title: Intracoronary enalaprilat during angioplasty for acute myocardial infarction: alleviation of postischaemic neurohumoral and inflammatory stress?
abstract: OBJECTIVE
  Reperfusion after myocardial ischaemia is associated with a distinct ischaemia/reperfusion injury. Since ACE-inhibition, beyond its influence on cardiac angiotensin II formation and kinin metabolism, has been shown to be cardioprotective by decreasing leucocyte adhesion and endothelin-1 (ET-1) release, we investigated the effects of intracoronary (i.c.) enalaprilat during primary angioplasty in acute myocardial infarction.
  
  
  RESULTS
  Twenty-two patients were randomized to receive i.c. enalaprilat (50 micro g) or placebo immediately after reopening of the infarct-related artery (IRA). Plasma concentrations of soluble L-selectin, P-selectin, intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), ET-1 and nitric oxide metabolite concentrations (NOx) were measured in pulmonary arterial blood. Coronary blood flow was assessed using corrected thrombolysis in myocardial infarction (TIMI) frame counts (CTFC). During reperfusion, there was a significant increase in sL-selectin, sP-selectin and ET-1 in the placebo group, which was greatly diminished by enalaprilat. Levels of sVCAM-1 and sICAM-1 were not affected in either group. CTFC in the placebo group remained higher than normal in both the IRA and nonculprit vessels, whereas myocardial blood flow improved with enalaprilat.
  
  
  CONCLUSIONS
  Enalaprilat as adjunct to primary angioplasty might be a protective approach to prevent leucocyte adhesion and the release of ET-1, thereby improving coronary blood flow.
authors.affiliation: Medizinische Klinik II, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Germany. ulrich.schaefer@ukl.uni-luebeck.de
authors.forename: U
authors.initials: U
authors.lastname: Schaefer
authors.forename: T
authors.initials: T
authors.lastname: Kurz
authors.forename: H
authors.initials: H
authors.lastname: Bonnemeier
authors.forename: A
authors.initials: A
authors.lastname: Dendorfer
authors.forename: F
authors.initials: F
authors.lastname: Hartmann
authors.forename: H
authors.initials: H
authors.lastname: Schunkert
authors.forename: G
authors.initials: G
authors.lastname: Richardt
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage* / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D003131:Combined Modality Therapy; D003331:Coronary Vessels; D015773:Enalaprilat / Q000008:administration & dosage* / Q000627:therapeutic use; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006801:Humans; D007267:Injections; D019041:L-Selectin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy / Q000628:therapy*; D015425:Myocardial Reperfusion; D009569:Nitric Oxide / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D019007:P-Selectin / Q000097:blood; D011651:Pulmonary Artery; D012008:Recurrence; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D019332:Endothelin-1; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D019041:L-Selectin; D009569:Nitric Oxide; D015773:Enalaprilat; D009638:Norepinephrine