(Circulation. 2001;104:974.)
© 2001 American Heart Association, Inc.
Editorial |
C-Reactive Protein
Linking Inflammation to Cardiovascular Complications
From the Department of Cardiology (E.T.H.Y.), University of Texas M.D. Anderson Cancer Center; Department of Medicine (E.T.H.Y., H.V.A., J.T.W.) and the Institute of Molecular Medicine for the Prevention of Human Diseases (E.T.H.Y.), University of Texas Health Science Center; and Texas Heart Institute, St Luke’s Episcopal Hospital (E.T.H.Y., H.V.A., V.P., J.T.W.), Houston, Tex.
Correspondence to Edward T.H. Yeh, MD, Department of Cardiology, 1515 Holcombe Blvd, Box 449, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030-4095. E-mail eyeh@mdanderson.org
Key Words: Editorials • angioplasty • inflammation
In the present issue, Chew and colleagues1 show that elevated baseline C-reactive protein (CRP) levels before percutaneous coronary intervention (PCI) are associated with a progressive increase in the risk of death or myocardial infarction at 30 days. The independent association of risk attributable to the marker CRP remained, even after adjusting for a number of baseline variables that are known to influence early events after PCI. This finding is not a surprise to those who have followed the trail of CRP in the last few years. However, to those who have not followed the CRP story, some explanation is in order.
See p 992
Our understanding of atherosclerosis has evolved immensely over the years. When William Osler wrote his textbook of medicine more than a century ago, atherosclerosis was viewed as being caused by the hardening of blood vessels as a consequence of the aging process. More recently, the perils of hypercholesterolemia and its causative association with atherosclerosis at all ages were uncovered through many large epidemiological studies.2 However, cholesterol deposits in the arterial wall do not fully explain all the features of the proliferation of smooth muscle cells that attempt to form scars to wall off these lipid deposits. With the discovery of growth factors and their role in tissue repair, the "response to injury" hypothesis has become a dominant paradigm. In the last decade, however, a new perspective on atherosclerosis has been developed based on accumulating evidence that the entry of inflammatory cells such as monocytes into the
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