Intensifying Platelet Inhibition With Tirofiban in Poor Responders to Aspirin, Clopidogrel, or Both Agents Undergoing Elective Coronary Intervention

Author:

Valgimigli Marco1,Campo Gianluca1,de Cesare Nicoletta1,Meliga Emanuele1,Vranckx Pascal1,Furgieri Alessandro1,Angiolillo Dominick J.1,Sabatè Manel1,Hamon Martial1,Repetto Alessandra1,Colangelo Salvatore1,Brugaletta Salvatore1,Parrinello Giovanni1,Percoco Gianfranco1,Ferrari Roberto1

Affiliation:

1. From the Department of Cardiology, University of Ferrara, Ferrara, Italy (M.V., G.C., R.F.); Cardiovascular Research Centre, Salvatore Maugeri Foundation, IRCCS, Gussago, BS, Italy (M.V., R.F.); Policlinico S. Marco, Zingonia, BG, Italy (N.d.C.); Cardiovascular Intervention Laboratory San Giovanni Bosco Hospital, Turin, Italy (E.M.); Virga Jesseziekenhuis, Hasselt, Belgium (P.V.); Department of Medical and Surgical Cardiology, Villa Maria, Cecilia Hospital, Cotignola, RA, Italy (A.F.); Division of...

Abstract

Background— Inhibition of platelet aggregation after aspirin or clopidogrel intake varies greatly among patients, and previous studies have suggested that poor response to oral antiplatelet agents may increase the risk of thrombotic events, especially after coronary angioplasty. Whether this reflects suboptimal platelet inhibition per se, which might benefit from more potent antiplatelet agents such as tirofiban, is unknown. Methods and Results— We screened 1277 patients to enroll 93 aspirin, 147 clopidogrel, and 23 dual poor responders, based on a point-of-care assay, who underwent elective coronary angioplasty at 10 European sites for stable or low-risk unstable coronary artery disease. Patients were randomly assigned in a double-blind manner to receive either tirofiban (n=132) or placebo (n=131) on top of standard aspirin and clopidogrel therapy. The primary end point, consisting of troponin I/T elevation at least 3 times the upper limit of normal, was attained in 20.4% (n=27) in the tirofiban group compared with 35.1% (n=46) in the placebo group (relative risk, 0.58; 95% confidence interval, 0.39 to 0.88; P =0.009). The rate of major adverse cardiovascular events within 30 days in the tirofiban group also was reduced (3.8% versus 10.7%; P =0.031). The overall incidence of bleeding was low, likely explained by a substantial use of the transradial approach, and did not differ between the 2 groups. Conclusions— In low-risk patients according to clinical presentation who had poor responsiveness to standard oral platelet inhibitors via a point-of-care assay, intensified platelet inhibition with tirofiban lowers the incidence of myocardial infarction after elective coronary intervention.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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