<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sabe SA</submitter><funding>NHLBI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>e028623</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9973570</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>Background Sodium-glucose cotransporter-2 inhibitors are cardioprotective independent of glucose control, as demonstrated in animal models of acute myocardial ischemia and clinical trials. The functional and molecular mechanisms of these benefits in the setting of chronic myocardial ischemia are poorly defined. The purpose of this study is to determine the effects of canagliflozin therapy on myocardial perfusion, fibrosis, and function in a large animal model of chronic myocardial ischemia. Methods and Results Yorkshire swine underwent placement of an ameroid constrictor to the left circumflex artery to induce chronic myocardial ischemia. Two weeks later, pigs received either no drug (n=8) or 300 mg sodium-glucose cotransporter-2 inhibitor canagliflozin orally, daily (n=8). Treatment conti</pubmed_abstract><journal>Journal of the American Heart Association</journal><pubmed_title>Canagliflozin Improves Myocardial Perfusion, Fibrosis, and Function in a Swine Model of Chronic Myocardial Ischemia.</pubmed_title><pmcid>PMC9973570</pmcid><funding_grant_id>F32 HL160063</funding_grant_id><funding_grant_id>R56 HL133624</funding_grant_id><funding_grant_id>R01 HL046716</funding_grant_id><funding_grant_id>T32 HL160517</funding_grant_id><funding_grant_id>R01 HL128831</funding_grant_id><funding_grant_id>T32 GM065085</funding_grant_id><funding_grant_id>R01 HL133624</funding_grant_id><pubmed_authors>Xu CM</pubmed_authors><pubmed_authors>Sellke FW</pubmed_authors><pubmed_authors>Harris DD</pubmed_authors><pubmed_authors>Sabe SA</pubmed_authors><pubmed_authors>Aboulgheit A</pubmed_authors><pubmed_authors>Stanley M</pubmed_authors><pubmed_authors>Sabra M</pubmed_authors><pubmed_authors>Malhotra A</pubmed_authors><pubmed_authors>Abid MR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Canagliflozin Improves Myocardial Perfusion, Fibrosis, and Function in a Swine Model of Chronic Myocardial Ischemia.</name><description>Background Sodium-glucose cotransporter-2 inhibitors are cardioprotective independent of glucose control, as demonstrated in animal models of acute myocardial ischemia and clinical trials. The functional and molecular mechanisms of these benefits in the setting of chronic myocardial ischemia are poorly defined. The purpose of this study is to determine the effects of canagliflozin therapy on myocardial perfusion, fibrosis, and function in a large animal model of chronic myocardial ischemia. Methods and Results Yorkshire swine underwent placement of an ameroid constrictor to the left circumflex artery to induce chronic myocardial ischemia. Two weeks later, pigs received either no drug (n=8) or 300 mg sodium-glucose cotransporter-2 inhibitor canagliflozin orally, daily (n=8). Treatment conti</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T13:07:32.985Z</modification><creation>2025-04-04T13:07:32.985Z</creation></dates><accession>S-EPMC9973570</accession><cross_references><pubmed>36583437</pubmed><doi>10.1161/JAHA.122.028623</doi></cross_references></HashMap>