{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T21:27:39Z","timestamp":1790976459084,"version":"4.1.0"},"reference-count":27,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2008,4,21]],"date-time":"2008-04-21T00:00:00Z","timestamp":1208736000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cathet Cardio Intervent"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:styled-content>Background:<\/jats:styled-content> Vascular interventions, such as percutaneous coronary interventions (PCI), lead to endothelial damage and cause an inflammatory response. Endothelial progenitor cells (EPC) have been shown to have a prominent role in re\u2010endothelialization and repair following vascular injury. Studies have implicated a role for the chemokine, stromal\u2010cell\u2010derived factor\u20101 alpha (SDF1\u2010alpha) in the recruitment of circulating EPCs to sites of vascular injury. However, the relationship between the inflammatory response, SDF1\u2010alpha, and EPC levels after PCI is unclear. <jats:styled-content>Methods:<\/jats:styled-content> We enrolled one hundred patients (mean age 65.5 \u00b1 10.9 years, 32% females)\u201420 patients with NSTEMI, 27 patients with unstable angina, and 53 patients with stable angina who underwent PCI with stenting. EPC levels were measured by quantifying colony forming units in the 20 NSTEMI patients, whereas SDF1\u2010alpha levels and hs\u2010CRP levels were measured in all 100 patients by enzyme\u2010linked immunosorbent assay. All three markers were measured in blood samples drawn before and 24 hr after PCI. <jats:styled-content>Results:<\/jats:styled-content> EPC colonies increased from 9.6 colonies per million cells before PCI to 13.2 colonies per million cells after PCI (37% increase, <jats:italic>P<\/jats:italic> = 0.03). Circulating SDF1\u2010alpha levels increased mildly from 1707.1 \u00b1 480 pg\/mL at baseline to 1758.6 \u00b1 501 pg\/mL after PCI (3% increase, <jats:italic>P<\/jats:italic> = 0.0425). There was a 95% increase in the levels of hs\u2010CRP (pre\u2010PCI: 4.5 \u00b1 5.3 mg\/L vs. post\u2010PCI: 8.8 \u00b1 9.5 mg\/L; <jats:italic>P<\/jats:italic> = 0.0004). <jats:styled-content>Conclusions:<\/jats:styled-content> A robust rise in hs\u2010CRP levels in our study suggests that PCI induced a potent inflammatory response. This combined with a proportional increase in the levels of EPCs and mild elevation in SDF1\u2010alpha after PCI suggests the possibility that the potent inflammatory response induced by PCI may be associated with EPC recruitment. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ccd.21611","type":"journal-article","created":{"date-parts":[[2008,4,21]],"date-time":"2008-04-21T17:23:03Z","timestamp":1208798583000},"page":"205-209","source":"Crossref","is-referenced-by-count":24,"title":["The effect of percutaneous coronary intervention on inflammatory response and endothelial progenitor cell 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