Rapid Fire Abstracts
Csenge E. Fogarasi, MD
PhD student
Karolinska Institutet, Sweden
Csenge E. Fogarasi, MD
PhD student
Karolinska Institutet, Sweden
David Makari, N/A
Medical student
Karolinska Institutet, Sweden
Fabricio Espinosa-Ortega, MD, PhD
Physician Scientist
Karolinska Institutet and Karolinska University Hospital, Sweden
Simon Thalén, MD, PhD
Physician Scientist, Postdoctoral Researcher
Karolinska Institutet and Karolinska University Hospital, Sweden
Ingrid Lundberg, MD, PhD
Professor
Karolinska Institutet and Karolinska University Hospital, Sweden
Daniel F. Andersson, MD
PhD-student, junior physician
Department of Molecular Medicine and Surgery, Sweden
Jonas Faxén, MD, PhD
Physician Scientist
Karolinska Institutet and Karolinska University Hospital, Sweden
Louise E. Ekholm, MD, PhD
Physician Scientist
Karolinska Institutet and Karolinska University Hospital, Sweden
Peder Sörensson, MD, PhD
Associate professor
Karolinska Institute, Sweden
Peter Kellman, PhD
Director of the Medical Signal and Image Processing Program
National Heart, Lung, and Blood Institute, National Institutes of Health
.jpg "Martin Ugander, MD, PhD photo")
Martin Ugander, MD, PhD
Professor of Cardiac Imaging
Kolling Institute, Royal North Shore Hospital and University of Sydney/ Karolinska University Hospital and Karolinska Institutet, Australia
Maryam Dastmalchi, MD, PhD
Physician Scientist
Karolinska Institutet, Sweden
Jannike Nickander, MD, PhD
MD, PhD
Karolinska Institutet, Sweden
Idiopathic inflammatory myopathies (IIM) are systemic inflammatory diseases with diverse clinical presentations, often summarized as myositis. Patients with myositis have elevated mortality risk ( >3.5-fold overall), with the greatest risk occurring in the first year after diagnosis (9-fold), compared to the general population. Cardiovascular (CV) disease are common and major drivers for excess mortality in myositis patients.1 While systemic inflammation is likely to play a key role in the development of CV disease in myositis patients, its direct impact on myocardial tissue remains unclear. Therefore, this study aimed to elucidate inflammatory effects on the myocardium using cardiovascular magnetic resonance quantitative perfusion imaging.
Methods:
Newly diagnosed patients with myositis, between February 2018 and October 2020 who were over 18 years old were prospectively enrolled. Patients were matched with healthy, sex- and age-matched controls, on a case-by-case basis. Patients underwent first-pass perfusion imaging with adenosine stress at 3T, while controls at 1.5T. Native T1 maps were acquired with modified Look-Locker inversion recovery (MOLLI) in three short-axis slices, and post-contrast to produce extracellular volume maps (ECV), calibrated by hematocrit. One native T1 map and three perfusion maps were acquired during adenosine stress (140 µg/kg/min or in inadequate stress response increased to 210 µg/kg/min). Mean native T1, ECV and perfusion values were acquired by delineating endo- and epicardial borders using the software Segment (Medviso AB, Lund, Sweden). Segments with suspected ischemia were excluded.
Results:
Previous in-house data show no difference in quantitative stress myocardial perfusion between healthy controls at 1.5T and 3T (n=55, 3.6±0.7 vs n=23, 3.6±0.7 ml/min/g, p=0.86). Patients with myositis (n=14, mean age 49±15 years, 64 % female) had reduced stress perfusion (3.2±0.7 vs 4.0±0.9 ml/g/min, p=0.016, Figures 1. and 2.), myocardial perfusion reserve (MPR) (median: 2.8 [2.2-3.4] vs 4.3 [2.6-5.1] ml/min/g, p=0.04) and native T1 reactivity (3.5±2.5 vs 5.9±2.2 %, p=0.01) compared to controls. These differences persisted in the endocardial and epicardial perfusion (endocardial: 3.0±0.7 vs 3.8±0.9 ml/min/g, p=0.02 and epicardial: 3.3±0.7 vs 4.1±0.9 ml/min/g, p=0.01). However, there was no difference in the stress endo-to-epicardial ratio, rest perfusion or ECV (p >0.05 for all).
Conclusion: Patients with myositis in the inflammatory phase have reduced stress perfusion, MPR and native T1 reactivity as a sign of inflammatory-induced microvascular dysfunction. The reduced stress perfusion is global, affecting the endo- and epicardial layers equally, thus shedding light on pathophysiological mechanisms in inflammatory associated CV disease.
