{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:48:30Z","timestamp":1787014110517,"version":"build-2736575974"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,10,13]],"date-time":"2019-10-13T00:00:00Z","timestamp":1570924800000},"content-version":"am","delay-in-days":341,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#am"},{"start":{"date-parts":[[2018,11,6]],"date-time":"2018-11-06T00:00:00Z","timestamp":1541462400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000001","name":"National Science Foundation","doi-asserted-by":"publisher","award":["3200B_163256\/1 to CS"],"award-info":[{"award-number":["3200B_163256\/1 to CS"]}],"id":[{"id":"10.13039\/100000001","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2019,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      To test the effect of long\u2010term pegfilgrastim on collateral function and myocardial ischaemia in patients with chronic stable coronary artery disease (\n                      <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This was a prospective clinical trial with randomized 2:1 allocation to pegfilgrastim or placebo for 6\u00a0months. The primary study endpoint was collateral flow index (\n                      <jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content>\n                      ) as obtained during a 1\u2010minute ostial coronary artery balloon occlusion.\n                      <jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content>\n                      is the ratio of mean coronary occlusive divided by mean aortic pressure both subtracted by central venous pressure (mm\u00a0Hg\/mm\u00a0Hg). Secondary endpoints were signs of myocardial ischaemia determined during the same coronary occlusion, that is quantitative intracoronary (i.c.)\n                      <jats:styled-content style=\"fixed-case\">ECG ST<\/jats:styled-content>\n                      \u2010segment shift (\n                      <jats:styled-content style=\"fixed-case\">mV<\/jats:styled-content>\n                      ) and the occurrence of angina pectoris. Endpoints were obtained at baseline before and at follow\u2010up after three subcutaneous study drug injections.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Collateral flow index in the pegfilgrastim group changed from 0.096\u00a0\u00b1\u00a00.076 at baseline to 0.126\u00a0\u00b1\u00a00.070 at follow\u2010up (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0039), while in the placebo group\n                      <jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content>\n                      changed from 0.157\u00a0\u00b1\u00a00.146 to 0.122\u00a0\u00b1\u00a00.043, respectively (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.29); the\n                      <jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content>\n                      increment at follow\u2010up was +0.030\u00a0\u00b1\u00a00.075 in the pegfilgrastim group and \u22120.034\u00a0\u00b1\u00a00.148 in the placebo group (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0172). In the pegfilgrastim group, i.c.\n                      <jats:styled-content style=\"fixed-case\">ECG ST<\/jats:styled-content>\n                      \u2010segment shift changed from +1.23\u00a0\u00b1\u00a01.01\u00a0mV at baseline to +0.93\u00a0\u00b1\u00a00.97\u00a0mV at follow\u2010up (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0049), and in the placebo group, it changed from +0.98\u00a0\u00b1\u00a01.02\u00a0mV to +1.43\u00a0\u00b1\u00a01.09\u00a0mV, respectively (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.05). At follow\u2010up, the fraction of patients free from angina pectoris during coronary occlusion had increased in the pegfilgrastim but not in the placebo group.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Pegfilgrastim given over the course of 6\u00a0months improves collateral function in chronic stable\n                      <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                      , which is reflected by reduced myocardial ischaemia during a controlled coronary occlusion.\n                    <\/jats:p>\n                  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