SCAI KERN CHAP 3 Antiplatelets Flashcards
(20 cards)
Q1: What is the main mechanism leading to acute coronary syndrome (ACS)?
Q2: Can rupture of an atherosclerotic plaque be iatrogenic?
Q3: In what medical procedure can iatrogenic plaque rupture occur?
Q4: What happens after exposure of subendothelial collagen following plaque rupture?
Q5: What process does exposure of tissue factor trigger?
Q6: What is the result of platelet adhesion, activation, and aggregation at the injury site?
Q7: What cascade pathway is involved in thrombus formation after plaque rupture?
Q8: Why is understanding plaque rupture important for therapy development?
Q9: What type of therapies have been developed due to advances in understanding thrombus formation?
Q10: What is the focus of the chapter mentioned in the text?
A1: The rupture or erosion of an atheromatous plaque and subsequent thrombus formation
A2: Yes
A3: Percutaneous coronary interventions (PCIs)
A4: Platelet adhesion, activation, and aggregation
A5: The extrinsic pathway of the coagulation cascade
A6: Thrombus formation
A7: Extrinsic coagulation cascade
A8: It has been pivotal for developing safer and more efficacious therapies
A9: Antithrombotic and antiplatelet therapies
A10: Reviewing currently available antiplatelet therapies in the setting of PCI
Q1: What event exposes subendothelial components leading to platelet-mediated thrombosis?
Q2: During platelet adhesion, what mediates the rolling phase interaction?
Q3: Which platelet receptor complexes interact with von Willebrand factor (vWF) during adhesion?
Q4: Which platelet receptors bind to collagen at the site of vascular injury?
Q5: Binding of collagen to which receptor induces release of activating factors?
Q6: Name two activating factors released upon collagen binding to GP VI.
Q7: What processes are promoted by the release of activating factors during platelet activation?
Q8: What changes occur in platelets upon activation?
Q9: Which platelet integrin is activated and plays a key role in platelet aggregation?
Q10: What extracellular ligands does activated GP IIb/IIIa bind to?
Q11: What does vascular injury leads to after exposing subendothelial tissue factor?
Q12: Tissue factor forms a complex with which coagulation factor?
Q13: What complex formation leads to conversion of prothrombin to thrombin?
Q14: What does thrombin convert fibrinogen into?
Q15: Through which receptors does thrombin further activate platelets?
A1: Plaque rupture
A2: Platelet adhesion during the rolling phase is mediated by interactions between tissular vWF and GP Ib/V/IX ( 1b/5/9 ) receptor complexes located on the platelet surface AND between platelet collagen receptors (GP VI and GP Ia ( 6 and 1a) ) and collagen exposed at the site of vascular injury.
A3: GP Ib/V/IX ( GP 1b/5/9 ) or VWF receptors at platelet membrane
A4: GP VI and GP Ia ( GP 6 and 1a ) or collagen receptors at platelet membrane
A5: GP VI ( GP6 )
A6: ADP and thromboxane A2 (also serotonin, epinephrine, and thrombin)
A7: Interactions between adherent platelets and recruitment/activation of circulating platelets
A8: Changes in shape, expression of proinflammatory molecules, procoagulant activity, and activation of integrin GP IIb/IIIa GP2b/3a ( so activation of GP2b3a is not the first step, it is a middle step )
A9: GP IIb/IIIa ( it is a platelet Integrin )
A10: Fibrinogen and soluble von Willebrand factor (vWF)
A11: Vascular injury exposes subendothelial tissue factor, which forms a complex with factor VIIa (7a) and sets off a chain of events that culminates in formation of the prothrombinase complex
A12: Factor VIIa (7a)
A13: Prothrombinase complex
A14: Fibrin ( clot is fibrin rich )
A15: Protease-activated receptors PAR-1 and PAR-4
Fibrin likes PAR 1 and 4
Tissue factor likes factor 7
Platelet’s Gp2b3a likes fibrinogen
Collagen likes platelets’ GP6 and GP1a
vWF likes platelets GP1b/5/9
Q1: How many families of antiplatelet agents are currently used in PCI treatment and prevention?
