title: Multiple plaque rupture and C-reactive protein in acute myocardial infarction.
abstract: OBJECTIVE
  This study sought to investigate the relationship between multiple plaque ruptures, C-reactive protein (CRP), and clinical prognosis in acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Several studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some acute coronary syndrome (ACS) patients. Recent studies have reported that a ruptured plaque at the culprit lesion is associated with elevated CRP, which indicates a poor prognosis in patients with ACS.
  
  
  METHODS
  We performed intravascular ultrasound in 45 infarct-related arteries and another 84 major coronary arteries in 45 first AMI patients.
  
  
  RESULTS
  Plaque rupture was observed in 21 patients (47%) at the culprit site. Intravascular ultrasound revealed 17 additional plaque ruptures at remote sites in 11 patients (24%). Patients with multiple risk factors were more frequently found in our multiple-plaque rupture patients compared with single-plaque rupture or nonrupture patients (82% vs. 40% vs. 29%, p = 0.01). High-sensitive CRP levels had a positive correlation with the number of plaque ruptures (p < 0.01). All culprit lesions were successfully treated by percutaneous coronary intervention. Patients with multiple plaque rupture showed significantly poor prognosis compared with others (p = 0.01).
  
  
  CONCLUSIONS
  Multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Our results suggest that AMI treatment should focus not only on stabilization of the culprit site but also a systemic approach to systemic stabilization of the arteries.
authors.affiliation: Department of Cardiology, Baba Memorial Hospital, Sakai, Japan. m4497147@msic.med.osaka-cu.ac.jp
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tanaka
authors.forename: Kenei
authors.initials: K
authors.lastname: Shimada
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Sano
authors.forename: Masashi
authors.initials: M
authors.lastname: Namba
authors.forename: Tsunemori
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Yukio
authors.initials: Y
authors.lastname: Nishida
authors.forename: Takahiko
authors.initials: T
authors.lastname: Kawarabayashi
authors.forename: Daiju
authors.initials: D
authors.lastname: Fukuda
authors.forename: Junichi
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000276:immunology* / Q000628:therapy; D003328:Coronary Thrombosis / Q000000981:diagnostic imaging / Q000276:immunology* / Q000628:therapy; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000276:immunology* / Q000628:therapy; D011379:Prognosis; D012307:Risk Factors; D012422:Rupture, Spontaneous; D018746:Systemic Inflammatory Response Syndrome / Q000000981:diagnostic imaging / Q000276:immunology / Q000628:therapy; D014463:Ultrasonography
chemical_list: D002097:C-Reactive Protein