Part I Low-grade systemic inflammationCardiovascular disease and cancer; two pieces of the same puzzle?In addition to the risk of recurrent cardiovascular disease, patients with established cardiovascular disease are also at a higher risk for cancer compared to the general population [12][13][14][15] (standardized incidence ratio of 1. 19; 95%CI 1. 10-1.29 adjusted for age, sex and calendar year 14 ). Especially cancer of the respiratory tract, bladder, colorectum, and kidney are more common in patients with cardiovascular disease. 14 Although generally regarded as two separate entities, increasing evidence shows an overlap in risk factors for cardiovascular disease and cancer, suggesting common pathways of etiology and progression of disease. [16][17][18] Shared risk factors for cardiovascular disease and cancer include lifestyle habits such as smoking, diet, and physical activity, diabetes mellitus, obesity, and hypertension. 16 Underlying proposed pathophysiological pathways leading from these well-established cardiovascular risk factors to cancer are several. One of the mechanisms through which diabetes and obesity are related to the development of certain malignancies, is chronic hyperinsulinemia and consequent elevated unbounded insulin-like growth factor (IGF-1) levels, resulting in promotion of cell proliferation. 12, 16, 18 Hypertension in turn, is associated with elevated levels of plasma vascular endothelial growth factor, a hormone that enables tumor cells to induce new blood-vessel formation. 16 Most importantly, inflammation is thought be one of the major common pathways leading from several risk factors such as diabetes mellitus, obesity, hypertension, and lifestyle habits to development and progression of both cardiovascular disease and cancer. 16 Inflammation, cardiovascular disease, and cancerChronic low-grade systemic inflammation is a well established risk factor for cardiovascular disease, and plays a role in the etiology and progression of disease by initiating and accelerating arterial plaque formation and destabilization, causing acute atherosclerotic events. 19 The interleukin (IL) 1β, IL-6, C-reactive protein (CRP) pathway is involved in the pathogenesis; cholesterol crystals, neutrophil extracellular traps, atheroprone flow, and local tissue hypoxia activate the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome resulting in production of pro-IL1β and IL1β. 20 Moving downstream, IL-1β leads to IL-6 activation and consequent CRP production by the liver. 20 IL-6 signaling has been linked to plaque initiation and transformation to vulnerable plaques, [20][21][22] and microvascular flow dysfunction. 20,23 The involvement of the IL1β, IL-6, CRP pathway in the pathophysiology of atherothrombosis is illustrated by the combined results of two trials; the Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS) and the Cardiovascular Inflammation Reduction Trial (CIRT), both enrolling patients with established cardiovascular disease. 20,24 In the CANTOS trial...
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