Prediction of enzymatic infarct size in ST-segment elevation myocardial infarction.
OBJECTIVE
Predictors of adverse outcomes following myocardial infarction (MI) are well established; however, little is known about what predicts enzymatically estimated infarct size in patients with acute ST-elevation MI. The Complement And Reduction of INfarct size after Angioplasty or Lytics trials of pexelizumab used creatine kinase (CK)-MB area under the curve to determine infarct size in patients treated with primary percutaneous coronary intervention (PCI) or fibrinolysis.


METHODS
Prediction of infarct size was carried out by measuring CK-MB area under the curve in patients with ST-segment elevation MI treated with reperfusion therapy from January 2000 to April 2002. Infarct size was calculated in 1622 patients (PCI=817; fibrinolysis=805). Logistic regression was used to examine the relationship between baseline demographics, total ST-segment elevation, index angiographic findings (PCI group), and binary outcome of CK-MB area under the curve greater than 3000 ng/ml.


RESULTS
Large infarcts occurred in 63% (515) of the PCI group and 69% (554) of the fibrinolysis group. Independent predictors of large infarcts differed depending on mode of reperfusion. In PCI, male sex, no prior coronary revascularization and diabetes, decreased systolic blood pressure, sum of ST-segment elevation, total (angiographic) occlusion, and nonright coronary artery culprit artery were independent predictors of larger infarcts (C index=0.73). In fibrinolysis, younger age, decreased heart rate, white race, no history of arrhythmia, increased time to fibrinolytic therapy in patients treated up to 2 h after symptom onset, and sum of ST-segment elevation were independently associated with a larger infarct size (C index=0.68).


CONCLUSIONS
Clinical and patient data can be used to predict larger infarcts on the basis of CK-MB quantification. These models may be helpful in designing future trials and in guiding the use of novel pharmacotherapies aimed at limiting infarct size in clinical practice.
Duke Clinical Research Institute, Durham, North Carolina, USA. james.s.mills@duke.edu
James S
JS
Mills
Kenneth W
KW
Mahaffey
Yuliya
Y
Lokhnygina
Jose C
JC
Nicolau
Witold
W
Ruzyllo
Peter X
PX
Adams
Thomas G
TG
Todaro
Paul W
PW
Armstrong
Christopher B
CB
Granger
D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000627:therapeutic use*; D017023:Coronary Angiography; D052279:Creatine Kinase, MB Form / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000201:enzymology / Q000628:therapy; D009204:Myocardial Revascularization / Q000379:methods*; D009206:Myocardium / Q000201:enzymology*; D011379:Prognosis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D057127:Single-Chain Antibodies / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome
D061067:Antibodies, Monoclonal, Humanized; D057127:Single-Chain Antibodies; C402724:pexelizumab; D052279:Creatine Kinase, MB Form