title: Association between serum C-reactive protein elevation and left ventricular thrombus formation after first anterior myocardial infarction.
abstract: OBJECTIVE
  Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI.
  
  
  METHODS
  We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI.
  
  
  RESULTS
  LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (+/- SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 +/- 12.6 vs 9.4 +/- 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of > or =20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (> or =60 years old), peak CK level (> or =3,000 IU/L), and peak WBC count (> or =12,000 cells/ microL).
  
  
  CONCLUSIONS
  A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.
authors.affiliation: Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. anzai@cpnet.med.keio.ac.jp
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Anzai
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Kaneko
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Maekawa
authors.forename: Shiro
authors.initials: S
authors.lastname: Iwanaga
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Asakura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ogawa
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000379:methods; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D006328:Cardiac Catheterization; D015331:Cohort Studies; D017023:Coronary Angiography; D015150:Echocardiography, Doppler; D005260:Female; D006331:Heart Diseases / Q000150:complications / Q000175:diagnosis* / Q000628:therapy; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000175:diagnosis* / Q000628:therapy; D011336:Probability; D011379:Prognosis; D012189:Retrospective Studies; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D015912:Thrombolytic Therapy / Q000379:methods; D013927:Thrombosis / Q000150:complications / Q000175:diagnosis* / Q000628:therapy; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein