Title:Torsades de Pointes in Patients with Polymyalgia Rheumatica
Volume: 24
Issue: 3
Author(s): Pietro Enea Lazzerini*, Iacopo Bertolozzi, Maurizio Acampa, Rosella Fulceri, Franco Laghi-Pasini and Pier Leopoldo Capecchi
Affiliation:
- Department of Medical Sciences, Surgery and Neurosciences, University of Siena, Siena,Italy
Keywords:
Torsades de Pointes, polymyalgia rheumatica, giant cell arteritis, cardiovascular disease, coronary artery disease, arrhythmias,
systemic inflammation, interleukin-6, sudden death.
Abstract: Polymyalgia rheumatica (PMR) represents the most common inflammatory rheumatic disease of the
elderly. It is characterized by synovitis of proximal joints and extra-articular synovial structures, along with
chronic high-grade systemic inflammation. PMR is closely related to giant cell arteritis (GCA), a large–vessel
vasculitis that involves the major branches of the aorta, particularly the extracranial branches of carotid artery
including temporal arteries. It is currently believed that PMR and GCA may represent different manifestations of
the same disease process.
Chronic systemic inflammation is presently recognized as one of the key pathogenic mechanisms underlying
cardiovascular disease and associated complications, including cardiac arrhythmias and sudden death. In this
regard, several studies demonstrated that besides promoting structural heart disease, inflammatory activation may
also be per se arrhythmogenic, via cytokine-mediated effects on cardiac electrophysiology. In particular, increasing
evidence points to inflammation as a novel risk factor for QTc prolongation and related life-threatening arrhythmias,
specifically Torsade de Pointes (TdP).
Starting from the report of two cases of TdP occurring in PMR patients with active disease and elevated circulating
IL-6 levels, we here reviewed literature data regarding heart involvement and arrhythmic events in
PMR/GCA, as well as TdP risk in inflammatory diseases. Potential underlying mechanisms were dissected, by
focusing on the driving role of inflammatory activation.
