{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:54:53Z","timestamp":1787018093443,"version":"build-2736575974"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,4,3]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Current recommendations for lipoprotein(a) (Lp[a]) focus on the control of other risk factors, including lowering low\u2010density lipoprotein cholesterol (\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C), with little evidence to support this approach. Identifying interactions between Lp(a) and other risk factors could identify individuals at increased risk for Lp(a)\u2010mediated disease.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We used a case\u2010only study design and included 939 participants (median age=49\u00a0years, interquartile range 46\u201353, women=33.1%) from the\n                      <jats:styled-content style=\"fixed-case\">GENdE<\/jats:styled-content>\n                      r and Sex determInantS of cardiovascular disease: from bench to beyond\u2010Premature Acute Coronary Syndrome (\n                      <jats:styled-content style=\"fixed-case\">GENESIS<\/jats:styled-content>\n                      \u2010\n                      <jats:styled-content style=\"fixed-case\">PRAXY<\/jats:styled-content>\n                      ) study, a multicenter prospective cohort study of premature acute coronary syndrome. There was a higher prevalence of elevated Lp(a) levels (&gt;50\u00a0mg\/dL; 80th percentile) in\n                      <jats:styled-content style=\"fixed-case\">PRAXY<\/jats:styled-content>\n                      participants as compared to the general population (31% versus 20%;\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001). Lp(a) was strongly associated with\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C (adjusted \u03b2 0.17;\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001). Individuals with high Lp(a) were more likely to have\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C &gt;2.5\u00a0mmol\/L, indicating a synergistic interaction (adjusted odds ratio 1.51; 95%\n                      <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                      1.08\u20132.09;\n                      <jats:italic>P<\/jats:italic>\n                      =0.015). The interaction with high Lp(a) was stronger at increasing\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C levels (\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C &gt;3.5, adjusted odds ratio 1.87;\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C &gt;4.5, adjusted odds ratio 2.72). In a polytomous logistic model comparing mutually exclusive\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C categories, the interaction with high Lp(a) became attenuated at\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C \u22643.5\u00a0mmol\/L (odds ratio 1.16; 95%\n                      <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                      0.80\u20131.68,\n                      <jats:italic>P<\/jats:italic>\n                      =0.447). Other risk factors were not associated with high Lp(a).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      In young acute coronary syndrome patients, high Lp(a) is more prevalent than in the general population and is strongly associated with high\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C, suggesting that Lp(a) confers greater risk for acute coronary syndrome when\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C is elevated. Individuals with high Lp(a) and\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C &gt;3.5\u00a0mmol\/L may warrant aggressive\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      \u2010C lowering.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.115.003012","type":"journal-article","created":{"date-parts":[[2016,4,23]],"date-time":"2016-04-23T20:57:43Z","timestamp":1461445063000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":73,"title":["Lipoprotein(a) Interactions With Low\u2010Density Lipoprotein Cholesterol and Other Cardiovascular Risk Factors in Premature Acute Coronary Syndrome (ACS)"],"prefix":"10.1161","volume":"5","author":[{"given":"Mehdi","family":"Afshar","sequence":"first","affiliation":[{"name":"Department of Medicine, McGill University, Montreal, Quebec, Canada"},{"name":"Preventive and Genomic Cardiology, McGill University Health Center and Research Institute, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louise","family":"Pilote","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University, Montreal, Quebec, Canada"},{"name":"Department of Clinical Epidemiology, McGill University Health Center, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Line","family":"Dufresne","sequence":"additional","affiliation":[{"name":"Preventive and Genomic Cardiology, McGill University Health Center and Research Institute, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James C.","family":"Engert","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University, Montreal, Quebec, Canada"},{"name":"Department of Human Genetics, McGill University, Montreal, Quebec, Canada"},{"name":"Preventive and Genomic Cardiology, McGill University Health Center and Research Institute, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Thanassoulis","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University, Montreal, Quebec, Canada"},{"name":"Preventive and Genomic Cardiology, McGill University Health Center and Research Institute, Montreal, Quebec, Canada"},{"name":"Department of Clinical Epidemiology, McGill University Health Center, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehq386"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2009.801"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1109034"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacl.2010.07.002"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacl.2011.07.005"},{"key":"e_1_3_5_7_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a008915"},{"key":"e_1_3_5_8_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a009346"},{"key":"e_1_3_5_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115855"},{"key":"e_1_3_5_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.102.10.1082"},{"key":"e_1_3_5_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinchem\/40.4.571"},{"key":"e_1_3_5_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.clinbiochem.2014.04.023"},{"key":"e_1_3_5_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2012.01.022"},{"key":"e_1_3_5_14_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.107.699579"},{"key":"e_1_3_5_15_2","doi-asserted-by":"publisher","DOI":"10.1002\/sim.4780130206"},{"key":"e_1_3_5_16_2","doi-asserted-by":"publisher","DOI":"10.1006\/pmed.1996.0117"},{"key":"e_1_3_5_17_2","doi-asserted-by":"publisher","DOI":"10.1002\/gepi.20427"},{"key":"e_1_3_5_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-620990-7.50014-0"},{"key":"e_1_3_5_19_2","volume-title":"R: A Language and Environment for Statistical Computing","author":"R Core Team","year":"2015","unstructured":"R Core Team . 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