Research has lead to a better understanding of the pathophysiology and history of atherosclerotic heart disease, which has reached epidemic proportions in industrialized countries in this century. Atherosclerosis should be seen as a chronic, protracted process that encompasses complex and dynamic interactions between cellular, biochemical, and biophysical factors in the microcosmos of the arterial vessel wall and blood circulation. In this context, the ultimate consequences of this disease process, namely coronary artery disease, must be seen as the "tip of the iceberg." The most dramatic manifestation of coronary artery disease, the acute coronary syndrome, usually occurs as the result of different forces and factors, which lead to abrupt plaque disruption, rupture, and vessel thrombosis. In contrast, the genesis of this atherosclerotic lesion is a slow process. Despite considerable experimental clinical evidence accrued during the past decade, atherosclerosis remains a complex pathophysiological process that is not fully understood. It is clear, however, that the interaction between the cellular elements of the vessel wall and the circulation are the determinants of atheroma formation. In this regard, the vascular endothelium appears to play a pivotal role because of its strategic location and metabolic activity. Antilipidemic therapy influences the outcome of coronary disease through a variety of mechanisms, including direct and indirect effects on the endothelium.
CAVH can be effective in severe hypervolemic states, which are generally major hemodynamic abnormalities associated with refractory congestive heart failure, and not infrequently may have a poor renal response to diuretics and vasodilators. Reduced vascular volume with CAVH is accompanied by lower preload and afterload and thus decreased heart size. As a result, cardiac efficiency and contractility improve and oxygen demand is reduced. The temporal progression of congestive heart failure from a mild to a severe state need not be a sign of progressive pathology of heart muscle but rather a result of feedback circuits in which failure begets failure and leads to progressive cardiac enlargement, progressive hypervolemia, and peripheral edema. An appreciation of this concept permits a more optimistic approach to the management of congestive heart failure. Thus, the effective use of CAVH in reducing vascular volume and peripheral edema may reverse "refractory" congestive heart failure and prolong life.