BACKGROUND: Rapid loss of collateral support has been reported after percutaneous coronary intervention (PCI), leaving the myocardium susceptible to subsequent infarction. However, well-developed collaterals have been found in normal hearts, suggesting that collaterals exist even in the absence of an ischemic stimulus. We assessed the plasticity and determinants of collateral supply after PCI. METHODS AND RESULTS: Collateral flow index (CFI) was calculated in 60 patients as (P(w)-P(v))/(P(a)-P(v)) by measurement of aortic (P(a)), central venous (P(v)), and coronary wedge (P(w)) pressures. CFI was reassessed during transient balloon occlusion 5 minutes and 24 hours after PCI in the first 29 patients and at 6 months in the subsequent 25 patients. We also evaluated the relationship between collateral supply, lesion characteristics, and circulating hemopoietic cells numbers before and after successful PCI. CFI at baseline was 0.23+/-0.10, with no change 5 minutes and 1 day later (0.21+/-0.12, P=0.62; and 0.22+/-0.11, P=0.96, respectively). At 6 months, CFI was 0.14+/-0.07 or 63+/-27% of the baseline value (P<0.001). CFI was proportional to severity of the coronary lesion at baseline (r=0.63, P<0.0001) but not 6 months after PCI (r=-0.04, P=0.87). The number of circulating CD133+ and CD34+ cells was associated with CFI 6 months after PCI (CD133, r=0.59, P=0.035; CD34, r=0.63, P=0.037). CONCLUSIONS: Coronary collateral flow remains undiminished for at least 24 hours after successful PCI. Functional collateral support subsequently declines but does not regress completely.
BACKGROUND: Rapid loss of collateral support has been reported after percutaneous coronary intervention (PCI), leaving the myocardium susceptible to subsequent infarction. However, well-developed collaterals have been found in normal hearts, suggesting that collaterals exist even in the absence of an ischemic stimulus. We assessed the plasticity and determinants of collateral supply after PCI. METHODS AND RESULTS: Collateral flow index (CFI) was calculated in 60 patients as (P(w)-P(v))/(P(a)-P(v)) by measurement of aortic (P(a)), central venous (P(v)), and coronary wedge (P(w)) pressures. CFI was reassessed during transient balloon occlusion 5 minutes and 24 hours after PCI in the first 29 patients and at 6 months in the subsequent 25 patients. We also evaluated the relationship between collateral supply, lesion characteristics, and circulating hemopoietic cells numbers before and after successful PCI. CFI at baseline was 0.23+/-0.10, with no change 5 minutes and 1 day later (0.21+/-0.12, P=0.62; and 0.22+/-0.11, P=0.96, respectively). At 6 months, CFI was 0.14+/-0.07 or 63+/-27% of the baseline value (P<0.001). CFI was proportional to severity of the coronary lesion at baseline (r=0.63, P<0.0001) but not 6 months after PCI (r=-0.04, P=0.87). The number of circulating CD133+ and CD34+ cells was associated with CFI 6 months after PCI (CD133, r=0.59, P=0.035; CD34, r=0.63, P=0.037). CONCLUSIONS: Coronary collateral flow remains undiminished for at least 24 hours after successful PCI. Functional collateral support subsequently declines but does not regress completely.
Authors: Pascal Meier; Andreas Indermuehle; Bertram Pitt; Tobias Traupe; Stefano F de Marchi; Tom Crake; Guido Knapp; Alexandra J Lansky; Christian Seiler Journal: BMC Med Date: 2012-06-21 Impact factor: 8.775
Authors: Muhammad Aetesam-Ur-Rahman; Adam J Brown; Catherine Jaworski; Joel P Giblett; Tian X Zhao; Denise M Braganza; Sarah C Clarke; Bobby S K Agrawal; Martin R Bennett; Nick E J West; Stephen P Hoole Journal: J Am Heart Assoc Date: 2021-06-30 Impact factor: 6.106