Dr. Jean-Claude Tardif is the Director of the Montréal Heart Institute's Research Centre and a University of Montréal Professor of Medicine. Dr. Tardif received his medical degree from the University of Montréal in 1987 and finished his cardiology and research studies in Montréal and Boston in 1994. Dr. Tardif is the endowed research chair in atherosclerosis at the University of Montréal. He is the Scientific Director of the Montréal Heart Institute Coordinating Centre and the Chairman of the Canadian Atherosclerosis Imaging Network and the Medical Imaging Trials NEtwork of Canada. In this video Dr. Tardif discusses the Colchicine Cardiovascular Outcomes Trial.
Link to Abstract-
The trial examines whether long-term colchicine medication reduces the risk of cardiovascular events in people who have had a myocardial infarction. Patients who have had a documented acute myocardial infarction in the previous 30 days are treated according to national guidelines and, after completing any planned percutaneous revascularization procedures associated with their initial infarction, are given either colchicine (0.5 mg per day) or matching placebo (1:1 allocation ratio) for an estimated 2 years or until the target of 301 primary endpoints is met.
Description in detail:
Myocardial infarction, stroke, and peripheral arterial disease are all caused by atherosclerosis. Inflammation plays a critical role in the genesis, progression, and symptoms of atherosclerosis, according to research. Atherosclerotic lesions begin as an accumulation of lipid-laden cells (mainly macrophages) underneath the endothelium and proceed through immunological and inflammatory activation to an accumulation of cells, connective-tissue elements, lipids, and debris. Atherosclerotic lesions in acute coronary syndromes have been demonstrated to be invaded by neutrophils and other inflammatory cells. Despite major breakthroughs in the treatment of risk factors such as hypercholesterolemia and hypertension, it is likely that the inflammatory process is to blame for the high rate of cardiovascular events. Improved understanding of the inflammatory aspect of atherosclerotic disease is critical, as is the ability to modulate the inflammatory process with targeted therapeutics. In numerous populations, prospective cohort studies have repeatedly shown that high sensitivity C-reactive protein (hs-CRP) and several other inflammatory biomarkers are independently related with an increased risk of future cardiovascular events. This, together with animal models indicating that reduced inflammation has anti-atherosclerotic effects, gives rise to the premise that treating the underlying inflammatory process will lead to better cardiovascular clinical outcomes. Colchicine is a low-cost, high-potency anti-inflammatory medication licensed for acute and chronic usage in individuals with gout and Familial Mediterranean Fever. Tubulin polymerization inhibition, as well as impacts on cellular adhesion molecules and inflammatory chemokines, are thought to be the mechanism of action. Colchicine may also have direct anti-inflammatory effects by blocking the inflammasome and pro-inflammatory cytokines, two major inflammatory signaling networks. Colchicine is thought to decrease cytokine and chemokine release as well as in vitro platelet aggregation via disrupting the cytoskeleton. Colchicine has been studied extensively for its potential in the treatment of cardiovascular disorders caused by pro-inflammatory processes. Colchicine's influence on cardiovascular events in patients with coronary artery disease has recently been studied (CAD).