Platelet Function Tests in Clinical Cardiology

• Published in: Journal of the American College of Cardiology 2013-05, Vol.61 (21), p.2115-2129
• Main Authors: Gorog, Diana A., MD, PhD, Fuster, Valentin, MD, PhD
• Format: Article
• Language: English
• Subjects: Acute coronary syndromes; aggregation; Agreements; Aspirin; Blood platelets; Cardiology; Cardiovascular; Cardiovascular disease; Drug therapy; Heart attacks; Internal Medicine; Laboratories; PCI; platelets; Thrombosis
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2012.11.080

This review is a critical evaluation of publications in the past decade on the usefulness of platelet function tests (PFTs) in clinical cardiology, in aiding diagnosis, predicting risk, and monitoring therapy. The ideal PFT should: 1) detect baseline platelet hyperreactivity; 2) allow individualization of antiplatelet medication; 3) predict thrombotic risk; and 4) predict bleeding risk. The practicalities of clinical cardiology demand rapid, accurate, and reliable tests that are simple to operate at the bedside and available 24 h a day, 7 days a week. Point-of-care PFTs most widely evaluated clinically include PFA-100 and VerifyNow. None of these tests can reliably detect platelet hyperreactivity and thus identify a prothrombotic state. Identification of antiplatelet nonresponsiveness or hyporesponsiveness is highly test specific, and does not allow individualization of therapy. The power of PFTs in predicting thrombotic events for a given individual is variable and often modest, and alteration of antithrombotic treatment on the basis of the results of PFTs has not been shown to alter clinical outcome. PFTs in current mainstream use cannot reliably assess bleeding risk. These tests have been in use for over a decade, but the hopes raised by PFTs in clinical practice remain unfulfilled. Although physiologically relevant measurement of platelet function now is more important than ever, a critical reappraisal of available techniques in light of clinical requirements is needed. The use of native blood, global stimulus instead of individual agonists, contribution of thrombin generation by activated platelets to the test results, and establishment of a PFT therapeutic range for each antiplatelet drug should be considered and is discussed.