Q2: Name the three main families of antiplatelet agents used in PCI.
Q3: What enzyme do COX-1 inhibitors target?
Q4: What receptor do ADP P2Y12 receptor inhibitors block?
Q5: What is the role of glycoprotein IIb/IIIa inhibitors (GPIs)?
Q6: Name one antiplatelet agent that is a protease-activated receptor-1 antagonist.
Q7: For what indication is vorapaxar approved?
Q8: Vorapaxar is used as an adjunct to which medications?
Q9: Does dipyridamole have a clinical indication for preventing *recurrent ischemic events in CAD patients?
Q10: Are cilostazol and pentoxifylline clinically indicated for *recurrent ischemic event prevention in CAD?
A1: Three
A2: Cyclooxygenase-1 (COX-1) inhibitors, ADP P2Y12 receptor inhibitors, glycoprotein IIb/IIIa inhibitors (GPIs) [ Other agents with antiplatelet properties are available, such as vorapaxar, cilostazol, dipyridamole, and pentoxifylline ]
A3: Cyclooxygenase-1 (COX-1) enzyme
A4: Adenosine diphosphate (ADP) P2Y12 receptor
A5: They inhibit platelet aggregation by blocking the final common pathway of platelet activation ( AI generated )
A6: Vorapaxar
A7: *Secondary prevention of thrombotic cardiovascular events in patients with history of myocardial infarction or peripheral arterial disease, as an adjunct to aspirin and/or clopidogrel.
A8: Aspirin and/or clopidogrel
A9: No
A10: No
Fibrin likes Platelets’ PAR 1 and 4
Tissue factor likes factor 7
Platelet’s Gp2b3a likes fibrinogen and soluble vWF
Collagen likes platelets’ GP6 and GP1a
vWF likes platelets GP1b/5/9
Q1: What enzyme activity does aspirin *irreversibly inhibit?
Q2: What are the two isoenzymes inhibited by aspirin?
Q3: What substrate do COX-1 and COX-2 catalyze the conversion of?
Q4: What is the substrate PGH2 used to generate?
Q5: What prostanoid derived from platelet COX-1 amplifies platelet activation?
Q6: What is the vascular prostanoid derived largely from COX-2 that acts as a platelet inhibitor and vasodilator?
Q7: Which prostanoid is highly sensitive to inhibition by aspirin?
Q8: Are low doses of aspirin sufficient to inhibit COX-1 or COX-2?
Q9: What effects are associated with COX-2 ( the good enzyme, in general ) inhibition at high aspirin doses? ( Only high doses of aspirin can inhibit COX-2 )
Q10: Where is plain aspirin rapidly absorbed?
Q11: How long does it take for plain aspirin to lead to platelet inhibition?
Q12: What is the plasma half-life of aspirin?
Q13: How long does enteric-coated aspirin **delay absorption?
Q14: For how long does aspirin prevent COX-mediated thromboxane A2 synthesis?
Q15: What is the lifespan of a platelet affected by aspirin’s irreversible COX-1 blockade?
A1: Cyclooxygenase (COX) activity
A2: COX-1 and COX-2 ( also known as prostaglandin H *synthase 1 and 2 or PGH1 synthase and PGH2 synthase). The enzyme synthetizes PGH1 and 2
A3: Arachidonic acid ( COX2 uses PGH2 to synthetize arachidonic acid )
A4: Several prostanoids including thromboxane A2 (TXA2) and prostacyclin (PGI2)
A5: Thromboxane A2 (TXA2). It’s a vasoconstrictor.
