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Previous Volume 345:1022-1029 October 4, 2001 Number 14 Next

	Full Text PDF Editorial by Rabbani, L. E. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background Circulating markers indicating the instability of atherosclerotic plaques could have diagnostic value in unstable angina or acute myocardial infarction. We evaluated pregnancy-associated plasma protein A (PAPP-A), a potentially proatherosclerotic metalloproteinase, as a marker of acute coronary syndromes.

Methods We examined the level of expression of PAPP-A in eight culprit unstable coronary plaques and four stable plaques from eight patients who had died suddenly of cardiac causes. We also measured circulating levels of PAPP-A, C-reactive protein, and insulin-like growth factor I (IGF-I) in 17 patients with acute myocardial infarction, 20 with unstable angina, 19 with stable angina, and 13 controls without atherosclerosis.

Results PAPP-A was abundantly expressed in plaque cells and extracellular matrix of ruptured and eroded unstable plaques, but not in stable plaques. Circulating PAPP-A levels were significantly higher in patients with unstable angina or acute myocardial infarction than in patients with stable angina and controls (P<0.001). A PAPP-A threshold value of 10 mIU per liter identified patients who had acute coronary syndromes with a sensitivity of 89.2 percent and a specificity of 81.3 percent. PAPP-A levels correlated with levels of C-reactive protein and free IGF-I, but not with markers of myocardial injury (troponin I and the MB isoform of creatine kinase).

Conclusions PAPP-A is present in unstable plaques, and circulating levels are elevated in acute coronary syndromes; these increased levels may reflect the instability of atherosclerotic plaques. PAPP-A is a new candidate marker of unstable angina and acute myocardial infarction.

Source Information

From the Division of Cardiovascular Diseases (A.B.-G., D.R.H., R.S.S.), Endocrine Research Unit (C.A.C.), and Statistics Department (K.R.B.), Mayo Clinic and Foundation, Rochester, Minn.; the Department of Molecular and Structural Biology, University of Aarhus, Aarhus, Denmark (M.T.O., C.O.); the Department of Clinical Biochemistry, Statens Serum Institute, Copenhagen, Denmark (M.C.); and the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D.C. (R.V.).

Address reprint requests to Dr. Schwartz at the Division of Cardiovascular Diseases, Mayo Clinic, 200 First St., SW, Rochester, MN 55905.

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