CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY
Value of Platelet Reactivity in Predicting Response to Treatment and Clinical Outcome in Patients Undergoing Primary Coronary Intervention
Insights Into the STRATEGY Study
Gianluca Campo, MD*,
Marco Valgimigli, MD, PhD*, , ,*,
Donato Gemmati, MS ,
Gianfranco Percoco, MD*,
Silvia Tognazzo, MS,
Giordano Cicchitelli, MD*,
Linda Catozzi, MS,
Patrizia Malagutti, MD*,
Maurizio Anselmi, MD||,
Corrado Vassanelli, MD||,
Gianluigi Scapoli, MD and
Roberto Ferrari, MD, PhD*,
* Department of Cardiology
Center for the Study of Hemostasis and Thrombosis, University of Ferrara, Ferrara, Italy
Cardiovascular Research Center, Salvatore Maugeri Foundation, IRCCS, Gussago, Italy
Erasmus Medical Center, Thoraxcenter, Rotterdam, the Netherlands
|| Dipartimento di Scienze Biomediche e Chirurgiche, Cardiologia, Verona, Italy
Manuscript received October 3, 2005;
revised manuscript received December 5, 2005,
accepted December 19, 2005.
* Reprint requests and correspondence: Dr. Marco Valgimigli, Chair of Cardiology, University of Ferrara, Cardiovascular Institute, Arcispedale S. Anna Hospital, C.rso Giovecca 203, 44100 Ferrara, Italy (Email: vlgmrc{at}unife.it).
OBJECTIVES: 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.
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Abbreviations and Acronyms
| | CADP-CT = cartridge ADP closure time | | CPI = complete platelet inhibition | | LTA = light transmission aggregometry | | PA = platelet aggregation | | PCI = percutaneous coronary intervention | | PR = platelet reactivity | | SA = stable angina | | STEMI = ST-segment elevation myocardial infarction |
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