viral load were measured. All patients were asymptomatic from a cardiac perspective. Myocardial structure, function and tissue characterization with native T1, T2, ECV and LGE assessed.
Results: Compared with healthy controls, HIV-infected patients had reduced left ventricular function (EF 61%±4 vs 65±3, P=0.02). Inflammation and diffuse fibrosis were higher: native T1 (1289±42 vs 1227±56, p=0.03); T2 (38.4±1.9 vs 36.5±1.6, p=0.02), figure 1. Pericardial effusions and the presence of LGE was three times more common. The LGE was predominantly sub and mid-epicardium, in the septal and inferolateral wall, figure 2. The LV EF reduction was present in both treated and untreated HIV patients (respectively 60.5%±5 vs 62±3, p=ns). Both had T1 and T2 elevation. Measured ECV correlated inversely with CD4 count (p=0.04), figure 3
Conclusion: Asymptomatic HIV patients have pericardial effusions, reduced LV function and subclinical myocardial inflammation with T1, T2, ECV elevation and LGE. Here we demonstrate this in both treated and untreated patients, and that the ECV correlated inversely with the CD4 count