{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T12:53:26Z","timestamp":1768568006602,"version":"3.49.0"},"posted":{"date-parts":[[2024,7,10]]},"group-title":"Cardiovascular Medicine","reference-count":66,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,7,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>\n                    High Lp(a) levels contribute to atherosclerotic cardiovascular disease and are tightly regulated by the\n                    <jats:italic>LPA<\/jats:italic>\n                    gene. Lp(a) levels have an inverse correlation with\n                    <jats:italic>LPA<\/jats:italic>\n                    Kringle IV Type-2 (KIV-2) copy number (CN). Black (B) and Hispanic (H) individuals exhibit higher levels of Lp(a), and rates of CVD compared to non-Hispanic Whites (NHW). Therefore, we investigated genetic variations in the\n                    <jats:italic>LPA<\/jats:italic>\n                    KIV-2 region across three ancestries and their associations with metabolic risk factors.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Using published pipelines, we analyzed a multi-ethnic whole exome dataset comprising 3,817 participants from the Washington Heights and Inwood Columbia Aging Project (WHICAP): 886 [NHW (23%), 1,811 Caribbean (C) H (47%), and 1,120 B individuals (29%). Rare and common variants (alternative allele carrier frequency, CF &lt; 0.01 or &gt; 0.99 and 0.01 &lt; CF &lt; 0.99, respectively) were identified and KIV-2 CN estimated. The associations of variants and CN with history of heart disease, hypertension (HTN), stroke, lipid levels and clinical diagnosis of Alzheimer\u2019s disease (AD) was assessed. A small pilot provided in-silico validation of study findings.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    We report 1421 variants in the\n                    <jats:italic>LPA<\/jats:italic>\n                    KIV-2 repeat region, comprising 267 exonic and 1154 intronic variants. 61.4% of the exonic variants have not been previously described. Three novel exonic variants significantly increase the risk of HTN across all ethnic groups: 4785-C\/A (frequency = 78%, odds ratio [OR] = 1.45, p = 0.032), 727-T\/C (frequency = 96%, OR = 2.11, p = 0.032), and 723-A\/G (frequency = 96%, OR = 1.97, p = 0.038). Additionally, six intronic variants showed associations with HTN: 166-G\/A, 387-G\/C, 402-G\/A, 4527-A\/T, 4541-G\/A, and 4653-A\/T. One intronic variant, 412-C\/T, was associated with decreased blood glucose levels (frequency = 72%, \u03b2 = \u221214.52, p = 0.02).\n                  <\/jats:p>\n                  <jats:p>\n                    Three of the associations were not affected after adjusting for\n                    <jats:italic>LPA<\/jats:italic>\n                    KIV-2 CN: 412-C\/T (\u03b2 = \u221214.2, p = 0.03), 166-G\/A (OR = 1.41, p = 0.05), and 387-G\/C (OR = 1.40, p = 0.05). KIV CN itself was significantly associated with 314 variants and was negatively correlated with plasma total cholesterol levels.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>\n                    In three ancestry groups, we identify novel rare and common\n                    <jats:italic>LPA<\/jats:italic>\n                    KIV-2 region variants. We report new associations of variants with HTN and Glucose levels. These results underscore the genetic complexity of the\n                    <jats:italic>LPA<\/jats:italic>\n                    KIV-2 region in influencing cardiovascular and metabolic health, suggesting potential genetic regulation of pathways that can be studied for research and therapeutic interventions.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Clinical Perspective<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>\n                        Lp(a) levels are mostly controlled by the\n                        <jats:italic>LPA<\/jats:italic>\n                        gene and are higher in Blacks and Hispanics.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:italic>Novel LPA<\/jats:italic>\n                        KIV-2 variants found in three ancestry groups, including data on Caribbean Hispanics, show strong positive associations to hypertension and negative associations to glucose levels.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Further characterization of these variants and identifying links to disease can help precision medicine efforts to understand disease mechanisms in all populations.<\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>","DOI":"10.1101\/2024.07.09.24310176","type":"posted-content","created":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T13:15:18Z","timestamp":1720617318000},"source":"Crossref","is-referenced-by-count":0,"title":["Ancestry specific distribution of LPA Kringle IV-Type-2 genetic variants highlight associations to apo(a) copy number, glucose, and hypertension"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-8722-3437","authenticated-orcid":false,"given":"Yihao","family":"Li","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2229-1120","authenticated-orcid":false,"given":"Florian","family":"Kronenberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5677-8979","authenticated-orcid":false,"given":"Stefan","family":"Coassin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Badri","family":"Vardarajan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6746-4569","authenticated-orcid":false,"given":"Gissette","family":"Reyes-Soffer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"54368","reference":[{"key":"2024071204550433000_2024.07.09.24310176v1.1","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R067314"},{"key":"2024071204550433000_2024.07.09.24310176v1.2","doi-asserted-by":"crossref","unstructured":"Gencer B KF , Stroes ES , Mach F . 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