April 19th, 2012
Should We Pull the Trigger on Platelet Reactivity Testing (and Put It out of Its Misery)?
Richard A. Lange, MD, MBA and L. David Hillis, MD
In a previous blog about the GRAVITAS trial — which showed that high-dose clopidogrel didn’t improve outcomes following PCI in patients with high on-treatment platelet reactivity (HTPR) when compared to clopidogrel given at conventional doses — we noted that an assessment of platelet reactivity by this method doesn’t effectively identify individuals at high risk for a cardiovascular event following PCI. Although more than 40% of patients have HTPR (according to the VerifyNow P2Y12 Test), very few have a cardiovascular event in the 6 months following PCI.
In the most recent issue of JACC, the TRIGGER-PCI (Testing Platelet Reactivity in Patients Undergoing Elective DES Placement on Clopidogrel to Guide Alternative Therapy with Prasugrel) trial investigated the effectiveness of prasugrel versus clopidogrel in 456 patients with HTPR undergoing elective PCI with DES.
The results shown in the table below demonstrate (a) a low rate of ischemic events in patients with HTPR and (b) no demonstrable benefit to switching from clopidogrel to prasugrel when HPTR is detected.
|
Prasugrel |
Clopidogrel |
P value |
|
| PRU * | |||
| Baseline |
245 |
249 |
NS |
| 3 mos |
80 |
241 |
<0.001 |
| Endpoints | |||
| CV death or MI |
0 (0%) |
1 (0.5%) |
NS |
| CV death |
0 (0%) |
0 (0%) |
NS |
| MI |
0 (0%) |
1 (0.5%) |
NS |
| Urgent TVR |
2 (1.0%) |
1 (0.5%) |
NS |
| Major bleeding |
3 (1.4%) |
1 (0.5%) |
NS |
*PRU=P2Y12 reaction units, according to the VerfiyNow P2Y12 Test
We said it before, and we’ll say it again: an assessment of platelet reactivity by this method doesn’t effectively identify individuals at high risk for a cardiovascular event following PCI.
We agree with the authors when they state, “The low observed ischemic event rate in the control group even without correction of HTPR demonstrates that testing platelet function in such patients for consideration of more intensive antiplatelet therapy is not warranted, especially given the potentially increased risk of bleeding.”
Critics of the GRAVITAS trial argued that the study may have been negative because the cut point for defining HTPR (P2Y12 reaction units [PRU] > 235) may have been too high. However, in Trigger-PCI, the cut point was much lower (PRU >208), yet switching to prasugrel yielded no improvement in clinical outcomes in patients with HTPR who were put on clopidogrel after elective PCI with DES.
It appears that the utility of VerifyNow platelet testing is………unverified.
Should we be routinely testing platelet reactivity in our PCI patients? If so, what should we do with that information?
One Response to “Should We Pull the Trigger on Platelet Reactivity Testing (and Put It out of Its Misery)?”
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To be fair, my friends Dr Lange and Hillis should note that TRIGGER PCI excluded patients with ACS and likely did not enroll a high proportion of patients with complex interventions – in other words, patients with a higher baseline risk for post PCI ischemic complications including stent thrombosis – and so this trial does not negate the potential value of platelet function testing entirely (as the authors note I their discussion). With this caveat, though, I do not routinely test platelet function testing in my elective PCI patients and TRIGGER PCI validates this practice. In an era where we are encouraged to choose tests wisely and spend health care resources judiciously, routine platelet function testing seems like an unnecessary expense given the absence of benefit in non-ACS elective patients.