ABSTRACT
INTRODUCTION Ischemic heart disease (IHD), the major cause of morbidity and mortality in the Western World, has its basis in the atherosclerosis that affects the epicardial coronary arteries. The term atherosclerosis originates from the Greek, athere (meaning “gruel”), which describes the soft, lipid-rich core of the plaque, and skleros (meaning “hard”) that describes the hard fibrous capsule that surrounds the core, a general description that is still useful today. Previously considered as a cholesterol-storage disease, it is now viewed as a chronic inflammatory disorder within the wall of the artery. Inflammation results from a complex interaction between modified lipoproteins, monocyte-derived macrophages, cytokines, and normal components of the arterial wall. In general, disease presentation results either from chronic and gradual reduction of the arterial lumen or instability of the plaque-producing acute luminal obstruction and/or distal vessel embolization. Within the context of IHD, this accounts for presentation as chronic stable angina, acute coronary syndromes (ACS), sudden ischemic coronary death, and heart failure (Table 1). This chapter will describe the fundamental processes involved in atherogenesis and the mechanisms of coronary instability.