A6: Prostacyclin (PGI2). It is a “ good “ mediator. Vascular PGI2, a platelet inhibitor and a vasodilator, is derived largely from COX-2 and is *less susceptible to inhibition by *low doses of aspirin
A7: Thromboxane A2 (TXA2)
A8: COX-1 ( the bad emzyme )
A9: COX2 has Anti-inflammatory and analgesic effects.
A10: Upper gastrointestinal tract
A11: Within 60 minutes
A12: Approximately 20 minutes
A13: Approximately 3 to 4 hours
A14: For the entire lifespan of the platelet ( Aspirin induces an irreversible COX-1 blockade )
A15: 7 to 10 days
- Mature platelets express only COX-1,
- Vascular endothelial cells express both COX-1 and COX-2 and represent the main site of prostacyclin generation.
- Low-dose aspirin selectively inhibits COX-1 activity, whereas higher doses inhibit both COX-1 and COX-2.
Q1: What is the mainstay of antiplatelet therapy for secondary prevention of recurrent ischemic events?
Q2: In high-risk patients undergoing PCI, what aspirin dosing strategy is recommended?
Q3: According to current guidelines, how long should aspirin be continued after PCI?
Q4: What is the class and level of evidence recommendation for aspirin continuation after PCI?
Q5: What aspirin dose range has registry data shown to be as effective as higher doses for long-term prevention?
Q6: Do aspirin doses higher than 150 mg offer greater protection from recurrent ischemic events?
Q7: What risk increases significantly with higher aspirin doses (>150 mg)?
Q8: What specific type of bleeding is most increased with higher aspirin doses?
Q9: What trial compared aspirin doses of 325 mg and 81 mg?
Q10: What were the findings of the ADAPTABLE trial regarding cardiovascular events between the two doses?
Q11: What were the findings of the ADAPTABLE trial regarding major bleeding between the two doses?
Q12: Which aspirin dose showed enhanced patient adherence in the ADAPTABLE trial?
Q13: What maintenance dose range does current guidelines endorse for aspirin?
Q14: Is aspirin given as a loading dose, maintenance dose, or both in high-risk PCI patients?
Q15: Why is aspirin important in patients with ACS undergoing PCI?
A1: Aspirin
A2: A loading dose followed by daily maintenance dose
A3: *Indefinitely
A4: Class I recommendation, level of evidence B
A5: 75 to 150 mg per day
A6: No
A7: Bleeding events
A8: Gastrointestinal bleeding
A9: ADAPTABLE trial
A10: No difference in cardiovascular events between 325 mg and 81 mg doses
A11: No difference in major bleeding between the two doses
A12: 81 mg
A13: 75 to 100 mg daily maintenance dose
A14: Both loading and maintenance doses
A15: For secondary prevention of recurrent ischemic events
Q1: What are the primary side effects of aspirin?
Q2: How can aspirin side effects be reduced?
Q3: Name three gastrointestinal side effects caused by aspirin use.
Q4: What mechanism causes aspirin’s gastrointestinal toxicity?
Q5: Why have different aspirin formulations been developed?
Q6: What are two examples of aspirin formulations designed to bypass the stomach?
Q7: What does enteric-coated aspirin resist in the stomach?
Q8: What is the purpose of phospholipid-aspirin liquid–filled capsules (PL-ASA)?
Q9: How does PL-ASA reduce gastrointestinal injury?
Q10: How does the absorption of PL-ASA compare to enteric-coated aspirin?
A1: Gastrointestinal side effects
A2: Using low doses (75-162 mg/day)
A3: Gastric erosions, hemorrhage, and ulcers
A4: Direct action of acetylsalicylic acid on gastric mucosa
A5: To bypass the stomach and reduce gastrointestinal toxicity
A6: Enteric-coated aspirin and phospholipid-aspirin liquid–filled capsules (PL-ASA)
A7: Disintegration
A8: To reduce gastrointestinal injury by limiting direct contact with stomach lining
A9: By releasing acetylsalicylic acid in the higher pH of the duodenum
A10: PL-ASA provides faster and more complete absorption than enteric-coated aspirin
Q1: Which nonsteroidal anti-inflammatory drugs (NSAIDs) can interfere with aspirin’s action?
