Abstract
Atherosclerosis is the leading cause of death worldwide. Over the past two decades, it has been clearly recognized that atherosclerosis is an inflammatory disease of the arterial wall. Accumulating data from animal experiments have supported this hypothesis, however, clinical applications making use of this knowledge remain scarce. In spite of optimal interventional and medical therapy, the risk for recurrent myocardial infarction remains by about 20% over 3 years after acute coronary syndromes, novel therapies to prevent atherogenesis or treat atherosclerosis are urgently needed. This review summarizes selected potential molecular inflammatory targets that may be of clinical relevance. We also review recent and ongoing clinical trails that target inflammatory processes aiming at preventing adverse cardiovascular events. Overall, it seems surprising that translation of basic science into clinical practice has not been a great success. In conclusion, we propose to focus on specific efforts that promote translational science in order to improve outcome and prognosis of patients suffering from atherosclerosis.
Highlights
Atherosclerosis is the leading cause of death worldwide
Apart from its lethal consequences such myocardial infarction or stroke, atherosclerosis underlies the cause of a huge burden of morbidity, associated with heart failure due to ischemic heart disease or neurological impairment due to stroke
There is still an enormous unmet need: after 3 years, 20% of ACS patients suffer from recurrent myocardial infarction despite optimal medial therapy (Cannon et al, 2005; Stone et al, 2011)
Summary
Atherosclerosis remains an epidemiologically highly prevalent disease and myocardial infarction and stroke represent the most important causes of death worldwide (Roger et al, 2011; Go et al, 2014). Antioxidants, inhibitors of lipoprotein-associated phospholipase A2 (Lp-PLA2), niacin, and cholesterol ester transfer protein (CETP) inhibitors either aim at decreasing LDL levels or increasing HDL levels or both This reflects the important role of lipids during atherogenesis. Darapladib inhibits Lp-PLA2 activity by roughly 95%, has no effects on blood lipids and has been shown to lower hs-CRP and IL-6 levels (Mohler et al, 2008) Both in a porcine model of atherosclerosis and in human individuals, darapladib significantly reduces the necrotic core of atherosclerotic plaques (Serruys et al, 2008). CHOLESTEROL ESTER TRANSFER PROTEIN (CETP) INHIBITION There is clear epidemiological evidence that increased high density lipoproteins (HDL) plasma levels are associated with beneficial outcome in coronary artery disease (Assmann et al, 2002). Raising HDL levels has been proposed to be beneficial and potentially prevent adverse cardiovascular events
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