P2y12 test Meaning, Normal Range, Interpretation, Low

P2y12 test Meaning, Normal Range, Interpretation, Low

P2y12 Test Meaning

Platelet aggregation is inhibited by P2Y12 antagonists such as clopidogrel, prasugrel, and ticagrelor. Cardiovascular disease’s etiology is greatly influenced by platelet activation and aggregation. 

Platelet dysfunction inhibition is becoming a primary treatment objective. Aspirin plus clopidogrel (Plavix) dual antiplatelet treatment has reduced risk in several big clinical trials. 

The P2Y12 lab test is used to evaluate the effects of anti-platelet medications such as prasugrel, clopidogrel, ticagrelor, and ticlopidine, which inhibit the P2Y12 receptor on platelets. P2Y12 reaction units (PRU) are used to report the test results. This test determines the degree to which platelets aggregate together in response to the presence of P2Y12 inhibitor medications such as ticlopidine, prasugrel, and clopidogrel. 

This test necessitates the use of a special tube that can only be filled to a single volume for accurate results. The time limit for running the test after collection is 4 hours. The specimen needs to be delivered by hand; it cannot be sent with the help of the Pneumatic Tube System (PTS). 

P2y12 Test Normal Range

P2Y12 Reaction Units (PRU) are used to evaluate the effects of antiplatelet medications that target the platelet P2Y12 receptor, like clopidogrel. The reference range is 180–376 PRU for people who are not on a P2Y12 inhibitor. PRU levels below 180 are a specific indicator of an antiplatelet effect caused by P2Y12 receptor blockade. A PRU value below 208 is considered a satisfactory response to anti-platelet medication in the medical literature for cardiology patients. PRU targets that are optimal for both pre-surgical treatment and therapeutic treatment are not determined yet.

P2y12 Test Interpretation

Platelet function is mostly checked with the VerifyNow assay (Accumetrics Inc., San Diego, California) to see how well the body responds to the three main types of antiplatelet drugs: aspirin, thienopyridines, and glycoprotein IIb/IIIa inhibitors (eptifibatide, abciximab, or tirofiban). The point-of-care technology known as VerifyNow is easy and quick, and it boasts several benefits, including the utilization of whole blood, the utilization of small sample quantities, and the absence of pipetting.

Glycoprotein IIb/IIIa inhibitor patients are not advised to be evaluated until platelet function recovers. This period is about 48 hours after eptifibatide and tirofiban are stopped, and 14 days after abciximab is stopped. The outcomes of this assay can also be impacted by other platelet medications such as NSAIDs, P2Y12 inhibitors (such as clopidogrel), and others.

The preliminary manufacturer data suggests that the 95-207 P2PRU range is the optimal therapeutic window for P2Y12 inhibitors (such as clopidogrel). Patients who have levels above or below this range are often more susceptible to cardiovascular problems, while those who have levels below or within this range are more susceptible to bleeding.

P2y12 Test Low

PRU assesses the degree of platelet aggregation when a P2Y12 inhibitor is present. <180 PRU shows the effect of the P2Y12 inhibitor. 180-376 PRU indicates that there is no P2Y12 inhibitor effect. P2Y12 levels lower than 194, which is the lower limit of the reference range, indicate definitive proof of a P2Y12 inhibitor action.

 Lower PRU is the outcome of clopidogrel’s platelet inhibition. The PRU for most responders is less than 180. PRU levels that are greater than 180 are typically referred to as having high on-treatment platelet reactivity (HPR), and they have been linked to an increased risk of ischemic events during PCI, such as mortality, MI, and stent thrombosis. These patients might benefit from either a larger dose of clopidogrel or an alternate antiplatelet therapy like cangrelor, ticagrelor, or prasugrel. Patients exhibiting low platelet reactivity (PRU 180), as opposed to those with HPR, have an increased risk of bleeding, particularly after PCI.

Clopidogrel’s ability to inhibit platelet aggregation is typically detectable 2 hours after a loading dose of 300 to 600 mg. The peak effect typically occurs 6 hours following therapy. Clopidogrel blocks platelets, which are affected during the remaining 7 to 10 days of their lives.

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