Q2: How do NSAIDs like naproxen and ibuprofen interfere with aspirin?
Q3: What effect does this interference have on aspirin’s antiplatelet effects?
Q4: Name the three types of aspirin sensitivity described.
Q5: What treatment can be considered for patients with aspirin sensitivity?
A1: Naproxen and ibuprofen
A2: They compete for the COX-1 active site
A3: Attenuation (reduction) of aspirin’s antiplatelet effects
A4: Respiratory sensitivity, cutaneous sensitivity, and systemic sensitivity
A5: Desensitization using escalating doses of oral aspirin
Q1: What is one of the main platelet-activating factors mentioned?
Q2: Through which receptor does ADP mainly exert its effect on platelets?
Q3: What type of receptor is P2Y12?
Q4: What does stimulation of the P2Y12 receptor lead to?
Q5: Why is inhibition of the P2Y12 signaling pathway critical in PCI?
Q6: Which first-generation thienopyridine was studied for P2Y12 inhibition?
Q7: What combination showed better outcomes compared to aspirin alone or aspirin plus warfarin in coronary stenting?
Q8: Name one major disadvantage of ticlopidine.
Q9: Why can’t ticlopidine be given as a loading dose?
Q10: Which second-generation thienopyridine has a more favorable safety profile than ticlopidine?
Q11: What is the drug of choice in PCI for patients with stable CAD?
Q12: What is a major limitation of clopidogrel?
Q13: What risk is increased in patients with high platelet reactivity despite clopidogrel therapy?
Q14: Name two newer-generation oral P2Y12 receptor inhibitors.
Q15: What class of drug is ticagrelor?
Q16: What is the mechanism of action of cangrelor?
Q17: How is cangrelor administered?
Q18: For what patient population is cangrelor FDA-approved?
Q19: What type of molecule is cangrelor an analogue of?
Q20: Why were newer P2Y12 inhibitors developed?
A1: ADP (adenosine diphosphate)
A2: P2Y12 receptor
A3: G-coupled receptor
A4: Sustained platelet aggregation and *stabilization of the platelet aggregate
A5: Because it prevents thrombotic complications during PCI
A6: Ticlopidine
A7: Aspirin plus ticlopidine
A8: Limited safety profile including agranulocytosis, rash, and gastrointestinal effects
A9: Due to risk of toxicity
A10: Clopidogrel
A11: Clopidogrel
A12: Broad range in interindividual antiplatelet effects
A13: Increased risk of recurrent ischemic events, including stent thrombosis ( a considerable number of patients persist with high platelet reactivity despite clopidogrel therapy )
A14: Prasugrel ( a third-generation thienopyridine ) and ticagrelor ( a first-in-class cyclopentyltriazolopyrimidine (CPTP) ).
A15: Cyclopentyltriazolopyrimidine (CPTP)
A16: *ATP analogue that antagonizes P2Y12 receptor
A17: Intravenously
A18: Patients with coronary artery disease undergoing PCI
A19: Adenosine triphosphate (ATP)
A20: To overcome clopidogrel limitations and improve efficacy and safety
TABLE 3.2 Large-Scale Randomized Clinical Trials Evaluating the Efficacy of Dual Antiplatelet Therapy With Aspirin and Clopidogrel in ACS/PCI Patients
TABLE 3.3 Large-Scale Randomized Clinical Trials Evaluating the Efficacy of Dual Antiplatelet Therapy With Aspirin and New-Generation P2Y12 Receptor Inhibitors in ACS/PCI Patients
Did not include those tables.
Q1: What issue does interindividual response to clopidogrel expose some patients to?
Q2: What risk is increased with the use of potent P2Y12 inhibitors?
