<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Algranati D</submitter><funding>NHLBI NIH HHS</funding><pagination>H1090-100</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3064294</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>300(3)</volume><pubmed_abstract>Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in de</pubmed_abstract><journal>American journal of physiology. Heart and circulatory physiology</journal><pubmed_title>Why is the subendocardium more vulnerable to ischemia? A new paradigm.</pubmed_title><pmcid>PMC3064294</pmcid><funding_grant_id>HL-055554-12</funding_grant_id><pubmed_authors>Lanir Y</pubmed_authors><pubmed_authors>Kassab GS</pubmed_authors><pubmed_authors>Algranati D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Why is the subendocardium more vulnerable to ischemia? A new paradigm.</name><description>Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in de</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Mar</publication><modification>2025-05-29T20:58:52.63Z</modification><creation>2025-05-29T20:58:52.63Z</creation></dates><accession>S-EPMC3064294</accession><cross_references><pubmed>21169398</pubmed><doi>10.1152/ajpheart.00473.2010</doi></cross_references></HashMap>