{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T07:21:39Z","timestamp":1791444099105,"version":"4.3.3"},"reference-count":48,"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":[[2026,2,17]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Insulin resistance (IR) and lipoprotein(a), Lp(a), are established contributors to cardiovascular disease (CVD) risk. Whether IR modifies the association between Lp(a) and CVD in primary prevention remains uncertain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">This prospective cohort study included UK Biobank participants without baseline CVD. IR at enrollment was assessed using the triglyceride\u2010glucose index (TyG). The primary outcome was first major adverse cardiovascular event, defined as peripheral arterial disease, coronary artery disease, myocardial infarction, ischemic stroke, or cardiovascular death. Cox models estimated adjusted hazard ratios (aHRs) with 95% CIs for log\u2010transformed Lp(a) and TyG, adjusting for each other. Lp(a) was categorized as &lt;125 or \u2265125\u2009nmol\/L; high IR was TyG \u226575th cohort percentile. Participants were stratified into 4 joint Lp(a)\/IR groups using low Lp(a)\/low IR as reference.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Among 328\u2009031 participants (mean age 56.4\u2009years; 54.7% women), 26\u2009865 CVD events occurred over 14.6\u2009years median follow\u2010up (interquartile range 13.7\u201315.4). Per 1\u2010SD increase, aHRs were 1.08 (95% CI, 1.06\u20131.09) for log\u2010Lp(a) and 1.06 (95% CI, 1.04\u20131.07) for TyG, each adjusted for the other. The\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      \u2010value for the multiplicative interaction between TyG and Lp(a) was 0.07. Relative to reference, aHRs (95% CI) were 1.15 (1.10\u20131.20) for \u2265125\/low IR, 1.09 (1.06\u20131.12) for &lt;125\/high IR, and 1.32 (1.24\u20131.41) for \u2265125\/high IR.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Lp(a) and IR each independently contribute to cardiovascular risk, with a combination offering improved risk stratification. This suggests that accounting for IR may enhance the assessment of Lp(a)\u2010associated risk in the context of primary CVD prevention setting.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.042361","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T10:58:00Z","timestamp":1770807480000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Lipoprotein(a), Insulin Resistance, and Cardiovascular Disease in the UK Biobank"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7085-3373","authenticated-orcid":false,"given":"Richard","family":"Kazibwe","sequence":"first","affiliation":[{"name":"Wake Forest University School of Medicine","place":["Winston\u2010Salem, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5302-0828","authenticated-orcid":false,"given":"Christopher 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