Q3: What types of testing have gained interest to guide antiplatelet treatment choice with Clopidogrel ?
Q4: What have many studies linked guided antiplatelet therapy to?
Q5: Did **initial trials show a benefit of guided antiplatelet therapy in reducing ischemic complications?
Q6: What do **recent clinical trials and meta-analyses suggest about platelet function- or genotype-guided therapy?
Q7: How does guided therapy compare to a standard approach in terms of efficacy and safety?
Q8: Are routine platelet function and genetic testing currently recommended by practice guidelines?
Q9: What is the main goal of using platelet function and genetic testing in antiplatelet therapy?
Q10: What patient risk might be reduced by genotype-guided antiplatelet therapy?
A1: Increased ischemic risk for nonresponder subjects
A2: Increased risk of bleeding
A3: Platelet function and genetic testing
A4: Clinical outcomes
A5: No, initial trials failed to show benefit
A6: *They suggest a favorable efficacy/safety profile
A7: Guided therapy has **better efficacy and safety compared to standard approach
A8: No, they are not currently recommended
A9: To guide the choice of antiplatelet treatment
A10: Risk of recurrent ischemic events
Q1: What class of drugs do ticlopidine, clopidogrel, and prasugrel belong to?
Q2: What must thienopyridines be metabolized by to become active?
Q3: Which enzyme system is responsible for metabolizing thienopyridines?
Q4: How many oxidation steps does clopidogrel require to become active?
Q5: What percentage of clopidogrel is hydrolyzed by prehepatic esterases to an **inactive form?
Q6: What percentage of clopidogrel is metabolized by the CYP system into an **active metabolite?
Q7: Which CYP enzyme is pivotal in the metabolism of clopidogrel?
Q8: What effect do genetic variants of CYP2C19 have on clopidogrel metabolism?
Q9: What type of drugs can interfere with CYP2C19 activity?
Q10: How does prasugrel metabolism differ from clopidogrel?
Q11: Where does hydrolysis of prasugrel mainly occur?
Q12: How many hepatic metabolism steps does prasugrel require to form its active metabolite?
Q13: How does the pharmacokinetic profile of prasugrel compare to clopidogrel?
Q14: What is the half-life of the **active metabolites of clopidogrel and prasugrel?
Q15: How long do the **irreversible effects of clopidogrel and prasugrel last on platelets?
A1: Thienopyridines ( ticlopidine, clopidogrel, and prasugrel ) are oral **prodrugs and thus need to be metabolized by the hepatic cytochrome P450 (CYP) system to give rise to an active metabolite that **irreversibly inhibits the P2Y12 receptor
A2: Hepatic cytochrome P450 (CYP) system
A3: Cytochrome P450 (CYP) enzyme system
A4: Two-step oxidation
A5: Approximately 85%
A6: Approximately 15%
A7: CYP2C19 ( C for clopidogrel )
A8: They reduce metabolic activity and antiplatelet effects
A9: Certain proton pump inhibitors (PPIs)
A10: Prasugrel has a *more efficient metabolism with a *single-step hepatic metabolism
A11: Intestine
A12: One single step hepatic metabolism ( unlike plavix ). It is also a prodrug like clopidogrel
A13: **Faster onset, more potent platelet inhibition, **lower interindividual variability
A14: Approximately 8 hours
A15: For the lifespan of platelets (7-10 days)
Q1: What class of P2Y12 inhibitors does ticagrelor belong to?
Q2: Is ticagrelor a thienopyridine or nonthienopyridine?
Q3: How is ticagrelor administered?
Q4: Does ticagrelor require metabolic activation?
Q5: What percentage of ticagrelor’s effects are attributed to its metabolite?
Q6: Which CYP isoenzyme is involved in metabolizing ticagrelor’s metabolite?
Q7: How does ticagrelor act on the P2Y12 receptor?
Q8: Compared to clopidogrel, how does ticagrelor’s platelet inhibition differ?
