{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T03:06:35Z","timestamp":1784603195203,"version":"3.55.0"},"reference-count":18,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T00:00:00Z","timestamp":1709856000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2024,4]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>Restoring ischaemic myocardial tissue perfusion is crucial for minimizing infarct size. Acute mechanical left ventricular (LV) support has been suggested to improve infarct tissue perfusion. However, its regulatory mechanism remains unclear. We investigated the physiological mechanisms in six Yorkshire pigs, which were subjected to 90\u2010min balloon occlusion of the left anterior descending artery. During the acute reperfusion phase, LV support using an Impella heart pump was initiated. LV pressure, coronary flow and pressure of the infarct artery were simultaneously recorded to evaluate the impact of LV support on coronary physiology. Coronary wave intensity was calculated to understand the forces regulating coronary flow. Significant increases in coronary flow velocity and its area under the curve were found after mechanical LV support. Among the coronary flow\u2010regulating factors, coronary pressure was increased mainly during the late diastolic phase with less pulsatility. Meanwhile, LV pressure was reduced throughout diastole resulting in significant and consistent elevation of coronary driving pressure. Interestingly, the duration of diastole was prolonged with LV support. In the wave intensity analysis, the duration between backward suction and pushing waves was extended, indicating that earlier myocardial relaxation and delayed contraction contributed to the extension of diastole. In conclusion, mechanical LV support increases infarct coronary flow by extending diastole and augmenting coronary driving pressure. These changes were mainly driven by reduced LV diastolic pressure, indicating\u00a0that the key regulator of coronary flow under mechanical LV support is downstream of the coronary artery, rather than upstream. Our study highlights the importance of LV diastolic pressure in infarct coronary flow regulation.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15973-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Restoring ischaemic myocardial tissue perfusion is crucial for minimizing infarct size. Although mechanical left ventricular (LV) support has been suggested to improve infarct coronary flow, its specific mechanism remains to be clarified.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>LV support reduced LV pressure, and elevated coronary pressure during the late diastolic phase, resulting in high coronary driving pressure.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>This study demonstrated for the first time that mechanical LV support extends diastolic phase, leading to increased infarct coronary flow.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Future studies should evaluate the correlation between improved infarct coronary flow and resulting infarct size.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp285586","type":"journal-article","created":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T17:19:57Z","timestamp":1709918397000},"page":"1669-1680","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Reduction of left ventricular diastolic pressure as a key regulator of infarct coronary flow under mechanical left ventricular support"],"prefix":"10.1113","volume":"602","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3841-9117","authenticated-orcid":false,"given":"Tomoki","family":"Sakata","sequence":"first","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"},{"name":"Division of Cardiac Surgery, Department of Surgery Thomas Jefferson University Hospital  Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1328-1708","authenticated-orcid":false,"given":"Spyros A.","family":"Mavropoulos","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata","family":"Mazurek","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco J.","family":"Romeo","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anjali J.","family":"Ravichandran","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonas M.","family":"Marx","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7678-3652","authenticated-orcid":false,"given":"Taro","family":"Kariya","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8287-3483","authenticated-orcid":false,"given":"Kiyotake","family":"Ishikawa","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,3,8]]},"reference":[{"key":"e_1_2_5_2_1","first-page":"281","volume-title":"A pig model of myocardial infarction: Catheter\u2010based approaches","author":"Bikou O.","year":"2018"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2006.08.054"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.603050"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12872-020-01673-0"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.117.310901"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2014.11.004"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.118.038269"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2022.08.011"},{"issue":"11","key":"e_1_2_5_10_1","first-page":"873","article-title":"Mechanical pre\u2010conditioning with acute circulatory support before reperfusion limits infarct size in acute myocardial infarction","volume":"3","author":"Kapur N. 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