Full Answer
Does platelet reactivity increase after a stroke?
The question whether greater platelet reactivity in patients with stroke merely reflects the body's inflammatory response to tissue damage is, however, clearly answered with a “no.” Increases in platelet activation not only may follow an acute stroke for many months but also may be chronically present before an episode of cerebral ischemia.
Is there a lower platelet reactivity cut-off for PCI patients?
Three recent studies support the concept of a lower platelet reactivity cut-off for bleeding risk in patients treated with PCI.
What was the first GWAS for platelet reactivity tested?
The first GWAS reported for platelet reactivity tested association of 2.5 million SNPs with platelet aggregation responses to ADP, collagen, and epinephrine.109 The primary cohorts were generally healthy, European-ancestry populations from the FHS (n=2,753) and the GeneSTAR cohorts (GS; n=1,238).
How much ADP is required for platelet aggregation?
Platelet aggregation by LTA in response to 5 µmol/L ADP and 10 µmol/L epinephrine, and by cone and plate (let) analysis expressed as the percent surface coverage by platelets and average size of surface-bound aggregates, was determined.
What does high platelet reactivity mean?
High platelet reactivity (HPR) is a risk factor for stent thrombosis, a potentially lethal complication of percutaneous coronary intervention. HPR is also associated with increased risk of myocardial infarction and death in invasively-treated patients with acute coronary syndrome (ACS).
What is on treatment platelet reactivity?
High on-treatment platelet reactivity (HTPR), referred to as a higher than expected platelet reactivity in patients under antiplatelet therapy, could influence outcome in cerebrovascular disease (CVD), but its prevalence and its stability over time is uncertain.
What is platelet reactivity index?
The platelet reactivity index (PR) is based on the ratio of platelet aggregates in blood samples obtained in different buffer solutions. Platelet aggregates are resolved when blood is sampled in EDTA-buffer, but remain fixed when EDTA-formalin-buffer is used.
How effective are antiplatelet drugs?
It is estimated that antiplatelet drugs reduce the risk of any serious vascular event by about 25% (this figure is calculated from a reduction in non-fatal MI of 34%, non-fatal stroke of 25%, and vascular death of 17%). The benefits in these high risk groups outweigh the risk such as major bleeding.
What is P2Y12 test?
Clinical Information. Test results are in P2Y12 reaction units (PRU). This test measures the extent of platelet aggregation in the presence of P2Y12 inhibitor drugs such as clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilinta) and ticlopidine (Ticlid).
What is the safest antiplatelet drug?
Clopidogrel monotherapy showed the most favourable benefit-harm profile (79% cumulative rank probability best and 77% cumulative rank probability safest). In conclusion, Clopidogrel should be the indicated antiplatelet agent in PAD patients.
What is a common side effect of antiplatelet medications?
Side effectsheadaches or dizziness.nausea.diarrhoea or constipation.indigestion (dyspepsia)stomach ache or abdominal pain.nosebleeds.increased bleeding (your blood taking longer to clot – for example, when you cut yourself), or easy bruising.
What is the most common antiplatelet drug?
The most common antiplatelet drug used in preventing further heart attacks is aspirin. Other drugs include clopidogrel, prasugrel and ticagrelor.
Biomarkers for Antiplatelet Therapy
Razvan T. Dadu MD, PhD, Neal S. Kleiman MD, in Biomarkers in Cardiovascular Disease, 2019
Laboratory Monitoring of Antiplatelet Therapy
Thomas Gremmel, ... Alan D. Michelson, in Platelets (Fourth Edition), 2019
Antiplatelet Therapy Monitoring
Connie H. Miller PhD, Mikhail Roshal MD, PhD, in Transfusion Medicine and Hemostasis (Third Edition), 2019
Monitoring of Antiplatelet Therapy
Similar to the upper platelet reactivity cut-off associated with ischemic event occurrence, there may be a lower platelet reactivity cut-off below which the risk for ischemic event occurrence may be minimal, whereas bleeding risk may be high (Fig. 30-10 ).
Antiplatelet Therapy for Secondary Prevention of Stroke
The question whether greater platelet reactivity in patients with stroke merely reflects the body's inflammatory response to tissue damage is, however, clearly answered with a “no.” Increases in platelet activation not only may follow an acute stroke for many months but also may be chronically present before an episode of cerebral ischemia.
P2Y12 Antagonists
A significant proportion of subjects (about 1/3) treated with clopidogrel are very poor responders, displaying almost no inhibition of platelet function. 101,102 Several lines of evidence strongly suggest that variability in active metabolite generation is the primary explanation for clopidogrel antiplatelet response variability.
Antiplatelet Therapy for Secondary Prevention of Stroke
Thalia S. Field, ... Oscar R. Benavente, in Stroke (Seventh Edition), 2022