Inflammation and atherosclerosis: fulfilling Koch’s postulates

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality in the Western world. Atherogenesis is an inflammatory process originating from a nascent fatty streak lesion culminating in plaque rupture.1–4 Various biomediators of inflammation, including adhesion molecules, cytokines, chemokines, etc., are known to play a role in atherosclerosis in both animal models and humans. The prototypic marker of inflammation, high-sensitivity C-reactive protein (hsCRP) for example, has previously been shown to independently predict cardiovascular events (CVE).1–