{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T20:37:56Z","timestamp":1793738276681,"version":"4.6.1"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"16","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2020,8,18]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>BACKGROUND<\/jats:title>\n            <jats:p xml:lang=\"en\">Sleep\u2010disordered breathing is associated with a poor prognosis (mortality) in patients with ischemic cardiomyopathy. The understanding of mechanisms linking intermittent hypoxia (IH), the key feature of sleep\u2010disordered breathing, to ischemic cardiomyopathy progression is crucial for identifying specific actionable therapeutic targets. The aims of the present study were (1) to evaluate the impact of IH on the time course evolution of cardiac remodeling and contractile dysfunction in a rat model of ischemic cardiomyopathy; and (2) to determine the impact of IH on sympathetic activity, hypoxia inducible factor\u20101 activation, and endoplasmic reticulum stress in the time course of ischemic cardiomyopathy progression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>METHODS AND RESULTS<\/jats:title>\n            <jats:p xml:lang=\"en\">Ischemic cardiomyopathy was induced by a permanent ligature of the left coronary artery in male Wistar rats (rats with myocardial infarction). Rats with myocardial infarction were then exposed to either IH or normoxia for up to 12\u00a0weeks. Cardiac remodeling and function were analyzed by Sirius red and wheat germ agglutinin staining, ultrasonography, and cardiac catheterization. Sympathetic activity was evaluated by spectral analysis of blood pressure variability. Hypoxia\u2010inducible factor\u20101\u03b1 activation and burden of endoplasmic reticulum stress were characterized by Western blots. Long\u2010term IH exposure precipitated cardiac remodeling (hypertrophy and interstitial fibrosis) and contractile dysfunction during the time course evolution of ischemic cardiomyopathy in rodents. Among associated mechanisms, we identified the early occurrence and persistence of sympathetic activation, associated with sustained hypoxia\u2010inducible factor\u20101\u03b1 expression and a delayed pro\u2010apoptotic endoplasmic reticulum stress.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>CONCLUSIONS<\/jats:title>\n            <jats:p xml:lang=\"en\">Our data provide the demonstration of the deleterious impact of IH on post\u2013myocardial infarction remodeling and contractile dysfunction. Further studies are needed to evaluate whether targeting sympathetic nervous system or HIF\u20101 overactivities could limit these effects and improve management of coexisting ischemic cardiomyopathy and sleep\u2010disordered breathing.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.120.016369","type":"journal-article","created":{"date-parts":[[2020,8,4]],"date-time":"2020-08-04T08:54:33Z","timestamp":1596531273000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":33,"title":["Intermittent Hypoxia Triggers Early Cardiac Remodeling and Contractile Dysfunction in the Time\u2010Course of Ischemic Cardiomyopathy in Rats"],"prefix":"10.1161","volume":"9","author":[{"given":"Guillaume","family":"Bourdier","sequence":"first","affiliation":[{"name":"Univ. 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