It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Aims
Anti‐mitochondrial antibody (AMA)‐positive myositis is frequently associated with various cardiac involvements, such as arrhythmia and left ventricular (LV) dysfunction. However, the efficacy of immunosuppressive therapy in these complications remains unknown. This study aimed to investigate the cardiac response to immunosuppressive therapy in patients with AMA‐positive myositis.
Methods and results
The clinical data of 15 AMA‐positive myositis patients with cardiac involvement were retrospectively collected at our centre. To evaluate the effects of immunosuppressive therapy, echocardiographic and laboratory data of patients who received glucocorticoid therapy with additional immunosuppressants (n = 6) and those who did not (n = 6) were compared. Also, the characteristics of patients with or without >5% LV ejection fraction (LVEF) decline during the follow‐up period (n = 5 vs. n = 7) were compared. Thirteen patients (87%) had arrhythmias, and eight patients (53%) had LV wall motion abnormalities. Although arrhythmias decreased after treatment, reduced LVEF and LV wall motion abnormalities persisted. Further investigation revealed an increased LV end‐systolic dimension and reduced LVEF in patients without additional immunosuppressive therapy, while those in patients with additional immunosuppressive therapy were maintained. Six of seven patients (86%) without LVEF decline received additional immunosuppressive therapy, whereas no patients with LVEF decline had additional immunosuppressive therapy.
Conclusions
Cardiac involvement in AMA‐positive myositis may worsen even with glucocorticoid monotherapy, and there might be some associations between the change of LV function and additional immunosuppressive therapy.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
; Maeda, Meiko Hashimoto 3 ; Ishida, Junichi 1 ; Hatano, Masaru 4 ; Ishizuka, Masato 1 ; Uehara, Masae 1 ; Oshima, Tsukasa 1 ; Kojima, Toshiya 1 ; Nakanishi, Koki 1 ; Daimon, Masao 1 ; Shimizu, Jun 5 ; Toda, Tatsushi 3 ; Komuro, Issei 1 1 Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
2 Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan, Department of Therapeutic Strategy for Heart Failure, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
3 Department of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
4 Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan, Advanced Medical Center for Heart Failure, University of Tokyo, Tokyo, Japan
5 Department of Physical Therapy, Tokyo University of Technology, Tokyo, Japan





