Platelet function predicts myocardial damage in patients with acute myocardial infarction.
BACKGROUND
Platelet activation is a hallmark of acute coronary syndromes. Numerous lines of evidence suggest a mechanistic link between von Willebrand factor or platelet hyperfunction and myocardial damage in patients with acute coronary syndromes. Thus, we assessed whether platelet function under high shear rates (collagen adenosine diphosphate closure times [CADP-CTs]) measured with the platelet function analyzer (PFA-100) may be enhanced in patients with myocardial infarction (MI) and whether it may predict the extent of myocardial damage as measured by creatine kinase (CK-MB) or troponin T (TnT) levels.


RESULTS
Patients with acute chest pain or symptoms suggestive of acute coronary syndromes (n=216) were prospectively examined at an emergency department. CADP-CT was significantly shorter in patients with MI, particularly in those with an ST-segment-elevation MI (STEMI) compared with the other patient groups (unstable angina, stable coronary artery disease, or controls). Furthermore, CADP-CT and collagen epinephrine-CT at presentation were independent predictors of myocardial damage as measured by CK-MB or TnT. Patients with MI whose CADP-CT values fell in the first quartile had 3-fold higher CK-MB and TnT levels than those in the fourth quartile.


CONCLUSIONS
Patients with STEMI have significantly enhanced platelet function when measured under high shear rates. CADP-CT is an independent predictor of the severity of MI, as measured by markers of cardiac necrosis. Measurement of platelet function with the PFA-100 may help in the risk stratification of patients presenting with MI.
Frossard
Martin
M
Department of Clinical Pharmacology, Medical University, Vienna, Austria.
Fuchs
Ingrid
I
Leitner
Judith M
JM
Hsieh
Kety
K
Vlcek
Marianne
M
Losert
Heidrun
H
Domanovits
Hans
H
Schreiber
Wolfgang
W
Laggner
Anton N
AN
Jilma
Bernd
B
D000077284:Abciximab; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use; D002317:Cardiovascular Agents / Q000627:therapeutic use; D000077144:Clopidogrel; D003094:Collagen / Q000494:pharmacology; D015897:Comorbidity; D000077542:Eptifibatide; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology / Q000627:therapeutic use; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology; D017202:Myocardial Ischemia / Q000097:blood / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D010455:Peptides / Q000494:pharmacology / Q000627:therapeutic use; D015539:Platelet Activation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D010979:Platelet Function Tests / Q000295:instrumentation; D011237:Predictive Value of Tests; D011446:Prospective Studies; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D014841:von Willebrand Factor / Q000032:analysis
D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D002317:Cardiovascular Agents; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor; D014443:Tyrosine; D000244:Adenosine Diphosphate; D003094:Collagen; D000077144:Clopidogrel; D000077466:Tirofiban; D000077542:Eptifibatide; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab