Georgios Tsivgoulis*, Aristeidis H. Katsanos, Georgios Giannopoulos, Vasiliki Panagopoulou, Dalius Jatuzis, Robin Lemmens, Spyridon Deftereos and Peter J. Kelly Pages 668 - 674 ( 7 )
Introduction: Despite the proven efficacy of anti-thrombotic, lipid-lowering, anti-hypertensive therapies and lifestyle modification changes for secondary ischemic stroke prevention, the risk of recurrent stroke, coronary events and vascular death remains substantial even for patients treated with high rates of established secondary preventive medications.
Methods: In the present review, we summarize available literature data on the association between systemic inflammation and symptomatic atherosclerosis including recurrent cerebral ischemia. We also highlight the potential role of colchicine in the suppression of atherosclerosis-induced inflammation, plaque stabilization and thromboembolism prevention.
Results: Accumulating evidence suggests that inflammation is of key importance in the pathophysiology of atherosclerotic plaque de-stabilization and thromboembolism, with inflammatory cells being involved in all stages of atherosclerosis development. Therefore, anti-inflammatory therapies targeting the atherosclerotic plaque inflammation may be important contributors in plaque stabilization and in the prevention of thromboembolic events. Colchicine is known to have multiple anti-inflammatory properties including inhibition of microtubule polymerization, leading to reduced secretion in monocyte-macrophages. Currently the randomized controlled CONVINCE trial is enrolling stroke patients to evaluate the effect of a daily low-dose of colchicine in reducing the rate of recurrent stroke and major vascular events.
Conclusion: Inflammatory pathways seem to be key mediators in the development of atherosclerotic process, atheromatous plaque destabilization and thromboembolism. Colchicine as a novel therapeutic agent could be a safe and effective inhibitor of the inflammation cascade in patients with extra- or intracranial atherosclerosis or arteriolosclerosis, resulting in reduced vascular events.
Colchicine, inflammation, stroke, cerebral ischemia, transient ischemic attack, macrophages, prevention.
Department of Neurology, University of Tennessee Health Science Center, Memphis, TN, Department of Neurology, University of Ioannina School of Medicine, Ioannina, Second Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens, Athens, Second Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens, Athens, Department of Neurology and Neurosurgery, Center for Neurology, Vilnius University, Vilnius, Department of Neurology, University Hospitals Leuven, B-3000 Leuven, Second Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens, Athens, Health Research Board Irish Stroke Clinical Trials Network and Mater University Hospital/ University College Dublin