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Cardiovascular diseases cause considerable health and economic burden, as they are the leading cause of disability and death in the western world. Inactivity, hypertension, obesity, diabetes, and smoking are among the classic risk factors for cardiovascular disease. From a pathophysiological point of view, the arteries of our body bear the harmful stimuli produced by these factors and respond to them with a series of intricate adaptive mechanisms. Vascular remodeling constitutes an adaptive response to hemodynamic and inflammatory alterations associated with hypertension, diabetes, and other illnesses. Thickening of the arterial walls leads to endothelial dysfunction and increases the risk of cerebrovascular and coronary events. During the last decades, antiplatelet, lipid-lowering, and antihypertensive therapies have been the cornerstone of primary and secondary prevention of cardiovascular events. However, it is still unknown whether their efficacy is strictly associated with the control of the classical risk factors or their additive effects on vascular inflammation. Since inflammation of arterial walls is related to the pathogenesis of atherosclerosis, it has been hypothesized that anti-inflammatory therapies could prevent and treat vascular remodeling. Clinical trials based on canakinumab or hydroxychloroquine provide further insight into the role of inflammation in the pathophysiology of cardiovascular diseases. In this review, we have analyzed evidence and suggested that inflammation may play an important role in the final pathway of many cardiovascular risk factors.
García et al. (Wed,) studied this question.