{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T01:38:36Z","timestamp":1790386716382,"version":"4.1.0"},"reference-count":64,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2025,3,18]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Classically, hypertrophic cardiomyopathy (HCM) has been viewed as a single-gene (monogenic) disease caused by pathogenic variants in sarcomere genes. Pathogenic sarcomere variants are individually rare and convey high risk for developing HCM (highly penetrant). Recently, important polygenic contributions have also been characterized. Low penetrance sarcomere variants (LowSVs) at intermediate frequencies and effect sizes have not been systematically investigated. We hypothesize that LowSVs may be common in HCM with substantial influence on disease risk and severity.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              Among all sarcomere variants observed in the Sarcomeric Human Cardiomyopathy Registry (SHaRe), we identified putative LowSVs defined by (1) population frequency greater than expected for highly penetrant (monogenic) HCM (allele frequency &gt;5\u00d710\n              <jats:sup>-5<\/jats:sup>\n              in the Genome Aggregation Database, gnomAD) and (2) moderate enrichment (&gt;2\u00d7) in patients with HCM compared with gnomAD. LowSVs were examined for their association with disease severity and clinical outcomes. Functional effects of selected LowSVs were assessed using induced pluripotent stem cell\u2013derived cardiomyocytes. Association of LowSVs with HCM-adjacent traits in the general population was tested using UK Biobank cardiac magnetic resonance imaging data.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Among 6045 patients and 1159 unique variants in sarcomere genes, 12 LowSVs were identified. LowSVs were collectively common in the general population (1:350) and moderately enriched in HCM (aggregate odds ratio, 14.9 [95% CI, 12.5\u201317.9]). Isolated LowSVs were associated with an older age of HCM diagnosis and fewer adverse events. However, LowSVs in combination with a pathogenic sarcomere variant conferred higher morbidity (eg, composite adverse event hazard ratio, 5.4 [95% CI, 3.0\u20139.8] versus single pathogenic sarcomere variant, 2.0 [95% CI, 1.8\u20132.2];\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001). An intermediate functional impact was validated for 2 specific LowSVs\u2014\n              <jats:italic>MYBPC3<\/jats:italic>\n              c.442G&gt;A (partial splice gain) and\n              <jats:italic>TNNT2<\/jats:italic>\n              c.832C&gt;T (intermediate effect on contractile mechanics). Cardiac magnetic resonance imaging analysis of the general population revealed 5 of 12 LowSVs were significantly associated with HCM-adjacent traits without overt HCM.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>This study establishes a new class of low penetrance sarcomere variants that are relatively common in the population. When penetrant, isolated LowSVs cause mild HCM. In combination with pathogenic sarcomere variants, LowSVs markedly increase disease severity, supporting a clinically significant additive effect. Last, LowSVs also contribute to age-related remodeling even in the absence of overt HCM.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.124.069398","type":"journal-article","created":{"date-parts":[[2024,12,5]],"date-time":"2024-12-05T10:00:36Z","timestamp":1733392836000},"page":"783-798","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Low Penetrance Sarcomere Variants Contribute to Additive Risk in Hypertrophic Cardiomyopathy"],"prefix":"10.1161","volume":"151","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1049-8351","authenticated-orcid":true,"given":"Joshua K.","family":"Meisner","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Cardiology (J.K.M., M.W.R.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8782-9342","authenticated-orcid":true,"given":"Aaron","family":"Renberg","sequence":"additional","affiliation":[{"name":"Cellular and Molecular Biology Program, Medical School (A.R.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5915-9492","authenticated-orcid":true,"given":"Eric D.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Cardiovascular Medicine (E.D.S., Y.-C.T., B.E., A.B., O.L.M., S.S., A.S.H.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0373-1290","authenticated-orcid":true,"given":"Yao-Chang","family":"Tsan","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Cardiovascular Medicine (E.D.S., Y.-C.T., B.E., A.B., O.L.M., S.S., A.S.H.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5353-6683","authenticated-orcid":true,"given":"Brynn","family":"Elder","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Cardiovascular Medicine (E.D.S., Y.-C.T., B.E., A.B., O.L.M., S.S., A.S.H.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abbey","family":"Bullard","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Cardiovascular Medicine (E.D.S., Y.-C.T., B.E., A.B., O.L.M., S.S., A.S.H.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Owen L.","family":"Merritt","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Cardiovascular Medicine (E.D.S., Y.-C.T., B.E., A.B., O.L.M., S.S., A.S.H.), University of Michigan, Ann Arbor."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean L.","family":"Zheng","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute and Medical Research Council Laboratory of Medical Sciences, Imperial College London, United Kingdom (S.L.Z., J.S.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6458-5421","authenticated-orcid":true,"given":"Neal K.","family":"Lakdawala","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, Brigham and Women\u2019s Hospital, Boston, MA (N.K.L., C.Y.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9669-8495","authenticated-orcid":true,"given":"Anjali T.","family":"Owens","sequence":"additional","affiliation":[{"name":"Penn Center for Inherited Cardiovascular Disease, Hospital of the University of Pennsylvania &amp; 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