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Nearly all the risk associated with elevated Lp(a) was found to be restricted to persons with historically elevated plasma total cholesterol (6.72 mmol\/L [260 mg\/dL] or higher) or with a total\/HDL cholesterol ratio &gt;5.8. Nonlipid risk factors were also found to at least multiply the risk associated with Lp(a). When Lp(a) was over 40 mg\/dL and plasma total\/HDL cholesterol &gt;5.8, relative odds for CAD were 25 (<jats:italic>P<\/jats:italic>=.0001) in multiple logistic regression. If two or more nonlipid risk factors were also present (including hypertension, diabetes, cigarette smoking, high total homocysteine, or low serum bilirubin), relative odds were 122 (<jats:italic>P<\/jats:italic>&lt;1\u00d710<jats:sup>\u221212<\/jats:sup>). The ability of nonlipid risk factors to increase risk associated with Lp(a) was dependent on at least a mildly elevated total\/HDL cholesterol ratio. In conclusion, high Lp(a) was found to greatly increase risk only if the total\/HDL cholesterol ratio was at least mildly elevated, an effect exaggerated by other risk factors. Aggressive lipid lowering in those with elevated Lp(a) therefore appears indicated.<\/jats:p>","DOI":"10.1161\/01.atv.17.11.2783","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T19:44:19Z","timestamp":1308339859000},"page":"2783-2792","source":"Crossref","is-referenced-by-count":56,"title":["Lipoprotein(a) Interactions With Lipid and Nonlipid Risk Factors in Early Familial Coronary Artery Disease"],"prefix":"10.1161","volume":"17","author":[{"given":"Paul N.","family":"Hopkins","sequence":"first","affiliation":[{"name":"From Cardiovascular Genetics, Department of Internal Medicine, Cardiology Division, University of Utah School of Medicine, (P.N.H., L.L.W., S.C.H., R.D.W.); the Department of Pathology, University of Utah School of Medicine, Associated Regional and University Pathologists (L.L.W.); Intermountain Health Care and University of Utah School of Medicine, (B.C.J.); and the Cardiology Division, LDS Hospital, and University of Utah School of Medicine (G.M.V.), Salt Lake City, Utah."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lily L.","family":"Wu","sequence":"additional","affiliation":[{"name":"From Cardiovascular Genetics, Department of Internal Medicine, Cardiology Division, University of Utah School of Medicine, (P.N.H., L.L.W., S.C.H., R.D.W.); the Department of Pathology, University of Utah School of Medicine, Associated Regional and University Pathologists (L.L.W.); Intermountain Health Care and University of Utah School of Medicine, (B.C.J.); and the Cardiology Division, LDS Hospital, and University of Utah School of Medicine (G.M.V.), Salt Lake City, Utah."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven C.","family":"Hunt","sequence":"additional","affiliation":[{"name":"From Cardiovascular Genetics, Department of Internal Medicine, Cardiology Division, University of Utah School of Medicine, (P.N.H., L.L.W., S.C.H., R.D.W.); the Department of Pathology, University of Utah School of Medicine, Associated Regional and University Pathologists (L.L.W.); Intermountain Health Care and University of Utah School of Medicine, (B.C.J.); and the Cardiology Division, LDS Hospital, and University of Utah School of Medicine (G.M.V.), Salt Lake City, Utah."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brent C.","family":"James","sequence":"additional","affiliation":[{"name":"From Cardiovascular Genetics, Department of Internal Medicine, Cardiology Division, University of Utah School of Medicine, (P.N.H., L.L.W., S.C.H., R.D.W.); the Department of Pathology, University of Utah School of Medicine, Associated Regional and University Pathologists (L.L.W.); Intermountain Health Care and University of Utah School of Medicine, (B.C.J.); and the Cardiology Division, LDS Hospital, and University of Utah School of Medicine (G.M.V.), Salt Lake City, Utah."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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