{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T23:42:56Z","timestamp":1791934976448,"version":"4.3.4"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2010,11,23]]},"abstract":"<jats:sec>\n                    <jats:title>Background\u2014<\/jats:title>\n                    <jats:p>Aggressive blood pressure (BP) control has been advocated in patients with acute coronary syndrome, but few data exist in this population relative to cardiovascular outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results\u2014<\/jats:title>\n                    <jats:p>We evaluated 4162 patients enrolled in the PRavastatin Or atorVastatin Evaluation and Infection Therapy\u2013Thrombolysis In Myocardial Infarction (PROVE IT-TIMI) 22 trial (acute coronary syndrome patients randomized to pravastatin 40 mg versus atorvastatin 80 mg). The average follow-up BP (systolic and diastolic) was categorized into 10-mm Hg increments. The primary outcome was a composite of death due to any cause, myocardial infarction, unstable angina requiring rehospitalization, revascularization after 30 days, and stroke. The secondary outcome was a composite of death due to coronary heart disease, nonfatal myocardial infarction, or revascularization. The relationship between BP (systolic or diastolic) followed a J- or U-shaped curve association with primary, secondary, and individual outcomes, with increased events rates at both low and high BP values, both unadjusted and after adjustment for baseline variables, baseline C-reactive protein, and on-treatment average levels of low-density lipoprotein cholesterol. A nonlinear Cox proportional hazards model showed a nadir of 136\/85 mm Hg (range 130 to 140 mm Hg systolic and 80 to 90 mm Hg diastolic) at which the incidence of primary outcome was lowest. The curve was relatively flat for systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>After acute coronary syndrome, a J- or U-shaped curve association existed between BP and the risk of future cardiovascular events, with lowest event rates in the BP range of approximately 130 to 140 mm Hg systolic and 80 to 90 mm Hg diastolic and a relatively flat curve for systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg, which suggests that too low of a pressure (especially &lt;110\/70 mm Hg) may be dangerous.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Trial Registration\u2014<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/www.clinicaltrials.gov\">http:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      . Unique identifier: NCT00382460.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.109.905687","type":"journal-article","created":{"date-parts":[[2010,11,9]],"date-time":"2010-11-09T02:14:14Z","timestamp":1289268854000},"page":"2142-2151","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":190,"title":["What Is the Optimal Blood Pressure in Patients After Acute Coronary Syndromes?"],"prefix":"10.1161","volume":"122","author":[{"given":"Sripal","family":"Bangalore","sequence":"first","affiliation":[{"name":"From the New York University School of Medicine (S.B.), New York, NY, and TIMI Study Group (J.Q., S.S., S.A.M., C.P.C.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Qin","sequence":"additional","affiliation":[{"name":"From the New York University School of Medicine (S.B.), New York, NY, and TIMI Study Group (J.Q., S.S., S.A.M., C.P.C.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Sloan","sequence":"additional","affiliation":[{"name":"From the New York University School of Medicine (S.B.), New York, NY, and TIMI Study Group (J.Q., S.S., S.A.M., C.P.C.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabina A.","family":"Murphy","sequence":"additional","affiliation":[{"name":"From the New York University School of Medicine (S.B.), New York, NY, and TIMI Study Group (J.Q., S.S., S.A.M., C.P.C.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher P.","family":"Cannon","sequence":"additional","affiliation":[{"name":"From the New York University School of Medicine (S.B.), New York, NY, and TIMI Study Group (J.Q., S.S., S.A.M., C.P.C.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"for the PROVE IT-TIMI 22 Trial Investigators","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)11911-8"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(78)92288-2"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.19.2560"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1997.00440420033005"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(87)90231-5"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0954-6820.1985.tb08876.x"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-144-12-200606200-00005"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(79)91274-1"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.089797"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(98)22024-1"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1992.00400150007001"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)65599-7"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1991.03460040065031"},{"key":"e_1_3_3_15_2","first-page":"7","article-title":"Does therapeutic reduction of diastolic blood pressure cause death from coronary heart disease?","volume":"2","author":"Waller PC","year":"1988","unstructured":"Waller PC, Isles CG, Lever AF, Murray GD, McInnes GT. 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