{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T16:31:46Z","timestamp":1782837106248,"version":"3.54.5"},"reference-count":64,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Genomic and Precision Medicine"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Rare variant genetics have been associated with peripartum cardiomyopathy (PPCM), but the role of genetics remains unsettled. The study sought to compare dilated cardiomyopathy (DCM) genetic risk in first-degree relatives (FDRs) of female patients (probands) with DCM or PPCM to gain causal inference, and to assess DCM-relevant rare variant prevalence in DCM\/PPCM probands and population controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>Clinical and genetic data were analyzed from the DCM Precision Medicine Study. Risk of DCM or partial DCM, where partial DCM was defined as left ventricular enlargement or a left ventricular ejection fraction of &lt;50%, was estimated in 665 FDRs from 452 female probands, all of whom had been pregnant; 67 had PPCM and 385 had DCM; prevalence of pathogenic, likely pathogenic, or uncertain significance variants was estimated among probands.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>The risk of DCM\/partial DCM for FDRs of PPCM probands was similar to that for FDRs of DCM probands (hazard ratio, 0.77 [95% CI, 0.47\u20131.28]). Estimated DCM prevalence among the lowest-risk FDRs of non-Hispanic European ancestry probands with PPCM (7.0% [95% CI, 0%\u201314.1%] females, 9.0% [95% CI, 1.6%\u201316.3%] males) exceeded population estimates from a UK Biobank study (0.30% females, 0.63% males). Estimated prevalences of a pathogenic, likely pathogenic, or uncertain significance variant among African ancestry and European ancestry probands with PPCM were 55.4% (95% CI, 33.1%\u201377.7%) and 66.0% (95% CI, 38.6%\u201393.3%), respectively. The estimated prevalence of pathogenic\/likely pathogenic variants among European ancestry PPCM probands (26.6% [95% CI, 12.6%\u201340.6%]) exceeded a population estimate from a UK Biobank study (0.6%).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>The risk of DCM\/partial DCM among FDRs was similar regardless of whether their probands had PPCM or DCM. Also, DCM-relevant rare variant findings for females with PPCM or DCM were similar and greater than in population controls, suggesting a similar causal basis for PPCM and DCM. These findings underscore the need for genetic evaluations in all patients with PPCM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>REGISTRATION:<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      ; Unique identifier: NCT03037632.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circgen.125.005541","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T09:00:19Z","timestamp":1774429219000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Evaluation of Women With Peripartum or Dilated Cardiomyopathy and Their First-Degree Relatives: The DCM Precision Medicine Study"],"prefix":"10.1161","volume":"19","clinical-trial-number":[{"clinical-trial-number":"nct03037632","registry":"10.18810\/clinical-trials-gov"}],"author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0507-2412","authenticated-orcid":true,"given":"Evan P.","family":"Kransdorf","sequence":"first","affiliation":[{"name":"Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (E.P.K., R.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rashmi","family":"Jain","sequence":"additional","affiliation":[{"name":"Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (E.P.K., R.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-3833-1833","authenticated-orcid":true,"given":"Jonathan O.","family":"Mead","sequence":"additional","affiliation":[{"name":"Division of Human Genetics, Department of Internal Medicine (J.O.M., J. Cowan, P.P., J. Cao, N.S.H., E.J., H.N., D.D.K., R.E.H.), The Ohio State University, Columbus."},{"name":"The Davis Heart &amp; Lung Research Institute (J.O.M., G.H., J. Cowan, P.P., J. Cao, N.S.H., E.J., H.N., D.D.K., R.E.H.), The Ohio State University, Columbus."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4189-6136","authenticated-orcid":true,"given":"Garrie","family":"Haas","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine (G.H., R.E.H.), The Ohio State University, Columbus."},{"name":"The Davis Heart &amp; Lung Research Institute (J.O.M., G.H., J. Cowan, P.P., J. 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