{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T13:34:45Z","timestamp":1793108085790,"version":"4.5.0"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,11,6]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Heterozygous familial hypercholesterolemia increases the risk of adverse cardiovascular events. Whether affected relatives of probands are at increased risk remains unknown. We aimed to evaluate the long\u2010term cardiovascular risk in heterozygous familial hypercholesterolemia relatives with a low\u2010density lipoprotein receptor (\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">LDLR<\/jats:styled-content>\n                      <\/jats:italic>\n                      ) mutation who were all recommended statin therapy.\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                      Participants were identified by cascade screening at Aarhus University Hospital during 1992\u20131994. A comparison cohort from the Danish general population was matched 10:1 to relatives by birth year and sex. Using medical registries, participants were followed until the event of interest, migration, death, or end of follow\u2010up on December 31, 2014. The primary end point was all\u2010cause mortality and major adverse cardiovascular events comprising myocardial infarction, ischemic stroke, transient ischemic attack, peripheral artery disease, and coronary revascularization. We included 220 relatives. Median age was 37 years (interquartile range: 27\u201352 years) of which 118 (54%) had an\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">LDLR<\/jats:styled-content>\n                      <\/jats:italic>\n                      mutation. By 2004, when prescription data became available, 89% of mutation\u2010carrying participants were taking statins during their follow\u2010up period. Despite frequent use of lipid\u2010lowering medication, the adjusted hazard ratio of the primary end point was 1.65 (95% confidence interval, 1.17\u20132.33) in mutation\u2010carrying relatives compared with the general population cohort. The risk in non\u2013mutation\u2010carrying relatives was not different from that of the general population cohort (adjusted hazard ratio: 0.85; 95% confidence interval, 0.56\u20131.29). Comparing mutation\u2010carrying relatives with non\u2013mutation\u2010carrying relatives, the adjusted hazard ratio was 1.94 (95% confidence interval, 1.14\u20133.31). Results were driven by nonfatal events.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Heterozygous familial hypercholesterolemia relatives with an\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">LDLR<\/jats:styled-content>\n                      <\/jats:italic>\n                      mutation had an increased long\u2010term risk of adverse cardiovascular events.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.116.005435","type":"journal-article","created":{"date-parts":[[2017,6,26]],"date-time":"2017-06-26T20:20:17Z","timestamp":1498508417000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Long\u2010Term Cardiovascular Risk in Heterozygous Familial Hypercholesterolemia Relatives Identified by Cascade Screening"],"prefix":"10.1161","volume":"6","author":[{"given":"Kasper Aalb\u00e6k","family":"Kj\u00e6rgaard","sequence":"first","affiliation":[{"name":"Department of Cardiology, Aarhus University Hospital, Aarhus N, Denmark"},{"name":"Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus N, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morten Krogh","family":"Christiansen","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Aarhus University Hospital, Aarhus N, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morten","family":"Schmidt","sequence":"additional","affiliation":[{"name":"Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus N, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morten Sm\u00e6rup","family":"Olsen","sequence":"additional","affiliation":[{"name":"Department 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