{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T10:58:04Z","timestamp":1792666684361,"version":"4.5.0"},"reference-count":68,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,5,21]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Sepsis is the overwhelming host response to infection leading to shock and multiple organ dysfunction. Cardiovascular complications greatly increase sepsis\u2010associated mortality. Although murine models are routinely used for preclinical studies, the benefit of using genetically engineered mice in sepsis is countered by discrepancies between human and mouse sepsis pathophysiology. Therefore, recent guidelines have called for standardization of preclinical methods to document organ dysfunction. We investigated the course of cardiac dysfunction and myocardial load in different mouse models of sepsis to identify the optimal measurements for early systolic and diastolic dysfunction.<\/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\">\n              We performed speckle\u2010tracking echocardiography and assessed blood pressure, plasma inflammatory cytokines, lactate, B\u2010type natriuretic peptide, and survival in mouse models of endotoxemia or polymicrobial infection (cecal ligation and puncture, [\n              <jats:styled-content style=\"fixed-case\">CLP<\/jats:styled-content>\n              ]) of moderate and high severity. We observed that myocardial strain and cardiac output were consistently impaired early in both sepsis models. Suppression of cardiac output was associated with systolic dysfunction in endotoxemia or combined systolic dysfunction and reduced preload in the\n              <jats:styled-content style=\"fixed-case\">CLP<\/jats:styled-content>\n              model. We found that cardiac output at 2\u00a0hours post\u2010\n              <jats:styled-content style=\"fixed-case\">CLP<\/jats:styled-content>\n              is a negative prognostic indicator with high sensitivity and specificity that predicts mortality at 48\u00a0hours. Using a known antibiotic (ertapenem) treatment, we confirmed that this approach can document recovery.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We propose a non\u2010invasive approach for assessment of cardiac function in sepsis and myocardial strain and strain rate as preferable measures for monitoring cardiovascular function in sepsis mouse models. We further show that the magnitude of cardiac output suppression 2\u00a0hours post\u2010\n              <jats:styled-content style=\"fixed-case\">CLP<\/jats:styled-content>\n              can be used to predict mortality.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.012260","type":"journal-article","created":{"date-parts":[[2019,5,21]],"date-time":"2019-05-21T17:02:34Z","timestamp":1558458154000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":61,"title":["Myocardial Strain and Cardiac Output are Preferable Measurements for Cardiac Dysfunction and Can Predict Mortality in Septic Mice"],"prefix":"10.1161","volume":"8","author":[{"given":"Matthew","family":"Hoffman","sequence":"first","affiliation":[{"name":"Center for Translational Medicine and Department of Pharmacology Lewis Katz School of Medicine Temple University Philadelphia PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ioannis D.","family":"Kyriazis","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and Department of Pharmacology Lewis Katz School of Medicine Temple University Philadelphia PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna M.","family":"Lucchese","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and Department of Pharmacology Lewis Katz School of Medicine Temple University Philadelphia PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudio","family":"de Lucia","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and Department of Pharmacology Lewis Katz School of Medicine Temple University Philadelphia PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michela","family":"Piedepalumbo","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and Department of Pharmacology Lewis Katz School of Medicine Temple University Philadelphia PA"},{"name":"Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences University of Campania \u201cLuigi Vanvitelli\u201d Naples Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Bauer","sequence":"additional","affiliation":[{"name":"Department for Anesthesiology and Intensive Care Medicine Friedrich\u2010Schiller\u2010University Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. 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