TY - JOUR T1 - Systemic inflammation as a novel QT-prolonging risk factor in patients with torsades de pointes JF - Heart JO - Heart SP - 1821 LP - 1829 DO - 10.1136/heartjnl-2016-311079 VL - 103 IS - 22 AU - Pietro Enea Lazzerini AU - Franco Laghi-Pasini AU - Iacopo Bertolozzi AU - Gabriella Morozzi AU - Sauro Lorenzini AU - Antonella Simpatico AU - Enrico Selvi AU - Maria Romana Bacarelli AU - Francesco Finizola AU - Francesca Vanni AU - Deana Lazaro AU - Ademuyiwa Aromolaran AU - Nabil El Sherif AU - Mohamed Boutjdir AU - Pier Leopoldo Capecchi Y1 - 2017/11/01 UR - http://heart.bmj.com/content/103/22/1821.abstract N2 - Objective Increasing evidence indicates systemic inflammation as a new potential cause of acquired long QT syndrome (LQTS), via cytokine-mediated changes in cardiomyocyte ion channels. Torsade de pointes (TdP) is a life-threatening polymorphic ventricular tachycardia occurring in patients with LQTS, usually when multiple QT-prolonging factors are simultaneously present. Since classical risk factors cannot fully explain TdP events in a number of patients, we hypothesised that systemic inflammation may represent a currently overlooked risk factor contributing to TdP development in the general population.Methods Forty consecutive patients who experienced TdP (TdP cohort) were consecutively enrolled and circulating levels of C-reactive protein (CRP) and proinflammatory cytokines (interleukin-6 (IL-6), tumour necrosis factor alpha (TNFα), interleukin-1 (IL-1)) were compared with patients with active rheumatoid arthritis (RA), comorbidity or healthy controls. An additional 46 patients with different inflammatory conditions (acute infections, n=31; immune-mediated diseases, n=12; others, n=3) and elevated CRP (inflammatory cohort) were prospectively enrolled, and corrected QT (QTc) and cytokine levels were measured during active disease and after a CRP decrease of >75% subsequent to therapy.Results In the TdP cohort, 80% of patients showed elevated CRP levels (median: ~3 mg/dL), with a definite inflammatory disease identifiable in 18/40 cases (acute infections, n=12; immune-mediated diseases, n=5; others, n=1). In these subjects, IL-6, but not TNFα and IL-1, was ~15–20 times higher than in controls, and comparable to RA patients. In the inflammatory cohort, where QTc prolongation was common (mean values: 456.6±30.9 ms), CRP reduction was associated with IL-6 level decrease and significant QTc shortening (−22.3 ms).Conclusion The data are first to show that systemic inflammation via elevated IL-6 levels may represent a novel QT-prolonging risk factor contributing to TdP occurrence in the presence of other classical risk factors. If confirmed, this could open new avenues in antiarrhythmic therapy. ER -