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Cardiac Magnetic Resonance Imaging with Pharmacological Stress Perfusion and Delayed Enhancement in Asymptomatic Patients with Systemic Sclerosis HITOMI KOBAYASHI, ISAMU YOKOE, MASAHARU HIRANO, TETSUYA NAKAMURA, YASUO NAKAJIMA, KEVIN R. FONTAINE, JON T. GILES, and YASUYUKI KOBAYASHI
ABSTRACT. Methods. Ten asymptomatic patients with SSc (all female; mean age 59.5 ± 9.4 yrs) underwent contrast enhanced cardiac MRI on a 1.5 T MRI device. Adenosine triphosphate was used for stress and rest perfusion to assess perfusion defects due to microvascular impairment or ischemia, and delayed enhanced (DE) imaging was obtained for the assessment of myocardial necrosis and fibrosis. We evaluated the pathophysiological associations of stress perfusion combined with DE imaging with SSc disease severity measures. Results. Stress perfusion defects were seen in 5 out of 9 patients (56%): 4 had nonsegmental subendocardial perfusion defects and one had a segmental subendocardial perfusion defect. Three patients were found to have DE. DE was not observed in any patient without perfusion defect; and among the 5 patients with perfusion defects, 3 (60%) had DE. Two of the 3 had DE in segments not matching the region of nonsegmental perfusion defects. The remaining one had a segmental subendocardial DE matching the region of a segmental perfusion defect. Perfusion defects were seen in 75% of patients with a history of digital ulceration compared to only 20% of those without history of ulceration. Conclusion. Subclinical myocardial involvement, as detected by cardiac MRI, was frequent in asymptomatic patients with SSc. Cardiac MRI may aid in understanding the pathophysiological mechanism of SSc. (J Rheumatol First Release Dec 1 2008; doi:10.3899/jrheum.080377) Key Indexing Terms:
CARDIAC MAGNETIC RESONANCE IMAGING
From the Division of Rheumatology and Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Division of Rheumatology, Itabashi Chuo Medical Center, Tokyo; Division of Cardiology, Tokyo Medical School of Medicine, Tokyo; Division of Cardiology, Itabashi Chuo Medical Center, Tokyo; and Division of Radiology, St. Marianna University School of Medicine, Kawasaki, Japan. H. Kobayashi, MD, PhD, Division of Rheumatology, Johns Hopkins University School of Medicine; I. Yokoe, MD, Division of Rheumatology, Itabashi Chuo Medical Center; M. Hirano, MD, Division of Cardiology, Tokyo Medical School of Medicine; T. Nakamura, MD, Division of Cardiology, Itabashi Chuo Medical Center; Y. Nakajima, MD, PhD, Division of Radiology, St. Marianna University School of Medicine; K.R. Fontaine, PhD; J.T. Giles, MD, Division of Rheumatology, Johns Hopkins University School of Medicine; Y. Kobayashi, MD, Division of Cardiology, Johns Hopkins University School of Medicine. Address reprint requests to Dr. H. Kobayashi, Division of Rheumatology, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, Suite 4100, Baltimore, MD 21224, USA. E-mail: hkobaya6@jhmi.edu Accepted for publication August 25, 2008.
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