Hanne A Aulie1, Mette E Estensen2, Anne M Selvaag2, Vibke Lilleby2, Klaus Murbraech2, Berit Flatø2, Svend Aakhus2. 1. From the Department of Rheumatology, and Department of Cardiology, Oslo University Hospital, Rikshospitalet; Institute for Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway.H.A. Aulie, MD, Department of Rheumatology; M.E. Estensen, MD, PhD, Department of Cardiology; A.M. Selvaag, MD, PhD, Department of Rheumatology; V. Lilleby, MD, PhD, Department of Rheumatology; K. Murbraech, MD, Department of Cardiology, Oslo University Hospital, Rikshospitalet; B. Flatø, MD, PhD, Department of Rheumatology, Oslo University Hospital, Rikshospitalet, and Institute for Clinical Medicine, Medical Faculty, University of Oslo; S. Aakhus, MD, PhD, Department of Cardiology, Oslo University Hospital, Rikshospitalet. hanaul@ous-hf.no. 2. From the Department of Rheumatology, and Department of Cardiology, Oslo University Hospital, Rikshospitalet; Institute for Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway.H.A. Aulie, MD, Department of Rheumatology; M.E. Estensen, MD, PhD, Department of Cardiology; A.M. Selvaag, MD, PhD, Department of Rheumatology; V. Lilleby, MD, PhD, Department of Rheumatology; K. Murbraech, MD, Department of Cardiology, Oslo University Hospital, Rikshospitalet; B. Flatø, MD, PhD, Department of Rheumatology, Oslo University Hospital, Rikshospitalet, and Institute for Clinical Medicine, Medical Faculty, University of Oslo; S. Aakhus, MD, PhD, Department of Cardiology, Oslo University Hospital, Rikshospitalet.
Abstract
OBJECTIVE: To compare cardiac function in adults with longterm juvenile idiopathic arthritis (JIA) with that of healthy controls, and to investigate the influence of inflammation, disease severity, and use of antirheumatic medication on cardiac function. METHODS: Eighty-five patients with JIA (median age 38.6 yrs) with active disease for at least 15 years were reexamined at a median of 29 years after disease onset and compared with 46 matched controls. Echocardiography, including tissue Doppler imaging and longitudinal peak-systolic global strain, was used to assess diastolic and systolic myocardial function, and 12-channel electrocardiography was performed. RESULTS: The interventricular septum was thicker in patients than controls (mean ± SD 0.8 ± 0.2 cm vs 0.7 ± 0.1 cm, p = 0.036). Diastolic function in patients was altered compared with controls characterized by lower mitral E wave deceleration time (165 ± 36 ms vs 180 ± 40 ms, p = 0.029), higher surrogate marker of left ventricular (LV) filling pressure (median lateral E/e' 5.3, interquartile range 4.6-6.3 vs 4.8, 3.9-5.7, p = 0.036), and larger left atrial area (16.4 ± 2.9 cm(2) vs 15.1 ± 2.8 cm(2), p = 0.015). Systolic and diastolic blood pressures were higher in patients (120 ± 15 mmHg vs 114 ± 9 mmHg, p = 0.021 and 76 ± 10 mmHg vs 71 ± 8 mmHg, p = 0.009, respectively). QT corrected interval was similar in patients and controls. High high-sensitivity C-reactive protein (CRP), polyarticular disease course, and extended joint affection at 29-year followup, as well as duration of active disease, cumulative erythrocyte sedimentation rate, and CRP, and prednisolone use were associated with higher lateral E/e'. CONCLUSION: Adult patients with JIA did not differ from controls in LV systolic function, but had mildly thicker interventricular septum and indications for higher LV filling pressure, and most in patients with a higher disease burden.
OBJECTIVE: To compare cardiac function in adults with longterm juvenile idiopathic arthritis (JIA) with that of healthy controls, and to investigate the influence of inflammation, disease severity, and use of antirheumatic medication on cardiac function. METHODS: Eighty-five patients with JIA (median age 38.6 yrs) with active disease for at least 15 years were reexamined at a median of 29 years after disease onset and compared with 46 matched controls. Echocardiography, including tissue Doppler imaging and longitudinal peak-systolic global strain, was used to assess diastolic and systolic myocardial function, and 12-channel electrocardiography was performed. RESULTS: The interventricular septum was thicker in patients than controls (mean ± SD 0.8 ± 0.2 cm vs 0.7 ± 0.1 cm, p = 0.036). Diastolic function in patients was altered compared with controls characterized by lower mitral E wave deceleration time (165 ± 36 ms vs 180 ± 40 ms, p = 0.029), higher surrogate marker of left ventricular (LV) filling pressure (median lateral E/e' 5.3, interquartile range 4.6-6.3 vs 4.8, 3.9-5.7, p = 0.036), and larger left atrial area (16.4 ± 2.9 cm(2) vs 15.1 ± 2.8 cm(2), p = 0.015). Systolic and diastolic blood pressures were higher in patients (120 ± 15 mmHg vs 114 ± 9 mmHg, p = 0.021 and 76 ± 10 mmHg vs 71 ± 8 mmHg, p = 0.009, respectively). QT corrected interval was similar in patients and controls. High high-sensitivity C-reactive protein (CRP), polyarticular disease course, and extended joint affection at 29-year followup, as well as duration of active disease, cumulative erythrocyte sedimentation rate, and CRP, and prednisolone use were associated with higher lateral E/e'. CONCLUSION: Adult patients with JIA did not differ from controls in LV systolic function, but had mildly thicker interventricular septum and indications for higher LV filling pressure, and most in patients with a higher disease burden.