title: Coronary collateral function long after drug-eluting stent implantation.
abstract: OBJECTIVE
  This study was designed to compare coronary collateral function in patients after bare-metal stent (BMS) or drug-eluting stent (DES) implantation.
  
  
  BACKGROUND
  Drug-eluting stents have an inhibitory effect on the production of cytokines, chemotactic proteins, and growth factors, and may therefore negatively affect coronary collateral growth.
  
  
  METHODS
  A total of 120 patients with long-term stable coronary artery disease (CAD) after stent implantation were included. Both the BMS group and the DES group comprised 60 patients matched for in-stent stenosis severity of the vessel undergoing collateral flow index (CFI) measurement at follow-up and for the duration of follow-up. The primary end point of the investigation was invasively determined coronary collateral function 6 months after stent implantation. Collateral function was assessed by simultaneous aortic, coronary wedge, and central venous pressure measurements (yielding CFI) and by intracoronary electrocardiogram during balloon occlusion.
  
  
  RESULTS
  There were no differences between the groups regarding age, gender, body mass index, frequency of cardiovascular risk factors, use of cardiovascular drugs, severity of CAD, or site of coronary artery stenoses. Despite equal in-stent stenosis severity (46 +/- 34% and 45 +/- 36%) and equal follow-up duration (6.2 +/- 10 months and 6.5 +/- 5.4 months), CFI was diminished in the DES versus BMS group (0.154 +/- 0.097 vs. 0.224 +/- 0.142; p = 0.0049), and the rate of collaterals insufficient to prevent ischemia during occlusion (intracoronary electrocardiographic ST-segment elevation > or =0.1 mV) was higher with 50 of 60 patients in the DES group and 33 of 60 patients in the BMS group (p = 0.001).
  
  
  CONCLUSIONS
  Collateral function long after coronary stenting is impaired with DES (sirolimus and paclitaxel) when compared with BMS. Considering the protective nature of collateral vessels, this could lead to more serious cardiac events in the presence of an abrupt coronary occlusion.
authors.affiliation: Department of Cardiology, University Hospital, Bern, Switzerland.
authors.forename: Pascal
authors.initials: P
authors.lastname: Meier
authors.forename: Rainer
authors.initials: R
authors.lastname: Zbinden
authors.forename: Mario
authors.initials: M
authors.lastname: Togni
authors.forename: Peter
authors.initials: P
authors.lastname: Wenaweser
authors.forename: Stephan
authors.initials: S
authors.lastname: Windecker
authors.forename: Bernhard
authors.initials: B
authors.lastname: Meier
authors.forename: Christian
authors.initials: C
authors.lastname: Seiler
mesh_terms: D000368:Aged; D002630:Chemotactic Factors / Q000096:biosynthesis; D003097:Collateral Circulation / Q000187:drug effects*; D023921:Coronary Stenosis / Q000188:drug therapy / Q000628:therapy*; D003331:Coronary Vessels / Q000502:physiology; D016207:Cytokines / Q000096:biosynthesis; D016503:Drug Delivery Systems; D005260:Female; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D017239:Paclitaxel / Q000008:administration & dosage; D020123:Sirolimus / Q000008:administration & dosage; D015607:Stents
chemical_list: D002630:Chemotactic Factors; D016207:Cytokines; D007166:Immunosuppressive Agents; D036341:Intercellular Signaling Peptides and Proteins; D017239:Paclitaxel; D020123:Sirolimus