Quantitative Imaging, Risk Factors, Prevalence, and Change

Introduction and Background Coronary Atherosclerosis A Multifactorial Disease

Badimon, J.J.
Fuster, V.
Chesebro, J.H.
Badimon, L.

From the Cardiac Unit (J.J.B., V.F., J.H.C., L.B.), Massachusetts General Hospital, Harvard Medical School, Boston, and the Cardiovascular Research Lab (L.B.), Centro Investigacion y Desarrollo, Consejo Superior de Investigaciones Cientificas, Barcelona, Spain.
Supported in part by National Institutes of Health grants HL-39840, HL-38933, and HL-38393 and grants from CICYT-92 and FIS-92.
Address for correspondence: Juan Jose Badimon, PhD, Cardiovascular Biology Research, Cardiac Unit, Jackson Building, Room 1328, Massachusetts General Hospital, 32 Fruit Street, Boston, MA 02114.

Circulation 87(3S):p II3-II16, March 1993.

Background

Several of the theories on the pathogenesis of atherosclerosis may be integrated into a single multifactorial one. According to this theory, the most likely sequence of events involved in early atherosclerosis is vascular dysfunction and/or injury, monocyte recruitment and macrophage formation, lipid deposition, vascular smooth muscle cell proliferation (mitogenic factor mediated), and synthesis of extracellular matrix. The interaction of all these factors will configurate the typical characteristic of the atherosclerotic plaque.

Methods and Results.Accumulating experimental and clinical data suggest two pathways in atherosclerotic progression. In some cases, the very slow process of the pathogenesis of early lesions may be significantly accelerated by means of thrombus formation and organization. Thrombosis is a key process in the pathogenesis of late atherogenesis and in the development of acute ischemic syndromes.

Conclusions

The possibility of retarding human atherosclerosis or even inducing its regression is one of the present therapeutic challenges. Of the different approaches to this question, one approach aims at better control of risk factors, especially plasma lipid levels. Another approach attempts to enhance the removal of lipids from the arterial wall by increasing plasma high density lipoprotein levels. Each of these approaches, by acting on the lipid-rich plaques more prone to rupture, might prevent plaque progression and induce regression to prevent acute coronary events. A third approach, based on the key role of platelet thrombus formation in the conversion of chronic to acute events, would be the use of antithrombotic therapy. This last approach may partially prevent progression of the disease. (Circulation 1993;87(suppl II):II-3-II-16)