Brilinta
Brilinta
Generic Name
Brilinta
Mechanism
Brilinta (*ticagrelor*) is a rapid‑acting, reversible P2Y12 ADP receptor antagonist.
• Binds competitively to the purinoreceptor on platelet surfaces, prevents ADP‑induced activation and aggregation.
• Unlike thienopyridines, it does not require hepatic ½‑life metabolic activation; active drug is present immediately after absorption.
• Provides a stable, predictable antiplatelet effect with a short half‑life (~7 h), allowing rapid dose‑adjustment when needed.
Pharmacokinetics
- Absorption: ~80 % bioavailability, peak plasma concentration 1–2 h post‑dose.
- First‑pass metabolism: CYP3A4/5‑mediated; not a significant CYP inhibitor/inducer.
- Distribution: Volume of distribution ~210 L; moderate plasma protein binding (~54 %).
- Elimination: Predominantly renal (30 %) and hepatic; terminal half‑life ~7 h.
- Drug interactions: Caution with potent CYP3A4 inhibitors (e.g., ketoconazole) or inducers (e.g., rifampin). Avoid concomitant strong CYP3A4 induction due to potential subtherapeutic levels.
Indications
- Acute coronary syndrome (ACS) (ST‑segment and non‑ST‑segment) – as part of dual antiplatelet therapy (DAPT) with aspirin.
- Post‑percutaneous coronary intervention (PCI) – maintenance antiplatelet for at least 6 months, can be extended based on ischemic risk.
- Stable coronary artery disease – in high‑risk patients when DAPT is clinically indicated.
Contraindications
- Contraindicated:
- Known hypersensitivity to ticagrelor or any excipients.
- Concomitant use of strong CYP3A4 inhibitors (unless dose adjustment is justified).
- Severe hepatic impairment (Child‑Pugh C).
- Active pathological bleeding, ongoing major hemorrhage.
- Recent intracranial bleed or subarachnoid hemorrhage.
- Warnings:
- Pulmonary edema in patients with cardiogenic shock or left‑ventricular dysfunction.
- Tolerability issues: dyspnea, headaches; usually transient and self‑limited.
- Reversible bradycardia / tachyarrhythmias – monitor heart rhythm, especially in patients on β‑blockers or digoxin.
- Allergic reactions: rash, urticaria, anaphylaxis possible.
Dosing
| Situation | Dose | Frequency | Duration |
| ACS (hospital) | 180 mg single loading dose (two 90 mg tablets) | 90 mg BID | 12 months (extendable to 24 months per guideline) |
| Stable CAD, PCI | 90 mg BID (tablet) | 12 months DAPT post‑PCI | 3–6 months thereafter per risk profile |
| Long‑term DAPT | 90 mg BID | 12–24 months | Follow per ischemic risk assessment |
• Timing: Administer with food to enhance absorption.
• Direction: Swallow tablets whole; do not chew or crush.
• Missed dose: Take as soon as remembered; do not double‑dose.
Adverse Effects
- Common
- Dyspnea (≈6 %) – usually mild and improves with time.
- Headache, insomnia.
- Gastrointestinal upset (nausea, diarrhea).
- Serious
- Major bleeding (intracranial, gastrointestinal).
- Cardiogenic shock with pulmonary edema.
- Hypersensitivity reactions (rash, urticaria).
- Bradycardia or AV block events.
| Adverse Event | Incidence (≈10 % population) | Management |
| Major bleeding | 0.4–1.0 % | Hold drug, evaluate source, consider reversal agents (e.g., platelet transfusion) |
| Pulmonary edema | <0.1 % | Discontinue, treat heart failure, monitor oxygenation |
| Dyspnea | 6 % | Symptomatic relief, schedule follow‑up; consider dose taper if severe |
Monitoring
- Baseline: Hemoglobin, platelet count, PT/aPTT, CMP.
- After initiation: Monitor for signs of bleeding, renal and hepatic function.
- During therapy:
- Watch for dyspnea, cardiovascular symptoms, and signs of arrhythmias.
- Check platelet counts annually if prolonged DAPT.
- Special populations: Adjust dosing or avoid in severe renal dysfunction (CrCl < 30 mL/min).
Clinical Pearls
- “Rapid loading” is key: Unlike clopidogrel, ticagrelor’s active drug is present instantaneously, translating to early platelet inhibition in the cath‑lab setting.
- No prodrug concerns: Skip CYP3A4 issues of clopidogrel; worry less about genetic polymorphisms (CYP2C19).
- Dyspnea: cat‑thytherapy? – A transient, non‑cardiogenic dyspnea often resolves >24 h; educate patients to differentiate from ischemia.
- Caution with high‑dose aspirin (≥325 mg) – It can reduce ticagrelor absorption due to delayed gastric emptying; stick to 81–100 mg when possible.
- Stopped abruptly? – Rapidly declines antiplatelet effect due to short half‑life; if therapy must be interrupted, initiate bridging with IV heparin for patients at high thrombotic risk.
- Elderly & renal impairment – Still safe; no dose adjustment needed, but monitor bleed risk.
- PCI in chronic kidney disease – Ticagrelor offers superior platelet inhibition over clopidogrel with similar bleeding risk, advantageous in CKD patients.
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• *This drug card is for educational purposes only. For individualized patient care, consult updated prescribing information, guidelines, and specialist input.*