Coronary microvascular dysfunction by quantitative stress myocardial perfusion CMR in systemic lupus erythematosus patients compared to healthy controls

Saturday, February 1, 2025

9:50 AM – 10:00 AM East Coast USA Time

Location: Blue Room

Presenting Author(s)

ST

Simon Thalén, MD, PhD

Post doctoral fellow
Karolinska Institutet

Primary Author(s)

ST

Simon Thalén, MD, PhD

Post doctoral fellow
Karolinska Institutet

Co-Author(s)

IS

Isak Samuelsson, MD

Phd candidate
Karolinska Institutet, Sweden
JN

Jannike Nickander, MD, PhD

MD, PhD
Karolinska Institutet, Sweden
RT

Raquel Themudo, MD, PhD

Post doctoral fellow
Karolinska Institutet, Sweden
RS

Rebecka Steffen Johansson, MD

MD, PhD student
Karolinska Institutet, Sweden
GG

Giorgia Grosso, MD, PhD

Post doctoral fellow
Karolinska Institutet, Sweden
Magnus Lundin, MD, PhD

Post doctoral fellow
Karolinska Institutet, Sweden
PS

Peder Sörensson, MD, PhD

Docent
Department of Medicine, Solna, Sweden
Henrik Engblom, MD, PhD

Professor, MD
Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden, Sweden
ES

Elisabet Svenungsson, MD, PhD

Professor
Karolinska Institutet, Sweden
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

Background: Systemic Lupus Erythematosus (SLE) is an autoimmune disease that affects multiple organs, including the heart. Although pericarditis is the most widely recognized cardiac manifestation of SLE, chronic inflammation and corticosteroid exposure can lead to accelerated development of coronary artery disease. This study aimed to assess quantitative stress myocardial perfusion in patients with SLE compared to healthy controls.

Methods: Female patients with SLE underwent in-line quantitative adenosine stress myocardial perfusion mapping cardiovascular magnetic resonance imaging (Qperf-CMR) at 3T. Healthy volunteers underwent Qperf-CMR only at either 1.5T or 3T.

Results: There was 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). Compared to age-matched female healthy controls (n=25, age 45±15 years), female patients with SLE (n=23, aged 47±10 years) had lower quantitative stress myocardial perfusion (2.5±0.6 vs 3.7±0.6 ml/min/g, p< 0.001, Figure 1).

Conclusion:

Patients with SLE show reduced stress myocardial perfusion consistent with some degree of coronary microvascular dysfunction. These findings support the use of quantitative stress myocardial perfusion CMR for assessment of coronary microvascular dysfunction in patients, potentially guiding targeted cardiovascular risk management.

Figure 1. Comparison of quantitative stress myocardial perfusion between controls and patients with SLE.