BACKGROUND: Churg-Strauss syndrome (CSS) is a rare, systemic necrotising small and middle-sized vessel vasculitis, accompanied by blood eosinophilia, eosinophil infiltration of various tissues and bronchial asthma. Cardiac injury caused by myocardial eosinophilic infiltration and/or vasculitis in CSS seems to be very common. Active inflammatory process accompanied by myocardial fibrosis has been described in this population even despite disease remission. Nevertheless, little is known about the possible myocardial repolarisation abnormalities in CSS which may lead to life-threatening ventricular arrhythmias. AIM: To evaluate myocardial repolarisation in CSS patients at the time of initial diagnosis and during the last disease remission. METHODS: In 20 CSS patients (8 male, 12 female) QT dispersion (QTd) and QTc dispersion (QTcd) calculated from heart rate corrected QT (QTc) from the surface 12-lead electrocardiograms were measured at the time of initial diagnosis and during the last disease remission. As a control group, 20 sex- and age-matched healthy volunteers were studied. Transthoracic echocardiography was performed in all CSS patients at remission and in the control group. RESULTS: QTcd was higher in CSS (n = 20) than in healthy controls (n = 20) in each period of time: at the time of initial diagnosis (45.4 ± 14.2 vs 26.1 ± 6.5, p < 0.0001) and at the remission (38.6 ± 13.4 vs 26.1 ± 6.5, p = 0.002). At the time of initial diagnosis in CSS patients with heart involvement (n = 13), when compared to patients without heart involvement, (n = 7), both QTcd (52.2 ± 12.1 vs 34.7 ± 10.7, p = 0.007) and QTd (37.7 ± 12.7 vs 24 ± 11.4, p = 0.008) were higher, and this difference remained significant at remission only for QTcd (46.7 ± 13.2 vs 33.1 ± 10.8, p = 0.03). No significant correlation was observed between QTcd/QTd and disease activity (measured using the Birmingham Vasculitis Activity Score - BVAS), eosinophil blood count, presence of ANCA, nor the duration of the disease. CONCLUSIONS: The most pronounced increased QTcd was detected in the CSS patients with cardiac involvement at the time of initial diagnosis and remained higher at remission in all CSS patients when compared to healthy controls. Nevertheless, in the CSS patients, QTcd remains within the normal ranges, which may explain the relatively small number of ventricular arrhythmias in these patients.
BACKGROUND:Churg-Strauss syndrome (CSS) is a rare, systemic necrotising small and middle-sized vessel vasculitis, accompanied by blood eosinophilia, eosinophil infiltration of various tissues and bronchial asthma. Cardiac injury caused by myocardial eosinophilic infiltration and/or vasculitis in CSS seems to be very common. Active inflammatory process accompanied by myocardial fibrosis has been described in this population even despite disease remission. Nevertheless, little is known about the possible myocardial repolarisation abnormalities in CSS which may lead to life-threatening ventricular arrhythmias. AIM: To evaluate myocardial repolarisation in CSS patients at the time of initial diagnosis and during the last disease remission. METHODS: In 20 CSS patients (8 male, 12 female) QT dispersion (QTd) and QTc dispersion (QTcd) calculated from heart rate corrected QT (QTc) from the surface 12-lead electrocardiograms were measured at the time of initial diagnosis and during the last disease remission. As a control group, 20 sex- and age-matched healthy volunteers were studied. Transthoracic echocardiography was performed in all CSS patients at remission and in the control group. RESULTS:QTcd was higher in CSS (n = 20) than in healthy controls (n = 20) in each period of time: at the time of initial diagnosis (45.4 ± 14.2 vs 26.1 ± 6.5, p < 0.0001) and at the remission (38.6 ± 13.4 vs 26.1 ± 6.5, p = 0.002). At the time of initial diagnosis in CSS patients with heart involvement (n = 13), when compared to patients without heart involvement, (n = 7), both QTcd (52.2 ± 12.1 vs 34.7 ± 10.7, p = 0.007) and QTd (37.7 ± 12.7 vs 24 ± 11.4, p = 0.008) were higher, and this difference remained significant at remission only for QTcd (46.7 ± 13.2 vs 33.1 ± 10.8, p = 0.03). No significant correlation was observed between QTcd/QTd and disease activity (measured using the Birmingham Vasculitis Activity Score - BVAS), eosinophil blood count, presence of ANCA, nor the duration of the disease. CONCLUSIONS: The most pronounced increased QTcd was detected in the CSS patients with cardiac involvement at the time of initial diagnosis and remained higher at remission in all CSS patients when compared to healthy controls. Nevertheless, in the CSS patients, QTcd remains within the normal ranges, which may explain the relatively small number of ventricular arrhythmias in these patients.