title: Apolipoprotein A-I breakdown is induced by thrombolysis in coronary patients.
abstract: BACKGROUND
  The outcome of percutaneous coronary intervention (PCI) is apparently worse in patients receiving a prior thrombolytic therapy ('facilitated PCI'). Recombinant tissue-type plasminogen activator (rt-PA) can degrade circulating high-density lipoproteins (HDL) bound apolipoprotein A-I (apoA-I), thus possibly reducing the vascular protective activity. There have never been reports of the detection of apolipoprotein breakdown products in the circulation.
  
  
  OBJECTIVE
  We studied the potential interactions between the protein components of HDL and tenecteplase, infused as thrombolytic therapy.
  
  
  METHODS
  Sera from a total of 40 patients with acute myocardial infarction (AMI), unstable angina (UA), and dilative cardiomyopathy (controls) were investigated. AMI patients underwent either immediate PCI or were treated with tenecteplase thrombolysis.
  
  
  RESULTS
  Products of extensive proteolysis of apoA-I were found in many acute coronary patients treated with tenecteplase, and in some AMI patients before starting the treatment (time 0). These were not detected in controls, UA patients as well as AMI patients undergoing immediate PCI. Small pre-beta-HDLs were selectively degraded.
  
  
  CONCLUSIONS
  Significant apoA-I degradation occurs in AMI patients after thrombolytic treatment. This finding may provide a potential mechanism for the apparent reduction of benefit of facilitated versus nonfacilitated PCI.
authors.affiliation: Proteomics and Protein Structure Study Group, University of Milan, Milan, Italy.
authors.forename: Ivano
authors.initials: I
authors.lastname: Eberini
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Gianazza
authors.forename: Loranni
authors.initials: L
authors.lastname: Breghi
authors.forename: Silvio
authors.initials: S
authors.lastname: Klugmann
authors.forename: Laura
authors.initials: L
authors.lastname: Calabresi
authors.forename: Monica
authors.initials: M
authors.lastname: Gomaraschi
authors.forename: Giuliana
authors.initials: G
authors.lastname: Mombelli
authors.forename: Bruno
authors.initials: B
authors.lastname: Brusoni
authors.forename: Robin
authors.initials: R
authors.lastname: Wait
authors.forename: Cesare R
authors.initials: CR
authors.lastname: Sirtori
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000378:metabolism / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D016632:Apolipoprotein A-I / Q000187:drug effects* / Q000378:metabolism; D002311:Cardiomyopathy, Dilated / Q000378:metabolism / Q000628:therapy; D016022:Case-Control Studies; D005260:Female; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism / Q000628:therapy; D000077785:Tenecteplase; D015912:Thrombolytic Therapy / Q000009:adverse effects*; D010959:Tissue Plasminogen Activator / Q000009:adverse effects / Q000494:pharmacology*
chemical_list: D016632:Apolipoprotein A-I; D005343:Fibrinolytic Agents; D010959:Tissue Plasminogen Activator; D000077785:Tenecteplase