{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T11:46:29Z","timestamp":1788522389869,"version":"build-2803163510"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2021,3,16]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Obesity and hypertension are risk factors for myocardial infarction (MI); however, their potential interactions on post\u2010MI outcomes are unclear. We examined interactions of obesity and hypertensionon post\u2010MI function, remodeling, metabolic changes, and recovery.<\/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\">Male and female C57BL\/6J mice were provided standard chow or high\u2010fat\/fructose diet for 8\u00a0weeks and then infused with angiotensin II for 2\u00a0weeks to induce hypertension. MI was then induced by surgical ligation of the left coronary artery for 7\u00a0days. Obesity alone did not cause cardiac injury or exacerbate hypertension\u2010induced cardiac dysfunction. After MI, however, obese\u2010normotensive mice had lower survival rates compared with chow\u2010fed mice (56% versus 89% males; 54% versus 75% females), which were further decreased by hypertension (29% males; and 35% females). Surviving obese\u2010normotensive males displayed less left ventricular dilation and pulmonary congestion compared with chow\u2010fed males after MI; hypertension reversed left ventricular dilation because of high\u2010fat\/fructose diet and promoted significant pulmonary congestion compared with chow\u2010fed controls. Obese\u2010normotensive males displayed higher left ventricular \u03b1\u2010MHC (alpha\u2010myosin heavy chain) protein, phosphorylated Akt (protein kinase B) and AMPK (adenosine\u2010monophosphate activated kinase), PPAR\u2010\u03b3 (peroxisome proliferator activated receptor gamma), and plasma adiponectin levels after MI, indicating favorable contractile and metabolic changes. However, these favorable contractile and metabolic changes were attenuated by hypertension. Obese\u2010hypertensive males also had lower levels of collagen in the infarcted region, indicating decreased ability to promote an adaptive wound healing response to MI.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Obesity reduces post\u2010MI survival but is associated with improved post\u2010MI cardiac function and metabolism in surviving normotensive mice. When hypertension accompanies obesity, favorable metabolic pathways associated with obesity are attenuated and post\u2010MI cardiac function and remodeling are adversely impacted.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.120.018212","type":"journal-article","created":{"date-parts":[[2021,3,5]],"date-time":"2021-03-05T10:06:35Z","timestamp":1614938795000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":15,"title":["Interaction of Obesity and Hypertension on Cardiac Metabolic Remodeling and Survival Following Myocardial Infarction"],"prefix":"10.1161","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5973-3071","authenticated-orcid":false,"given":"Alan J.","family":"Mouton","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics University of Mississippi Medical Center Jackson MS"},{"name":"Mississippi Center for Obesity Research University of Mississippi Medical Center 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