{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T05:18:56Z","timestamp":1791350336718,"version":"4.3.1"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"14","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2006,4,11]]},"abstract":"\n \n Background\u2014<\/jats:italic>\n <\/jats:bold>\n Lipoprotein-associated phospholipase A\n 2<\/jats:sub>\n (Lp-PLA\n 2<\/jats:sub>\n ) is associated with the risk of cardiovascular (CV) events in population-based studies. The prognostic value of Lp-PLA\n 2<\/jats:sub>\n in patients with acute coronary syndromes (ACS) has not been established.\n <\/jats:p>\n \n \n Methods and Results\u2014<\/jats:italic>\n <\/jats:bold>\n Plasma levels of Lp-PLA\n 2<\/jats:sub>\n activity were measured at baseline (n=3648) and 30 days (n=3265) in patients randomized to atorvastatin 80 mg\/d or pravastatin 40 mg\/d after ACS in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy\u2013Thrombolysis In Myocardial Infarction) trial. The primary end point was death, myocardial infarction, unstable angina, revascularization, or stroke (mean follow-up 24 months). At baseline after ACS, the risk of recurrent CV events was similar across all quintiles of Lp-PLA\n 2<\/jats:sub>\n activity (\n P<\/jats:italic>\n trend<\/jats:sub>\n =0.88). Overall, mean levels of Lp-PLA\n 2<\/jats:sub>\n were lower at 30 days of follow-up than at baseline (35.7 versus 40.9 nmol \u00b7 min\n \u22121<\/jats:sup>\n \u00b7 mL\n \u22121<\/jats:sup>\n ,\n P<\/jats:italic>\n <0.001). In particular, treatment with atorvastatin 80 mg\/d was associated with a 20% reduction in Lp-PLA\n 2<\/jats:sub>\n activity (\n P<\/jats:italic>\n <0.001), whereas Lp-PLA\n 2<\/jats:sub>\n rose 3.6% with pravastatin 40 mg\/d (\n P<\/jats:italic>\n <0.001). Patients with 30-day Lp-PLA\n 2<\/jats:sub>\n activity in the highest quintile were at significantly increased risk of recurrent CV events compared with those in the lowest quintile (26.4% versus 17.6%,\n P<\/jats:italic>\n trend<\/jats:sub>\n =0.002). After adjustment for cardiac risk factors, treatments, achieved low-density lipoprotein (LDL), and C-reactive protein, Lp-PLA\n 2<\/jats:sub>\n activity in the highest quintile remained independently associated with a higher risk of recurrent CV events (adjusted hazard ratio 1.33, 95% confidence interval [CI] 1.01 to 1.74).\n <\/jats:p>\n \n \n Conclusions\u2014<\/jats:italic>\n <\/jats:bold>\n Lp-PLA\n 2<\/jats:sub>\n is not useful for risk stratification when measured early after ACS. At 30 days, Lp-PLA\n 2<\/jats:sub>\n activity is significantly lowered with high-dose statin therapy and is associated with an increased risk of CV events independent of C-reactive protein and LDL cholesterol levels.\n <\/jats:p>","DOI":"10.1161\/circulationaha.105.612630","type":"journal-article","created":{"date-parts":[[2006,3,15]],"date-time":"2006-03-15T02:23:44Z","timestamp":1142389424000},"page":"1745-1752","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":184,"title":["Lipoprotein-Associated Phospholipase A\n 2<\/sub>\n and Its Association With Cardiovascular Outcomes in Patients With Acute Coronary Syndromes in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy\u2013Thrombolysis In Myocardial Infarction) Trial"],"prefix":"10.1161","volume":"113","author":[{"given":"Michelle","family":"O\u2019Donoghue","sequence":"first","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Morrow","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc S.","family":"Sabatine","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabina A.","family":"Murphy","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolyn H.","family":"McCabe","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher P.","family":"Cannon","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugene","family":"Braunwald","sequence":"additional","affiliation":[{"name":"From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199901143400207"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.0000052939.59093.45"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)38724-1"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1066"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2005.058404"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/374549a0"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.103.20.2495"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3380479"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2362.1997.1570706.x"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvb.19.12.2909"},{"key":"e_1_3_2_11_2","first-page":"II-246","volume":"110","year":"2004","unstructured":"Kolodgie FD, Burke AP, Taye A, Liu W, Sudhir K, Virmani R. 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