{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:01:08Z","timestamp":1790870468815,"version":"4.1.0"},"reference-count":24,"publisher":"Wiley","license":[{"start":{"date-parts":[[2022,9,19]],"date-time":"2022-09-19T00:00:00Z","timestamp":1663545600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"The Jon Moulton Charity Trust","award":["203814\/Z\/16\/A, DN, APD"],"award-info":[{"award-number":["203814\/Z\/16\/A, DN, APD"]}]},{"name":"The Jon Moulton Charity Trust","award":["TG\/18\/4\/33770"],"award-info":[{"award-number":["TG\/18\/4\/33770"]}]},{"name":"The Jon Moulton Charity Trust","award":["RG64226"],"award-info":[{"award-number":["RG64226"]}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["203814\/Z\/16\/A, DN, APD"],"award-info":[{"award-number":["203814\/Z\/16\/A, DN, APD"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["TG\/18\/4\/33770"],"award-info":[{"award-number":["TG\/18\/4\/33770"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["RG64226"],"award-info":[{"award-number":["RG64226"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100018956","name":"NIHR Cambridge Biomedical Research Centre","doi-asserted-by":"publisher","award":["203814\/Z\/16\/A, DN, APD"],"award-info":[{"award-number":["203814\/Z\/16\/A, DN, APD"]}],"id":[{"id":"10.13039\/501100018956","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100018956","name":"NIHR Cambridge Biomedical Research Centre","doi-asserted-by":"publisher","award":["TG\/18\/4\/33770"],"award-info":[{"award-number":["TG\/18\/4\/33770"]}],"id":[{"id":"10.13039\/501100018956","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100018956","name":"NIHR Cambridge Biomedical Research Centre","doi-asserted-by":"publisher","award":["RG64226"],"award-info":[{"award-number":["RG64226"]}],"id":[{"id":"10.13039\/501100018956","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000735","name":"University of Cambridge","doi-asserted-by":"publisher","award":["203814\/Z\/16\/A, DN, APD"],"award-info":[{"award-number":["203814\/Z\/16\/A, DN, APD"]}],"id":[{"id":"10.13039\/501100000735","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000735","name":"University of Cambridge","doi-asserted-by":"publisher","award":["TG\/18\/4\/33770"],"award-info":[{"award-number":["TG\/18\/4\/33770"]}],"id":[{"id":"10.13039\/501100000735","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000735","name":"University of Cambridge","doi-asserted-by":"publisher","award":["RG64226"],"award-info":[{"award-number":["RG64226"]}],"id":[{"id":"10.13039\/501100000735","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Interventional Cardiology"],"published-print":{"date-parts":[[2022,9,19]]},"abstract":"<jats:p>Objective. Coronary microvascular dysfunction (CMD) can complicate successful percutaneous coronary intervention (PCI). The potent endogenous vasoconstrictor peptide Endothelin-1 (ET-1) may be an important mediator. To investigate the mechanism, we sought to define the peri-procedural trans-myocardial gradient (TMG-coronary sinus minus aortic root levels) of ET-1 and its precursor peptide \u2013 Big ET-1. We then assessed correlation with pressure-wire indices of CMD: coronary flow reserve (CFR) and index of microvascular resistance (IMR). Methods. Paired blood samples from the guide catheter and coronary sinus were collected before and after pressure-wire-guided PCI from patients with stable angina. Plasma was analysed using a specific enzyme-linked immunosorbent assay for quantification of ET-1 peptides and correlated with pressure-wire data. Non normally distributed continuous variables are presented as median [IQR]. Results. ET-1 and Big ET-1 increased post-PCI in the aorta (ET-1: 0.98 [0.76\u20131.26] pg\/ml to 1.20 [1.03\u20131.67] pg\/ml, <jats:inline-formula>\n                     <a:math xmlns:a=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\">\n                        <a:mi>P<\/a:mi>\n                        <a:mo>&lt;<\/a:mo>\n                        <a:mn>0.001<\/a:mn>\n                     <\/a:math>\n                  <\/jats:inline-formula> and Big ET-1: 2.74 [1.78\u20132.50] pg\/ml to 3.36 [2.33\u20133.97] pg\/ml, <jats:inline-formula>\n                     <c:math xmlns:c=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\">\n                        <c:mi>P<\/c:mi>\n                        <c:mo>&lt;<\/c:mo>\n                        <c:mn>0.001<\/c:mn>\n                     <\/c:math>\n                  <\/jats:inline-formula>) and coronary sinus (ET-1: 1.00 [0.81\u20131.28] pg\/ml