title: Evolution of spontaneous atherosclerotic plaque rupture with medical therapy: long-term follow-up with intravascular ultrasound.
abstract: BACKGROUND
  Ruptured coronary atheromatous plaque is generally considered to involve a high risk of subsequent clinical events. Few data are available on the natural evolution of non-culprit-lesion ruptured plaque. We therefore used serial intravascular ultrasound (IVUS) to study how such lesions, detected in the context of a first acute coronary syndrome with elevated troponin I levels, develop.
  
  
  RESULTS
  Fourteen patients with 28 distinct plaque ruptures (2+/-1 per patient) without significant associated stenosis (minimal lumen cross-sectional area >4 mm2) were included and systematically treated with 40 mg statin and antiplatelet agent (clopidogrel and aspirin for > or =9 months). Mean clinical and IVUS follow-up was 22+/-13 months (median, 22 months). No clinical event related to the lesion under study occurred. On final IVUS examination, half (14 of 28) of the ruptured plaques had healed, and the degree of stenosis tended to diminish (stenosis, 22+/-17% versus 29+/-17% at baseline; P=0.056). No healing-prediction criterion could be identified.
  
  
  CONCLUSIONS
  Nearly 2 years of follow-up found that spontaneous coronary atheromatous plaque rupture without significant stenosis detected on first acute coronary syndrome healed without significant plaque modification in 50% of cases with medical therapy.
authors.affiliation: Department of Hemodynamics and Interventional Cardiology, Cardiovascular Hospital and Claude Bernard University, B.P. Lyon-Monchat, 69394 Lyon Cedex 03, France. gilles.rioufol@univ-lyon1.fr
authors.forename: Gilles
authors.initials: G
authors.lastname: Rioufol
authors.forename: Martine
authors.initials: M
authors.lastname: Gilard
authors.forename: Gérard
authors.initials: G
authors.lastname: Finet
authors.forename: Isabelle
authors.initials: I
authors.lastname: Ginon
authors.forename: Jacques
authors.initials: J
authors.lastname: Boschat
authors.forename: Xavier
authors.initials: X
authors.lastname: André-Fouët
mesh_terms: D000368:Aged; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use*; D015415:Biomarkers; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging* / Q000188:drug therapy; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D012422:Rupture, Spontaneous; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D019210:Troponin I / Q000097:blood; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin