BCCCP Cardiology 2026: Mastering Acute Coronary Syndrome and Anticoagulation for the BPS Cardiology Board Exam

BCCCP Cardiology 2026: Mastering Acute Coronary Syndrome and Anticoagulation for the BPS Cardiology Board Exam

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Acute coronary syndrome (ACS) questions on the BPS Cardiology Board Exam reward clear, practical thinking. They test how you triage, choose antithrombotics, prevent bleeding, and adjust to real-world barriers like renal disease or planned surgery. This guide focuses on what matters for 2026-level practice: how to master antiplatelet and anticoagulant strategy across STEMI and NSTE-ACS, and why each decision lowers risk without inviting bleeding.

What the exam tests in ACS and anticoagulation

Expect cases that force tradeoffs. The exam checks whether you:

  • Recognize the clock. Reperfusion timing drives survival in STEMI. The earlier you open the artery, the more muscle you save.
  • Match drug to pathway. Aspirin and P2Y12 blockers target platelets (plaque rupture is platelet-rich). Heparins, bivalirudin, and fondaparinux target thrombin/Xa (the fibrin backbone). You need both in ACS because both processes drive clot growth.
  • Adapt to context. Kidney disease, prior stroke, active bleeding risk, need for CABG, or existing anticoagulation can flip the “right” regimen.
  • Prevent harm. Bleeding, especially intracranial, kills. The exam rewards dose checks, renal adjustments, radial access, PPIs, and the shortest effective duration of combination therapy.

Fast ECG and biomarker triage in ACS

You cannot pick the right drugs unless you classify the patient fast and correctly:

  • STEMI. ST elevation or new LBBB with ischemic symptoms. Goal is immediate reperfusion. You add potent antiplatelet and an anticoagulant because wire passage and device work trigger clot activation.
  • NSTE-ACS (NSTEMI/UA). No ST elevation. High-sensitivity troponin often reclassifies “UA” as NSTEMI. Treatment intensity depends on risk (TIMI/GRACE), ongoing ischemia, and timing to angiography.
  • Type 2 MI (supply/demand). Tachyarrhythmia, anemia, sepsis. Focus on the trigger; aggressive antithrombosis is not always right because the problem is not plaque rupture.

Antiplatelet therapy: the backbone of ACS care

Aspirin reduces mortality by blocking thromboxane and platelet activation.

  • Loading: 162–325 mg chewed once.
  • Maintenance: 81 mg daily long-term. Higher doses add bleeding without more benefit.
  • Aspirin intolerance: Aim for desensitization in true allergy if possible. If not, clopidogrel monotherapy is a fallback.

P2Y12 inhibitors prevent ADP-mediated platelet activation. More potent agents lower reinfarction but increase bleeding.

  • Clopidogrel
    • Load: 600 mg (PCI) or 300–600 mg (non-PCI).
    • Maintenance: 75 mg daily.
    • Why choose: Lower bleeding; preferred if triple therapy with oral anticoagulant is needed.
  • Ticagrelor
    • Load: 180 mg; Maintenance: 90 mg twice daily (then 60 mg twice daily after 12 months in extended therapy).
    • Why choose: Faster, stronger platelet inhibition; reduces ischemic events in ACS.
    • Avoid/Use caution: Severe dyspnea or bradyarrhythmias; strong CYP3A4 interactions; intracranial bleeding history.
  • Prasugrel
    • Load: 60 mg; Maintenance: 10 mg daily (5 mg if weight <60 kg; consider 5 mg or avoid if age ≥75 unless very high ischemic risk).
    • Why choose: Most potent oral option; best in PCI-defined anatomy.
    • Contraindicated: Prior stroke or TIA. Avoid pretreatment before anatomy is known in NSTE-ACS due to CABG bleeding risk.

Why pretreatment matters: In STEMI headed to PCI, pretreating helps because delays to CABG are rare. In NSTE-ACS, giving prasugrel or ticagrelor before the cath can backfire if CABG is needed; bleeding risk rises. The exam often rewards “wait until anatomy is known” in NSTE-ACS.

Anticoagulants in ACS: when and which one

Anticoagulants stop fibrin growth on top of platelet-rich clot. You use them during the acute phase, not indefinitely, because long-term benefit is minimal and bleeding risk accumulates.

  • Unfractionated heparin (UFH)
    • PCI bolus: 70–100 units/kg IV (lower dose if using GP IIb/IIIa). Adjust by ACT during PCI.
    • NSTE-ACS infusion: 60 units/kg IV bolus (max ~4000), then 12 units/kg/hr (max ~1000) with aPTT goal ~1.5–2.5× control.
    • Why choose: Rapid on/off; safe in severe CKD; reversible with protamine; ideal if urgent surgery is possible.
  • Enoxaparin (LMWH)
    • NSTE-ACS: 1 mg/kg SC every 12 h; if CrCl <30 mL/min, dose every 24 h.
    • STEMI with fibrinolysis, age <75: 30 mg IV bolus, then 1 mg/kg SC every 12 h (first two SC doses capped at 100 mg).
    • STEMI with fibrinolysis, age ≥75: no IV bolus; 0.75 mg/kg SC every 12 h (first two doses capped at 75 mg); if CrCl <30, give once daily.
    • Why choose: Lower HIT risk, predictable effect. But accumulation in CKD increases bleeding; this is tested often.
  • Bivalirudin
    • PCI: 0.75 mg/kg IV bolus, then 1.75 mg/kg/hr during PCI; reduce to 1.0 mg/kg/hr if CrCl <30.
    • Why choose: Lowers bleeding vs UFH + GP IIb/IIIa in primary PCI; ideal in HIT or high bleeding risk.
    • Watch for: Slightly higher acute stent thrombosis if infusion stops right at wire out; some centers extend a low-dose post-PCI infusion for 2–4 h.
  • Fondaparinux
    • NSTE-ACS: 2.5 mg SC daily.
    • Why choose: Lowest bleeding in NSTE-ACS among parenteral options.
    • Critical caution: Do not use as sole anticoagulant during PCI due to catheter thrombosis. Add a one-time UFH bolus in the lab.

Reperfusion in STEMI: primary PCI first, fibrinolysis if delayed

Reperfusion saves myocardium. The method depends on time and access:

  • Primary PCI is preferred when available promptly. It clears clot, treats the culprit lesion, and avoids fibrinolysis bleeding risks.
  • Fibrinolysis if PCI will be delayed beyond acceptable windows and symptoms are within 12 hours (or ongoing ischemia). The “why”: earlier microvascular flow beats later perfect epicardial flow.

Tenecteplase dosing (single IV bolus):

  • <60 kg: 30 mg; 60–69 kg: 35 mg; 70–79 kg: 40 mg; 80–89 kg: 45 mg; ≥90 kg: 50 mg.
  • Many protocols give a half-dose in patients ≥75 years to reduce intracranial hemorrhage.

Adjunct anticoagulation with fibrinolysis: Use enoxaparin (with age/renal adjustments above) or UFH infusion for at least 24 hours. Fondaparinux is another option in some centers. The “why”: lytics expose thrombin and can paradoxically propagate clot without anticoagulation.

Absolute contraindications to fibrinolysis include prior intracranial hemorrhage, known intracranial neoplasm or AVM, suspected aortic dissection, ischemic stroke within recent weeks (except acute disabling stroke under specific protocols), and active bleeding. The exam expects you to stop and switch to transfer for PCI if any are present.

PCI antithrombotics: putting it together

  • STEMI primary PCI:
    • Aspirin load + ticagrelor or prasugrel load (unless contraindicated) + UFH or bivalirudin.
    • Consider GP IIb/IIIa (eptifibatide/tirofiban) as bailout for thrombotic complications. Use renal dose reductions to avoid bleeding.
  • NSTE-ACS early invasive:
    • Begin aspirin + anticoagulant (UFH, enoxaparin, or fondaparinux). Withhold prasugrel until anatomy is known; ticagrelor or clopidogrel can be given per strategy and bleeding risk.
    • During PCI, if fondaparinux was started, add a UFH bolus to prevent catheter thrombosis.

NSTE-ACS: invasive vs ischemia-guided strategy

Why risk scores matter: high-risk patients (dynamic ST changes, positive troponin, high GRACE/TIMI) benefit from early invasive evaluation with upstream anticoagulation. Low-risk patients can pursue ischemia-guided care with careful monitoring and noninvasive testing.

  • Early invasive favors ticagrelor at the time of PCI, UFH/LMWH prior, and transition to DAPT x 12 months if stented.
  • Ischemia-guided favors clopidogrel if bleeding risk is higher, fondaparinux or dose-adjusted enoxaparin, and conservative anticoagulant duration.

Special populations: do the small things right

  • Renal impairment
    • Prefer UFH or bivalirudin (dose-adjust bivalirudin when CrCl <30).
    • Enoxaparin accumulates; reduce frequency to daily when CrCl <30 in NSTE-ACS; halve doses in STEMI protocols as noted. Fondaparinux is contraindicated when CrCl is severely reduced.
    • Why: accumulation raises bleeding risk, especially intracranial in the elderly.
  • Older adults
    • Higher bleeding risk with fibrinolysis and potent P2Y12s. Adjust lytic and LMWH doses; consider clopidogrel if recurrent falls, frailty, or planned surgery.
  • Low body weight
    • Prasugrel 5 mg daily if <60 kg; careful with enoxaparin (mg/kg without rounding up; cap first two doses in STEMI).
  • Hepatic disease
    • Argatroban preferred anticoagulant in HIT with renal impairment, but avoid if severe hepatic dysfunction. Ticagrelor use requires caution in significant hepatic impairment.
  • Pregnancy
    • UFH and enoxaparin are preferred; avoid fondaparinux unless no alternative. Fibrinolysis is considered if PCI is not rapidly available in STEMI.

AF or VTE on anticoagulation + ACS/PCI: minimize time on triple therapy

This is a high-yield exam theme: balance stroke prevention with stent protection while cutting bleeding.

  • Default path: Prefer a DOAC over warfarin if eligible.
  • Triple therapy (OAC + aspirin 81 mg + clopidogrel 75 mg) for the shortest period that protects the stent (often 1–4 weeks after PCI). Why: early stent thrombosis risk is highest in that window.
  • Then step down to dual therapy (OAC + clopidogrel) for 6–12 months depending on bleeding vs ischemic risk, then OAC alone.
  • Avoid prasugrel or ticagrelor with OAC unless compelling reasons; bleeding risk is higher.
  • Use a PPI and radial access to reduce GI and access-site bleeding.

Bleeding risk, HIT, reversal, and monitoring

Bleeding prevention is as important as ischemia prevention on the exam.

  • Risk reduction tactics:
    • Use radial access when possible.
    • Use weight-based dosing and renal adjustments.
    • Cap large boluses (e.g., UFH; first enoxaparin doses in STEMI), avoid duplicate anticoagulants.
    • Choose the shortest effective duration of combination therapy.
  • Monitoring:
    • UFH: aPTT or ACT in PCI; check platelets every 1–2 days for HIT when exposure lasts several days.
    • LMWH: anti-Xa in special populations (pregnancy, obesity, severe CKD) if needed.
    • DOACs: renal function at baseline and periodically.
  • HIT:
    • Suspect with platelet fall >50% 5–10 days after heparin, or sooner with prior exposure.
    • Use the 4Ts score to judge probability; switch to bivalirudin or argatroban if HIT likely.
    • Argatroban raises INR; this matters if you later bridge to warfarin.
  • Reversal (know these cold):
    • UFH/LMWH: protamine (full reversal for UFH; partial for LMWH).
    • Dabigatran: idarucizumab.
    • Apixaban/rivaroxaban: andexanet alfa or PCC per institutional protocol.
    • Bivalirudin: short half-life; no antidote; stop infusion and support.

Secondary prevention after ACS: what to continue and for how long

The exam often asks when to shorten or extend therapy.

  • DAPT duration
    • Standard after ACS with stent: 12 months of aspirin + a P2Y12 inhibitor.
    • Shorten to 3–6 months in high bleeding risk (e.g., recent bleed, frailty) with careful follow-up.
    • Extend beyond 12 months if ischemic risk is high and bleeding risk low. Ticagrelor 60 mg twice daily with aspirin is a common extended strategy.
  • Dual-pathway inhibition in chronic CAD/PAD (selected high-risk, low-bleeding-risk patients): rivaroxaban 2.5 mg twice daily + aspirin 81 mg can reduce events by adding anti-Xa to antiplatelet therapy. Not typically combined with full DAPT long term due to bleeding.
  • Foundational meds that reduce reinfarction and death:
    • High-intensity statin for all unless contraindicated.
    • Beta-blocker early post-MI unless shock, bradycardia, or severe asthma.
    • ACE inhibitor/ARB in LV dysfunction, diabetes, CKD, or hypertension.
    • Eplerenone in post-MI LV dysfunction with diabetes or heart failure symptoms.
    • Smoking cessation, cardiac rehab, diabetes optimization (SGLT2 inhibitors or GLP-1 RA when appropriate).

