Value of platelet reactivity in predicting response to treatment and clinical outcome in patients undergoing primary coronary intervention: insights into the STRATEGY Study.
OBJECTIVE
The purpose of this study was to evaluate the value of platelet reactivity (PR) in predicting the response to treatment and outcome in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention assisted by glycoprotein (GP) IIb/IIIa inhibition.


BACKGROUND
There is limited prognostic information on the role of spontaneous or drug-modulated PR in STEMI patients.


METHODS
The PR was measured with Platelet Function Analyzer (PFA)-100 and light transmission aggregometry (LTA) using adenosine diphosphate as agonist in 70 consecutive STEMI patients at entry (PR-T0), 10 min after GP IIb/IIIa bolus (PR-T1), and discharge (PR-T2) and in 30 stable angina (SA) patients (PR-SA). Complete platelet inhibition (CPI) was based on closure time >300 s by PFA-100 and percentage inhibition of platelet aggregation >95% by LTA. Clinical, electrocardiographic, and angiographic responses to treatment during 1-year follow-up were collected.


RESULTS
According to both techniques, PR-T0 was higher than: 1) PR-T2 and PR-SA; 2) in those without CPI at T1; and 3) in patients with final Thrombolysis In Myocardial Infarction (TIMI) flow grade <3. The PR-T0 assessed with PFA-100 correlated with: 1) corrected TIMI frame count (r = -0.6, p < 0.001); 2) ST-segment resolution (r = 45, p < 0.001); and 3) creatine kinase-MB (r = -0.47, p < 0.001). At 1 year, patients with high PR-T0 showed an adjusted 5- to 11-fold increase in the risk of death, reinfarction, and target vessel revascularization (hazard ratio [HR] 11, 95% confidence interval [CI] 1.5 to 78 [p = 0.02] in PFA-100; HR 5.2, 95% CI 1.1 to 23 [p = 0.03] in LTA).


CONCLUSIONS
The PR at entry affects response to GP IIb/IIIa inhibition, mechanical treatment, and long-term outcome in STEMI patients undergoing primary intervention.
Campo
Gianluca
G
Department of Cardiology, University of Ferrara, Ferrara, Italy.
Valgimigli
Marco
M
Gemmati
Donato
D
Percoco
Gianfranco
G
Tognazzo
Silvia
S
Cicchitelli
Giordano
G
Catozzi
Linda
L
Malagutti
Patrizia
P
Anselmi
Maurizio
M
Vassanelli
Corrado
C
Scapoli
Gianluigi
G
Ferrari
Roberto
R
D000077284:Abciximab; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001792:Blood Platelets; D017023:Coronary Angiography; D052279:Creatine Kinase, MB Form / Q000097:blood; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*; D010974:Platelet Aggregation; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011237:Predictive Value of Tests; D016032:Randomized Controlled Trials as Topic; D015607:Stents; D013997:Time Factors; D000077466:Tirofiban; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019210:Troponin I; D014443:Tyrosine; D052279:Creatine Kinase, MB Form; D000077466:Tirofiban; D000077284:Abciximab