QTc interval prolungation in systemic sclerosis: correlations with clinical variables

Among the abnormalities in SSc, QTc interval prolongation has been reported and associated with anti-RNA polymerase III antibodies, longer disease duration, and greater disease severity [4]. Accordingly, the aimof the study is to assess QTc prolongation in SSc and evaluate correlations with clinical variables and complications of the disease. Twenty scleroderma patients were enrolled in the current study. The epidemiological and clinical features of SSc are shown in Table 1.The median value of QTc is significantly (p b 0.0001) increased in SSc patients than healthy controls [447 (414–566) vs 386 (342–447)]. The median value of QTc is significantly (p b 0.01) different in three capillaroscopic groups: early 425 (421–454), active 437 (416–467), late 471 (445–566). The median value of QTc is significantly (p b 0.05) augmented in SSc patients with digital ulcers than in SSc patients without digital ulcers [459 (422–566) vs 436 (416–454)]. A positive correlation (p b 0.05) exists between QTc and mRSS (r = 0.53). The onset of skin lesions in SSc is largely related to vascular insufficiency and in our study QTc interval prolongation shows a linear correlation between clinical variables secondary to vascular and fibrosis complications as shown by a NVC pattern, onset of digital ulcers and skin thickening. Also, it is important to remark that QTc prolongation was found in SSc patients without clinical cardiac involvement and in the absence of echographic abnormality. QTc interval measured by 24-hour Holter ECG recording provides a more complete evaluation than standard ECG. QTc interval prolongation, with the concomitant autonomic dysfunction, suggests that SSc patients especially with specific features as late capillaroscopic pattern, presence of digitals ulcers, and skin thickening may have a particularly high risk of developing lifethreatening arrhythmias. We demonstrate that also left ventricular mass correlates with digital microvascular damage [10]. Finally, we can suppose that microvascular damage is present early in myocardium of SSc patients and it may be the pathogenic mechanism of autonomic dysfunction and arrhythmias.