title: Impaired myocardial perfusion score and inflammatory markers in patients undergoing primary angioplasty for acute myocardial infarction.
abstract: BACKGROUND
  Microcirculatory dysfunction during acute myocardial infarction is mediated by various mechanisms including inflammation, thrombus, or plaque embolization. We hypothesize that patients with acute myocardial infarction and admission Thrombolysis in Myocardial Infarction (TIMI) myocardial perfusion grade (TMP) < 2 had increased inflammatory status as measured by high sensitivity C-reactive protein (hs-CRP).
  
  
  METHODS
  From January 2002 to December 2003, 166 patients (178 lesions) were referred for primary percutaneous coronary intervention. Patients were stratified based on pre-PCI TMP < 2 or TMP 2. Univariate and multivariate predictors of in-hospital and 30-day death were determined with logistic regression.
  
  
  RESULTS
  Pre-PCI TMP < 2 was found in 66% vs 34% with TMP 2 (P < .001). Hs-CRP levels were high in both groups but not significantly different (37.9 +/- 6 vs 33.7 +/- 6 mg/L, P = .63). Patients with TMP < 2 had higher WBC (12.83 +/-4.55 x 10(-3) vs 10.83 +/- 3.00 x 10(-3), P = .04), lower ejection fraction (40 +/- 11% vs 46 +/- 12%, P < .001), and higher admission CK-MB levels (116 +/- 13 ng/mL vs 55 +/- 13 ng/mL, P = .006). Death occurred in 12% in the poorTMP group vs 1.8% in the good TMP group (P = .03). Advanced age, use of an intra-aortic balloon pump, and elevated admission WBC were independently associated with in-hospital and 30-day death.
  
  
  CONCLUSIONS
  High hs-CRP levels were not associated with impaired myocardial perfusion score. Microcirculatory impairment may be related to an increased inflammatory process, independent from high hs-CRP levels.
authors.affiliation: Instituto Nacional de Cardiología, Mexico City, Mexico. jeexaire@yahoo.com
authors.forename: J Emilio
authors.initials: JE
authors.lastname: Exaire
authors.forename: Robert B
authors.initials: RB
authors.lastname: Fathi
authors.forename: Sorin J
authors.initials: SJ
authors.lastname: Brener
authors.forename: Juhana
authors.initials: J
authors.lastname: Karha
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Ellis
authors.forename: Deepak L
authors.initials: DL
authors.lastname: Bhatt
mesh_terms: D000077284:Abciximab; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use*; D000925:Anticoagulants / Q000008:administration & dosage / Q000627:therapeutic use*; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use*; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis; D000077144:Clopidogrel; D003326:Coronary Circulation; D003627:Data Interpretation, Statistical; D004562:Electrocardiography; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D005500:Follow-Up Studies; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage / Q000627:therapeutic use*; D007249:Inflammation / Q000175:diagnosis*; D007423:Intra-Aortic Balloon Pumping; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D012307:Risk Factors; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D013997:Time Factors
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D015415:Biomarkers; D005343:Fibrinolytic Agents; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D002097:C-Reactive Protein; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab