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.
Keywords: Torsades de Pointes, polymyalgia rheumatica, giant cell arteritis, cardiovascular disease, coronary artery disease, arrhythmias, systemic inflammation, interleukin-6, sudden death.
Current Pharmaceutical Design
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.
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Cite this article as:
Lazzerini Enea Pietro*, Bertolozzi Iacopo , Acampa Maurizio, Fulceri Rosella, Laghi-Pasini Franco and Capecchi Leopoldo Pier , Torsades de Pointes in Patients with Polymyalgia Rheumatica, Current Pharmaceutical Design 2018; 24 (3) . https://dx.doi.org/10.2174/1381612824666180111111124
DOI https://dx.doi.org/10.2174/1381612824666180111111124 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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