to 1.09 [0.91\u20131.30] pg\/ml, <jats:inline-formula>\n                     <e:math xmlns:e=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\">\n                        <e:mi>P<\/e:mi>\n                        <e:mo>=<\/e:mo>\n                        <e:mn>0.03<\/e:mn>\n                     <\/e:math>\n                  <\/jats:inline-formula> and Big ET-1: 2.89 [1.95\u20133.83] pg\/ml to 3.56 [2.66\u20134.83] pg\/ml, <jats:inline-formula>\n                     <g:math xmlns:g=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\">\n                        <g:mi>P<\/g:mi>\n                        <g:mo>=<\/g:mo>\n                        <g:mn>0.01<\/g:mn>\n                     <\/g:math>\n                  <\/jats:inline-formula>). TMG of ET-1 shifted negatively compared with baseline following PCI reflecting significantly increased extraction (0.03 [\u22120.12\u20130.17] pg\/ml pre-PCI versus \u22120.16 [\u22120.36\u20130.07] pg\/ml post-PCI, <jats:inline-formula>\n                     <i:math xmlns:i=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\">\n                        <i:mi>P<\/i:mi>\n                        <i:mo>=<\/i:mo>\n                        <i:mn>0.01<\/i:mn>\n                     <\/i:math>\n                  <\/jats:inline-formula>). Increased ET-1 trans-myocardial extraction correlated with higher IMR (Pearson\u2019s r\u2009=\u20090.293, <jats:inline-formula>\n                     <k:math xmlns:k=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\">\n                        <k:mi>P<\/k:mi>\n                        <k:mo>=<\/k:mo>\n                        <k:mn>0.02<\/k:mn>\n                     <\/k:math>\n                  <\/jats:inline-formula>) and increased hyperemic transit time (Pearson\u2019s r\u2009=\u20090.333, <jats:inline-formula>\n                     <m:math xmlns:m=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\">\n                        <m:mi>P<\/m:mi>\n                        <m:mo>&lt;<\/m:mo>\n                        <m:mn>0.01<\/m:mn>\n                     <\/m:math>\n                  <\/jats:inline-formula>). In subgroup analysis, mean ET-1 trans-myocardial extraction was higher amongst patients with high IMR compared with low IMR (0.73\u2009pg\/ml, SD:0.78 versus 0.17\u2009pg\/ml, SD:0.42, <jats:inline-formula>\n                     <o:math xmlns:o=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\">\n                        <o:mi>P<\/o:mi>\n                        <o:mo>=<\/o:mo>\n                        <o:mn>0.02<\/o:mn>\n                     <\/o:math>\n                  <\/jats:inline-formula>). There was additionally a numerical trend towards increased ET-1 trans-myocardial extraction in subgroups of patients with low CFR and in patients with Type 4a Myocardial Infarction, albeit not reaching statistical significance. Conclusions. Circulating ET-1 increases post-PCI and upregulated ET-1 trans-myocardial extraction contributes to increased microcirculatory resistance.<\/jats:p>","DOI":"10.1155\/2022\/9154048","type":"journal-article","created":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T03:20:09Z","timestamp":1663644009000},"page":"1-7","source":"Crossref","is-referenced-by-count":2,"title":["Trans-myocardial Extraction of Endothelin-1 Correlates with Increased Microcirculatory Resistance following Percutaneous Coronary Intervention"],"prefix":"10.1155","volume":"2022","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1442-4835","authenticated-orcid":true,"given":"George R.","family":"Abraham","sequence":"first","affiliation":[{"name":"Royal Papworth Hospital NHS Foundation Trust, Cambridge, UK"},{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6212-9518","authenticated-orcid":true,"given":"Duuamene","family":"Nyimanu","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4673-1602","authenticated-orcid":true,"given":"Rhoda E.","family":"Kuc","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9254-7040","authenticated-orcid":true,"given":"Janet J.","family":"Maguire","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2096-3117","authenticated-orcid":true,"given":"Anthony P.","family":"Davenport","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3530-3808","authenticated-orcid":true,"given":"Stephen P.","family":"Hoole","sequence":"additional","affiliation":[{"name":"Royal Papworth Hospital NHS Foundation Trust, Cambridge, UK"},{"name":"Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, 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