Higher on-aspirin treatment platelet reactivity increased death, stent thrombosis

One year after PCI, patients who had elevated on-aspirin treatment platelet reactivity before the procedure were at increased risk for death and stent thrombosis, results published in the Journal of the American College of Cardiology concluded.

For the study, researchers of the ISAR-ASPI registry evaluated high on-aspirin treatment platelet reactivity (HAPR) as a possible prognostic biomarker among 7,090 consecutive PCI-treated patients from February 2007 to May 2013. On-aspirin treatment platelet aggregation values were measured directly before PCI.

Death or stent thrombosis at 1 year served as the primary endpoint. The HAPR cohort was composed of patients in the upper quintile (n=1,414), as determined by Multiplate (Roche Diagnostics) measurements.

Compared with the non-HAPR cohort (n=5,676), those in the HAPR arm were at increased risk for experiencing the primary outcome (6.2% vs. 3.7%; OR=1.78; P<.0001). In adjusted analysis, HAPR independently predicted the primary endpoint (HR=1.46; P=.005).

“Present data support the addition of HAPR to a panel of prognostic biomarkers in PCI-treated patients,” the researchers concluded.

In an accompanying editorial, Dominick J. Angiolillo, MD, PhD, and Jung Rae Cho, MD, of the University of Florida College of Medicine – Jacksonville, Fla., wrote that the major strengths of the study include: the large cohort of patients; the long-term follow-up with a clinically relevant primary endpoint; the detailed statistical approach; and the homogeneous conditions under which the pharmacodynamic (PD) assessments were performed.

Dominick J. Angiolillo

However, one of the considerations that should be addressed includes the fact that “a full PD effect of aspirin and complete COX-1-mediated inhibition of platelet thromboxane production can be achieved with low-dose therapy,” they wrote. “In fact, the prevalence of ‘aspirin resistance’ is approximately close to null when assays specifically measuring COX-1 activity are used, challenging the concept of ‘aspirin resistance.’ Many available assays are not specific for measuring platelet COX-1 activity, which may explain the broad prevalence of ‘aspirin resistance’ in published reports and the inconsistent association with clinical correlates.”

Angiolillo and Cho added that investigations corroborating these findings are necessary because of the controversial findings of the prognostic value of PD measures of aspirin-induced antiplatelet effects.

“Ultimately, defining the treatment strategies tailored to these high-risk patients that can improve outcomes, which thus far has yielded unsatisfactory results, remains the ultimate objective that would enable this biomarker to be incorporated into routine clinical practice,” they wrote.