Q9: What is the half-life of ticagrelor?
Q10: How often is ticagrelor dosed?
Q11: How long does it take for platelet function to return to baseline after stopping ticagrelor?
Q12: What is cangrelor’s route of administration?
Q13: Does cangrelor require metabolic activation?
Q14: How quickly does cangrelor reach steady-state concentrations?
Q15: What degree of platelet inhibition does cangrelor achieve?
Q16: What causes cangrelor’s fast offset of action?
Q17: What is the half-life of cangrelor?
Q18: How soon does platelet function return to baseline after stopping cangrelor infusion?
Q19: What is the recommended bolus dose of cangrelor?
Q20: What is the recommended infusion dose and duration for cangrelor?
A1: Cyclopentyltriazolopyrimidine (CPTP) class
A2: Nonthienopyridine
A3: Orally administered
A4: No, it is direct acting ( Although ticagrelor has direct-acting effects (no metabolism required), ~30% to 40% of its effects are attributed to a metabolite generated by the CYP system, in particular by the CYP3A4 isoenzyme )
A5: Approximately 30% to 40%
A6: CYP3A4 isoenzyme ( A like TicAgrelor )
A7: ***Reversible binding and noncompetitive ADP antagonist via allosteric modulation of the receptor
A8: Faster, more potent, and less variable platelet inhibition
A9: 7 to 12 hours ( rapid absorption )
A10: Twice daily
A11: Approximately 5 days
A12: Intravenous
A13: No metabolic activation required ( it is an ATP analogue )
A14: **Within a few minutes ( rapid onset of action )
A15: Greater than 90% inhibition of P2Y12 signaling pathway ( very potent and dose dependent effect )
A16: Rapid deactivation by plasmatic ectonucleotidases ( immediate onset of action )
A17: **3 to 5 minutes
A18: **Within 60 minutes
A19: 30 µg/kg bolus
A20: 4 µg/kg/min infusion for at least 2 hours or duration of PCI, up to 4 hours
*** Direct-acting antiplatelet agents (cangrelor and ticagrelor) have reversible effects and do not require hepatic metabolism for achieving pharmacodynamic activity.
Q1: What are the two purinergic G protein–coupled receptors expressed on platelets?
Q2: Activation of which receptor inhibits adenylate cyclase (AC) and decreases cAMP levels?
Q3: Activation of which receptor increases intracellular calcium (Ca2+) levels?
Q4: How does increased intracellular Ca2+ lead to platelet aggregation?
Q5: Name four drugs that bind to the P2Y12 receptor to inhibit platelet activation.
A1: P2Y1 and P2Y12
A2: P2Y12
A3: P2Y1
A4: By changing the ligand-binding properties of the glycoprotein IIb/IIIa receptor
A5: Clopidogrel, prasugrel, ticagrelor, and cangrelor ( inhibit platelet activation and aggregation processes by modulating intraplatelet levels of cAMP and VASP-P [ vasodilator-stimulated phosphoprotein] )
Q1: Adding P2Y12 receptor inhibitors to aspirin is particularly beneficial in which clinical settings?
Q2: What are the pivotal issues surrounding the optimal use of P2Y12 inhibitors in PCI patients?
Q3: Is there a consensus on the optimal timing of P2Y12 antagonist administration in PCI?
Q4: What is recommended for patients undergoing PCI with stenting regarding P2Y12 inhibitors?
Q5: Is routine pretreatment with P2Y12 inhibitors recommended before coronary angiography in stable CAD patients?
Q6: In patients with non-ST-segment elevation ACS undergoing early angiography, when is P2Y12 loading typically done?
Q7: *****Does preloading with P2Y12 inhibitors offer significantly more benefit than loading after anatomy is known in non-ST-elevation ACS?
Q8: Is prasugrel recommended as upfront therapy in non-ST-elevation ACS?
Q9: What is a significant trade-off of starting P2Y12 therapy before knowing coronary anatomy?
