(Circulation. 1999;100:2124.)
© 1999 American Heart Association, Inc.
Editorial |
A Tale of Two Diseases
Atherosclerosis and Rheumatoid Arthritis
From the Department of Internal Medicine and Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center, Houston, and the Texas Heart Institute, St Luke’s Episcopal Hospital, Houston.
Correspondence to Edward T.H. Yeh, MD, Department of Internal Medicine, 6431 Fannin St, Suite 4200, UT-Houston HSC, Houston, TX 77030.
Key Words: Editorials • atherosclerosis • immune system • lymphocytes
Acute coronary
syndromes are responsible for most of the morbidity and mortality
caused by coronary atherosclerosis. Both
unstable angina and acute myocardial infarction are characterized by
coronary thrombosis, usually caused by rupture or fissuring of
a coronary plaque. Yet the occurrence of plaque rupture and
coronary thrombosis is not related to severity of
coronary plaques, and functional factors other than the mere
presence of atherosclerotic lesions play an important
role.1 2 Recent studies have focused on the inflammatory
component of atherosclerosis, trying to highlight the
differences between stable and unstable coronary plaques. An
increasing body of evidence supports the hypothesis that
atherosclerosis shares many similarities with
other inflammatory/autoimmune diseases. Indeed, there are surprising
similarities in the inflammatory/immunologic response observed in
atherosclerosis, in unstable angina, and in rheumatoid
arthritis, the prototype of autoimmune disease
(Table
). However, although our understanding of
the molecular and immunological mechanisms of rheumatoid arthritis has
greatly progressed, due to the relatively easy access to the
diseased tissue (synovium) and to the availability of animal models,
the study of the inflammatory and immunological components of
atherosclerosis is still in its initial stages.
Unfortunately, it is more difficult for cardiologists to follow the
evolution of inflammatory response in plaques or make correlations with
the clinical course. Furthermore, although mice models of
atherosclerosis have been developed in the last
few years, there are still no animal models able to reproduce
the events occurring in acute coronary syndromes. Thus, the
study of the molecular mechanisms of rheumatoid arthritis may give
valuable
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