Abstract. Dilated cardiomyopathy of Doberman Pinschers (DCDP) is a progressive disease often presenting with a history of episodic weakness and syncope, or with clinical signs of predominantly left-sided congestive heart failure. A systematic dissection and histomorphologic evaluation of the heart from 32 Doberman Pinschers with a clinical diagnosis of dilated cardiomyopathy revealed a highly specific location for the characteristic myocardial lesions. The lesions of DCDP were found only in the left ventricular free wall, and in 30 cases, the lesions were characterized by myofiber degeneration and atrophy, and replacement of myocardium by dense bundles of collagen and clusters of adipocytes. In the two remaining hearts, myofiber atrophy and degeneration were accompanied by collagen deposition, but not adipocytes. In stained longitudinal (base to apex) tissue sections of the left ventricle, the lesions of DCDP were usually apparent to the unaided eye; appearing as a central linear pale zone, aligned in the long axis of the ventricular free wall. The lesions did not contain inflammatory cell infiltrates and often involved Ͼ50% of ventricular wall.
Objective
Fatigue is a common and disabling symptom amongst people with multiple sclerosis, however it has not been compared across the central nervous system (CNS) inflammatory diseases associated with aquaporin‐4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies (Ab). We explored the factors associated with fatigue within and across the two diseases, and compared fatigue levels between them.
Methods
We performed a cross‐sectional study of 90 AQP4‐Ab and 44 MOG‐Ab patients. Fatigue was assessed using the Modified Fatigue Impact Scale (MFIS). Clinical, demographic, and psychometric (anxiety, depression, pain) data were used as independent variables. Multivariable linear regression was used to identify significant independent variables associated with fatigue within and across the two diseases.
Results
Within AQP4‐Ab patients, age (P = 0.002), disease duration (P = 0.004), number of clinical attacks (P = 0.001), disability (P = 0.007), pain interference (P < 0.001), anxiety (P = 0.026), and depression (P < 0.001) were significant independent variables. Interestingly, disease duration had a negative association with fatigue (P = 0.004). Within MOG‐Ab patients, pain interference score (P < 0.001) and anxiety (P = 0.001) were significant independent variables. Although fatigue was worse in AQP4‐Ab patients compared to MOG‐Ab patients (P = 0.008) in all patients as well as in those who ever had transverse myelitis (P = 0.023), this was driven by the differences in age, disability and pain interference rather than antibody subtype itself.
Interpretation
Multiple factors, but not the antibody specificity, appear to contribute to fatigue in antibody positive CNS inflammatory diseases. A multifaceted treatment approach is needed to better manage the physical, cognitive, and psychosocial aspects of fatigue in these patients.
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