High-yield dosing pearls to memorize

  • Aspirin: 162–325 mg load; 81 mg daily maintenance.
  • Clopidogrel: 600 mg load for PCI; 75 mg daily.
  • Ticagrelor: 180 mg load; 90 mg twice daily, then 60 mg twice daily after 12 months if extended.
  • Prasugrel: 60 mg load; 10 mg daily (5 mg if <60 kg or age ≥75 use 5 mg or avoid unless high ischemic risk); contraindicated with prior stroke/TIA.
  • UFH (NSTE-ACS): 60 units/kg IV bolus, then 12 units/kg/hr; titrate to aPTT.
  • UFH (PCI): 70–100 units/kg IV bolus (lower if using GP IIb/IIIa); ACT-guided.
  • Enoxaparin (NSTE-ACS): 1 mg/kg SC q12h; q24h if CrCl <30.
  • Enoxaparin (STEMI lytics <75 y): 30 mg IV bolus + 1 mg/kg SC q12h (cap first two SC doses at 100 mg).
  • Enoxaparin (STEMI lytics ≥75 y): no IV bolus; 0.75 mg/kg SC q12h (cap first two at 75 mg); q24h if CrCl <30.
  • Bivalirudin (PCI): 0.75 mg/kg IV bolus; 1.75 mg/kg/hr infusion; 1.0 mg/kg/hr if CrCl <30.
  • Fondaparinux (NSTE-ACS): 2.5 mg SC daily; add UFH bolus in PCI lab.
  • Tenecteplase (STEMI): 30–50 mg single IV bolus by weight tier; consider half-dose in ≥75 years.

Common exam traps and how to avoid them

  • Pretreating prasugrel in NSTE-ACS before anatomy is known → higher CABG bleeding. Wait for the cath.
  • Using fondaparinux alone during PCI → catheter thrombosis. Always add a UFH bolus in the lab.
  • Full-dose enoxaparin in severe CKD → intracranial hemorrhage risk. Reduce frequency to daily or switch to UFH.
  • Prolonged triple therapy in AF + PCI → excess bleeding without extra protection after the first few weeks. Step down early.
  • Prasugrel in prior stroke/TIA → contraindicated. Choose a different P2Y12 inhibitor.
  • Skipping DAPT after lytics → re-occlusion risk rises. Give aspirin plus a P2Y12 unless contraindicated.
  • Not checking weight caps on initial enoxaparin doses in STEMI lysis protocols.

Case walk-throughs

  • Case 1: 62-year-old with STEMI, primary PCI planned in 45 minutes, no stroke history, normal kidneys.
    • Aspirin 325 mg chewed; ticagrelor 180 mg load; UFH 70–100 units/kg bolus in lab. Why: fast, potent platelet block; UFH is effective, reversible, and monitored by ACT.
  • Case 2: 78-year-old with STEMI, rural facility; PCI delayed; fibrinolysis considered; CrCl 28 mL/min.
    • Tenecteplase (half-dose per local protocol); enoxaparin 0.75 mg/kg SC q24h (omit IV bolus) or UFH infusion alternative. Why: age and CKD demand dose reduction to prevent ICH.
  • Case 3: 70-year-old NSTE-ACS, troponin positive, planned early invasive strategy, possible CABG.
    • Aspirin + UFH infusion; defer prasugrel; consider ticagrelor/clopidogrel at PCI. Why: avoid pretreatment that complicates surgical timing.
  • Case 4: 66-year-old with AF on apixaban needs PCI for STEMI.
    • Proceed with primary PCI; give clopidogrel load; keep aspirin low dose. After discharge: triple therapy 1–2 weeks, then apixaban + clopidogrel to 6–12 months, then apixaban alone. PPI on board. Why: shortest effective triple exposure limits bleeding.

Efficient study plan for the exam

  • Week 1: Memorize core doses and adjustments (section: High-yield dosing pearls). Drill contraindications to lytics and prasugrel.
  • Week 2: Work PCI pathways. Practice “if–then” branches for fondaparinux, bivalirudin, and GP IIb/IIIa. Add CABG timing holds: clopidogrel 5 days, prasugrel 7 days, ticagrelor 3–5 days, eptifibatide/tirofiban 4–8 hours, abciximab 12 hours, UFH 4–6 hours, bivalirudin 2–3 hours, enoxaparin 12–24 hours.
  • Week 3: Master special populations (CKD, elderly, low weight) and AF + PCI antithrombotic sequencing. Create flashcards for bleeding prevention tactics.
  • Week 4: Timed case sets. Aim for automatic recognition of traps and quick, safe choices.

Bottom line

In ACS, the right antiplatelet plus the right anticoagulant at the right time saves myocardium and lives. The exam rewards precise dosing, careful adjustments, and clear reasons for every choice. Think in pathways (platelet + thrombin), respect the clock, lower bleeding wherever possible, and tailor therapy to the person in front of you. If you can explain why each drug is there and when to stop it, you are ready for BCCCP Cardiology 2026.

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