Q10: How long should *Clopidogrel be suspended before surgical revascularization?
Q11: How long should *Prasugrel be suspended before surgical revascularization?
Q12: How long should *Ticagrelor be suspended before surgical revascularization?
Q13: Why is suspension of P2Y12 inhibitors necessary before surgery?
Q14: What risk is minimized by suspending P2Y12 inhibitors before surgery?
Q15: Are the recommendations about timing and duration of P2Y12 therapy consistent across guidelines?
A1: In the settings of PCI and across the spectrum of acute coronary syndrome (ACS) manifestations
A2: Timing of treatment, dosing, and duration of therapy
A3: No, it is still a matter of discussion
A4: A loading dose of a P2Y12 receptor inhibitor should be given
A5: *No, there is no compelling evidence to support routine *pretreatment
A6: After the coronary anatomy is known
A7: ***No, it appears to offer similar benefit
A8: No, it is not recommended for upfront therapy
A9: Patients may need to suspend ( postpone sx ) therapy if surgical revascularization is needed
A10: At least 5-7 days
A11: *7 days
A12: 5 days
A13: To minimize the risk of bleeding complications
A14: Bleeding complications
A15: Recommendations vary and are still being refined
Q1: What is the drug of choice for patients with stable ischemic heart disease undergoing PCI?
Q2: Which P2Y12 inhibitors are preferred over clopidogrel in the context of ACS?
Q3: At what dose is ticagrelor preferably considered in selected stable patients undergoing PCI?
Q4: Which patient group is especially considered for ticagrelor use in stable ischemic heart disease?
Q5: What factors should be considered when choosing between prasugrel and ticagrelor in ACS patients?
Q6: What does the ISAR-REACT 5 trial compare?
Q7: In the ISAR-REACT 5 trial, which drug showed a lower incidence of death, MI, or stroke?
Q8: Was there a significant difference in major bleeding between prasugrel and ticagrelor in ISAR-REACT 5?
Q9: Were the ISAR-REACT 5 results consistent in the subgroup treated with PCI?
Q10: What drug has received FDA approval as an adjunct to PCI for reducing periprocedural MI, repeat revascularization, and stent thrombosis?
Q11: Which trial provided evidence for cangrelor’s efficacy in PCI?
Q12: What was the comparison in the CHAMPION PHOENIX trial?
Q13: What was the outcome of using cangrelor followed by clopidogrel vs clopidogrel alone?
Q14: Has cangrelor been tested in clinical trials combined with ticagrelor or prasugrel?
Q15: What do pharmacodynamics studies show about combining cangrelor with potent oral P2Y12 inhibitors?
Q16: What are the primary ischemic events that cangrelor helps reduce during PCI?
Q17: Is clopidogrel effective in stable ischemic heart disease patients undergoing PCI?
Q18: What is the dosing frequency of ticagrelor when used in stable patients?
Q19: What is a major consideration when prescribing P2Y12 inhibitors in ACS?
Q20: What is the main benefit of using potent P2Y12 inhibitors in ACS compared to clopidogrel?
A1: Clopidogrel
A2: Prasugrel and ticagrelor
A3: 60 mg twice daily (bid)
A4: Patients with diabetes
A5: Clinical characteristics, contraindications, drug interactions, adherence, affordability
A6: Prasugrel versus ticagrelor in ACS patients
A7: Prasugrel
A8: No significant difference
A9: Yes
A10: Cangrelor
A11: CHAMPION PHOENIX trial
A12: Cangrelor followed by clopidogrel versus clopidogrel alone
A13: Reduction in peri-PCI ischemic events
A14: No
A15: Enhances platelet inhibition
A16: Periprocedural myocardial infarction, repeat revascularization, stent thrombosis
A17: Yes
A18: Twice daily
A19: Patient-specific factors including clinical profile and adherence
A20: Faster, more potent platelet inhibition and better outcomes
