{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T08:59:37Z","timestamp":1770973177218,"version":"3.50.1"},"reference-count":56,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2025,6,3]]},"abstract":"<jats:sec id=\"jah310886-sec-0001\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Ischemic cardiomyopathy with comorbid obstructive sleep apnea syndrome is associated with worse long\u2010term outcomes. Intermittent hypoxia (IH), a key feature of obstructive sleep apnea, exacerbates sympathetic activity, hastening cardiac dysfunction and remodeling in ischemic cardiomyopathy rat models. This study explores whether targeted cardiac sympathetic denervation (CSD) can limit IH\u2010induced progression of ischemic cardiomyopathy.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310886-sec-0002\" xml:lang=\"en\">\n            <jats:title>Methods<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Male Wistar rats underwent CSD, through ablation of the left middle cervical and stellate ganglions, and simultaneously myocardial infarction, via permanent left coronary artery ligation. Three days post surgery, rats were exposed to IH (21%\u20135% fraction of inspired O\n              <jats:sub>2<\/jats:sub>\n              , 60\u2010second cycle, 8\u2009hours\/day) or normoxia. At 6\u2009weeks, calcium transient, sarcomere shortening, and adrenergic reserve in response to isoproterenol (100\u2009nmol\/L) were assessed in isolated cardiomyocytes. At 14\u2009weeks, sympathovagal balance, cardiac function, and remodeling were evaluated.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310886-sec-0003\" xml:lang=\"en\">\n            <jats:title>Results<\/jats:title>\n            <jats:p xml:lang=\"en\">Post myocardial infarction, CSD prevented IH\u2010induced blunting of cardiomyocyte response to isoproterenol challenge and reduced cardiac sympathetic activity. In hypoxic animals, CSD reduced post\u2010myocardial infarction alterations in long\u2010term ejection fraction and mitigated cardiomyocyte hypertrophy and apoptosis. Transcriptomic analysis unveiled that CSD triggered biological processes related to cardiac repair and regeneration. Immunohistochemistry further supported these findings, demonstrating increased cardiomyocyte proliferation in the hypoxic group, as indicated by elevated Ki67 expression colocalized with MF20 markers.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310886-sec-0004\" xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Our data demonstrate that CSD prevents IH\u2010induced sympathetic hyperactivity, depletion of cardiac adrenergic reserve, and deterioration of cardiac function in a rat model of ischemic cardiomyopathy. This study highlights the intricate interplay between sympathetic activity and hypoxia in cardiac regeneration and underscores the importance of managing sympathetic hyperactivity in ischemic cardiomyopathy, particularly in the context of comorbid obstructive sleep apnea.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.124.038781","type":"journal-article","created":{"date-parts":[[2025,5,23]],"date-time":"2025-05-23T10:49:32Z","timestamp":1747997372000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Cardiac Sympathetic Denervation Mitigated Ischemic Cardiomyopathy Progression in a Rat Model of Sleep Apnea"],"prefix":"10.1161","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6380-540X","authenticated-orcid":false,"given":"Maximin","family":"D\u00e9trait","sequence":"first","affiliation":[{"name":"Univ. 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