title: Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study.
abstract: BACKGROUND
  To test the hypothesis of general atherosclerotic plaque destabilization during acute coronary syndrome (ACS), the present study sought to analyze the 3 coronary arteries by systematic intravascular ultrasound scan (IVUS).
  
  
  RESULTS
  Seventy-two arteries were explored in 24 patients referred for percutaneous coronary intervention after a first ACS with troponin I elevation. Fifty plaque ruptures (mean, 2.08 per patient; range, 0 to 6) were diagnosed by the association of a ruptured capsule with intraplaque cavity. Plaque rupture on the culprit lesion was found in 9 patients (37.5%). At least 1 plaque rupture was found somewhere other than on the culprit lesion in 19 patients (79%). These lesions were in a different artery than the culprit artery in 70.8% and were in both other arteries in 12.5% of these 24 patients. Complete IVUS examination of all 3 coronary axes in patients who had experienced a first ACS revealed that multiple atherosclerotic plaque ruptures were detected by IVUS; these multiple ruptures were present simultaneously with the culprit lesion; they were frequent and located (in three quarters of cases) on the 3 principal coronary trunks; and the multiple plaque ruptures in locations other than on the culprit lesion were less severe, nonstenosing, and less calcified.
  
  
  CONCLUSIONS
  Although one single lesion is clinically active at the time of ACS, the syndrome seems nevertheless associated with overall coronary instability.
authors.affiliation: Department of Hemodynamics, Cardiovascular Hospital and Claude Bernard University, Lyon, France. gilles.rioufol@univ-lyon1.fr
authors.forename: G
authors.initials: G
authors.lastname: Rioufol
authors.forename: G
authors.initials: G
authors.lastname: Finet
authors.forename: I
authors.initials: I
authors.lastname: Ginon
authors.forename: X
authors.initials: X
authors.lastname: André-Fouët
authors.forename: R
authors.initials: R
authors.lastname: Rossi
authors.forename: E
authors.initials: E
authors.lastname: Vialle
authors.forename: E
authors.initials: E
authors.lastname: Desjoyaux
authors.forename: G
authors.initials: G
authors.lastname: Convert
authors.forename: J F
authors.initials: JF
authors.lastname: Huret
authors.forename: A
authors.initials: A
authors.lastname: Tabib
mesh_terms: D000208:Acute Disease; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D015906:Angioplasty, Balloon, Coronary; D002114:Calcinosis / Q000175:diagnosis; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000628:therapy; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D012422:Rupture, Spontaneous / Q000000981:diagnostic imaging*; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014654:Vascular Patency
chemical_list: D000319:Adrenergic beta-Antagonists; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex