Intensity of inflammation as the most important predictor of myocardial involvement in JIA. A 3D echocardiographic study.
Authors
Antoine Fakhry AbdelMassih; Amr Salem; Salma Arabi; Lauris Malak; Huda Marzouk;
Introduction: Myocardial dysfunction is an important complication in the context of juvenile idiopathic arthritis (JIA). Several mechanisms might be involved in the induction of myocardial injury in such a disabling disease. Among several factors involved, myocardial inflammation and cardiotoxic drugs were thought to be the most incriminated factors. The aim of this paper was to determine the most important factors that implicated myocardial injury in JIA and to weigh whether the severity of inflammation varies significantly among the several subtypes or not.
Methods: Sixty JIA patients as well as sixty, age and surface area, matched controls were subjected to conventional Echocardiography, 3D Speckle tracking and the disease activity was measured as by Juvenile Arthritis Disease Score 27 (JADAS 27).
Results: JIA cases showed statistically significant systolic and diastolic dysfunction when compared to controls. Global longitudinal strain (GLS) (index of systolic function) was lower in cases compared to controls (JIA: 16.1±6.7 vs Controls: 23.9±1.4, P < 0.0001), Left Ventricular ratio of early diastolic mitral inflow velocity to average of early diastolic velocities of the mitral annulus and basal septum (LV E/E’) (index of diastolic function) was higher in cases compared to controls (JIA: 14.8±7 vs. Controls: 5.9±1.3). There was no statistically significant difference in echocardiographic parameters as well as JADAS 27 between subtypes of JIA patients. Multivariate analysis showed that the best predictor of both systolic and diastolic involvement of the myocardium in JIA patients was the severity of inflammation rather than the duration or the type of medications used.
Conclusion: This study points out the potential of inflammation as an important inducer of myocardial injury in JIA. It also underlines the fact that this inflammation does not differ significantly according to the disease subtype.
Antoine Fakhry AbdelMassih
Faculty of Medicine/Cairo University
Amr Salem
Faculty of Medicine/Cairo University
Salma Arabi
Faculty of Medicine/Cairo University
Lauris Malak
Faculty of Medicine/Cairo University
Huda Marzouk
Faculty of Medicine/Cairo University
Faculty of Medicine/Cairo University
Amr Salem
Faculty of Medicine/Cairo University
Salma Arabi
Faculty of Medicine/Cairo University
Lauris Malak
Faculty of Medicine/Cairo University
Huda Marzouk
Faculty of Medicine/Cairo University