Abstract

A growing amount of clinical and experimental evidence suggests a link between infections, with their consequent inflammation, and atherosclerotic diseases. In this sense, acute infections can promote the development of acute coronary syndromes (ACS), and clinical data strongly support a role for acute infections in triggering these events. On the one hand it is known that during the acute phase of myocardial infarction there is a proinflammatory state [1,2]. On the other hand several studies have demonstrated that infection causes a hypercoagulable state which increases the risk of thrombosis [3,4].

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