Immediate Management of Acute Coronary Syndrome
All patients with suspected ACS must receive aspirin 150-300 mg immediately (non-enteric formulation), obtain a 12-lead ECG within 10 minutes of first medical contact, and initiate continuous cardiac monitoring while simultaneously drawing high-sensitivity troponin with results available within 60 minutes. 1, 2, 3
Initial Assessment and Triage (First 10 Minutes)
ECG-Based Differentiation
- STEMI (persistent ST-elevation >20 minutes): Activate catheterization laboratory immediately for primary PCI within 120 minutes of presentation, or administer fibrinolytic therapy if PCI will be delayed beyond 120 minutes 1, 2, 4
- NSTE-ACS (no persistent ST-elevation): Proceed with risk stratification algorithm below—these patients show transient ST-depression, T-wave inversion, or non-diagnostic ECG changes 1
Immediate Pharmacotherapy (Administer While Awaiting Troponin)
Antiplatelet therapy:
- Aspirin 150-300 mg loading dose (chewed for faster absorption), then 75-100 mg daily indefinitely 1, 2, 3
- Add P2Y12 inhibitor immediately: Ticagrelor 180 mg loading dose, then 90 mg twice daily is preferred over clopidogrel for all NSTE-ACS patients regardless of management strategy 2, 3
- Do not administer prasugrel until coronary anatomy is known (contraindicated if prior stroke/TIA, age ≥75 years unless high-risk diabetes/prior MI, weight <60 kg requires dose reduction to 5 mg) 1, 5
Anticoagulation (select one):
- Fondaparinux 2.5 mg subcutaneously once daily has the best efficacy-safety profile 2, 3
- Alternative: Enoxaparin, unfractionated heparin, or bivalirudin based on institutional protocols 1
- Mandatory dose adjustment for renal dysfunction—assess creatinine clearance immediately 1, 3
Anti-ischemic therapy:
- Sublingual nitroglycerin 0.3-0.4 mg every 5 minutes up to 3 doses if systolic BP >90 mmHg and heart rate 50-100 bpm 3
- Transition to IV nitroglycerin if chest pain persists after sublingual doses 3
- Morphine IV/subcutaneous is reserved only for severe refractory chest pain—use sparingly as it may delay antiplatelet absorption 1, 3
- Oxygen only if saturation <90% or respiratory distress—routine oxygen is not indicated 1, 3
Risk Stratification for Invasive Strategy Timing
Very High-Risk: Immediate Angiography (<2 Hours)
Proceed directly to catheterization laboratory if ANY of the following present: 1, 3
- Hemodynamic instability or cardiogenic shock
- Recurrent/ongoing chest pain refractory to medical therapy
- Life-threatening arrhythmias or cardiac arrest
- Mechanical complications (acute severe mitral regurgitation, ventricular septal defect, free wall rupture)
- Acute heart failure with refractory angina or ST-segment deviation
High-Risk: Early Angiography (Within 24 Hours)
Perform coronary angiography within 24 hours if ANY of the following: 1, 2
- Confirmed NSTEMI (troponin rise/fall above 99th percentile)
- Dynamic ST-segment or T-wave changes on serial ECGs
- GRACE risk score >140
- Transient ST-segment elevation
Low-Risk: Selective Invasive Strategy
After stabilization, perform ischemia testing or coronary CT angiography to detect obstructive CAD before deciding on invasive approach 1, 2
Technical Considerations for Invasive Procedures
- Radial artery access is mandatory over femoral access to reduce bleeding complications 1, 3
- Drug-eluting stents are preferred over bare-metal stents for all PCI regardless of clinical presentation or anticipated DAPT duration 1
- Emergency CABG is indicated if coronary anatomy is not amenable to PCI in high-risk or cardiogenic shock patients 1, 2
- For mechanical complications, emergency surgical or catheter-based repair as decided by Heart Team 1
- Do not routinely use intra-aortic balloon pump in cardiogenic shock without mechanical complications—no mortality benefit demonstrated 1
Critical Monitoring and Laboratory Assessment
Biomarker strategy:
- High-sensitivity troponin at 0 and 1-2 hours allows rapid rule-in/rule-out with ≥99% sensitivity 1, 2, 3
- Conventional troponin requires 0 and 3-6 hour sampling 3
- Results must be available within 60 minutes of blood draw 1
Additional blood work on admission: 1, 3
- Serum creatinine and calculate eGFR (mandatory for anticoagulation dosing)
- Hemoglobin, hematocrit, platelet count
- Blood glucose
- Lipid profile in early admission phase
- INR if on warfarin
Continuous monitoring:
- Cardiac rhythm monitoring for minimum 24 hours 2
- Place defibrillator patches if ongoing ischemia until revascularization performed 1, 3
- Serial vital signs with frequent blood pressure monitoring if on IV nitroglycerin 3
Special Populations Requiring Modified Approach
Chronic kidney disease/ESRD:
- Apply same diagnostic and therapeutic strategies but mandatory dose adjustment of all anticoagulants and antiplatelet agents based on creatinine clearance 1, 3
- Use low- or iso-osmolar contrast at minimum volume during angiography 1, 3
- Chronically elevated baseline troponin requires assessment of dynamic changes rather than absolute values 3
- 2-3 fold increased bleeding risk—radial access and close hemoglobin monitoring essential 3
Age ≥75 years:
- Apply same invasive strategies as younger patients 1
- Prasugrel generally not recommended due to increased fatal/intracranial bleeding risk unless high-risk diabetes or prior MI 5
- Adjust antithrombotic dosing for renal function and bleeding risk 1
Diabetes mellitus:
- Screen all ACS patients for diabetes and monitor glucose frequently 1
- Avoidance of hypoglycemia is critical 1
Secondary Prevention (Initiate During Acute Phase)
Mandatory therapies to start before discharge: 1, 2
- High-intensity statin immediately regardless of baseline cholesterol
- Beta-blocker within first 24 hours if no heart failure, hypotension, bradycardia, or heart block
- ACE inhibitor or ARB for LVEF ≤40%, heart failure, hypertension, or diabetes
- Aspirin plus ticagrelor for 12 months, then aspirin monotherapy indefinitely
- Proton pump inhibitor for patients at higher than average GI bleeding risk 6
Critical pitfall: Discontinuing antiplatelet therapy, particularly in the first few weeks after ACS, dramatically increases risk of subsequent cardiovascular events and stent thrombosis 5