ABSTRACT
We are born and continue to live during a pandemic of cardiovascular disease(CVD). Coronary heart disease (CHD), a rare disease of the affluent and rich in the late 19th century, rapidly emerged as the main cause of death in the Western world by the mid 20th century and is rising to the number one cause of death in the developing countries as well. Atherosclerosis, the main underlying pathology for coronary artery disease, is a very common finding in adults living in the Western world and can be found even in the young. In fact, multiple autopsy studies have shown that atherosclerotic lesions can be found at very early ages.1,2 The relation between high plasma concentrations of cholesterol and especially low-density lipoprotein (LDL) cholesterol, smoking, diabetes, and hypertension with atherosclerosis is well established by now. However, new evidence generated during the past two decades has highlighted the critical role of inflammation in atherosclerosis.3 Atherosclerosis is an inflammatory disease characterized by multifocal lesions and systemic elevations of a number of inflammatory markers such as acute phase proteins, cytokines, and cell adhesion molecules.4 The natural history of atherosclerosis is one of slow progression over years with a possible abrupt disruption of plaques leading to acute coronary syndromes (ACS). The most common underlying pathophysiologic mechanism of ACS is plaque rupture and subsequent
thrombosis at the site of the plaque disruption.5 A majority of myocardial infarction (MI) cases and sudden cardiac deaths are caused by the rupture of a coronary atherosclerotic plaque.6 Plaque rupture may be precipitated by external stresses or ‘triggers’ superimposed on vulnerable coronary plaques.7 The mechanisms by which certain triggers can induce rupture and instability of the plaques are not completely understood but are believed to involve mechanical tension, chemical changes (low pH), tissue degradation (release of proteolytic enzymes), thinning of the fibrous cap (<65 µm) along with changes in platelet aggregability and blood viscosity.
