NSTEMI Diagnosis and Initial Management
For a patient diagnosed with NSTEMI, immediately place them on continuous ECG monitoring with defibrillator capacity, obtain a 12-lead ECG within 10 minutes, administer aspirin 162-325 mg (chewed), initiate dual antiplatelet therapy with a P2Y12 inhibitor, start anticoagulation, and perform risk stratification to determine timing of invasive coronary angiography. 1, 2, 3
Immediate Actions Upon Diagnosis
Monitoring and Environment
- Place the patient on continuous ECG monitoring with immediate defibrillator availability 1, 2
- Position emergency resuscitation equipment nearby 1
- Admit to a unit with continuous monitoring capability (chest pain unit, coronary care unit, or telemetry ward) 1
Oxygen Therapy
- Administer supplemental oxygen ONLY if arterial oxygen saturation is <90% or respiratory distress is present 1, 4, 2, 3
- Avoid routine oxygen therapy in patients with adequate saturation, as it provides no benefit 2, 3
Antiplatelet Therapy
Aspirin
- Administer aspirin 162-325 mg immediately (chewed for faster buccal absorption) 1, 2, 3
- Continue aspirin 75-100 mg daily indefinitely 2, 3
P2Y12 Inhibitor Selection
- Administer a P2Y12 inhibitor immediately upon diagnosis 2, 3
- For patients proceeding to PCI, ticagrelor or prasugrel are preferred over clopidogrel for higher-risk patients 2, 5
- Prasugrel dosing: 60 mg loading dose, then 10 mg daily 5
- Important timing consideration: In UA/NSTEMI patients, the loading dose should not be administered until coronary anatomy is established 5
- Continue dual antiplatelet therapy (aspirin plus P2Y12 inhibitor) for 12 months after PCI 3
Special Considerations for P2Y12 Inhibitors
- For patients weighing <60 kg on prasugrel, consider reducing maintenance dose to 5 mg daily due to increased bleeding risk 5
- Prasugrel is contraindicated in patients with prior stroke or TIA 5
- Discontinue clopidogrel 5-7 days before elective CABG 1
Anticoagulation Therapy
Initiate anticoagulation immediately with one of the following: 2, 3
- Unfractionated heparin: 60 U/kg IV bolus (maximum 4000 units), then 12 U/kg/hr infusion (maximum 1000 units/hr), adjusted to aPTT 1.5-2.5 times control 2
- Alternatively, low-molecular-weight heparin (enoxaparin) or fondaparinux may be used 1
- Continue anticoagulation for the duration of hospitalization, up to 8 days 1
Anti-Ischemic Therapy
Nitrates
- Administer sublingual nitroglycerin 0.4 mg every 5 minutes for up to 3 doses if ongoing ischemic chest pain 1, 2
- Initiate IV nitroglycerin starting at 10 mcg/min for persistent ischemia, heart failure, or hypertension, titrating to reduce blood pressure by 10-20% 1, 4, 2
- Contraindications: systolic BP <90 mmHg, suspected right ventricular infarction 2
Beta-Blockers
- Initiate oral beta-blocker therapy within the first 24 hours 1, 4, 2
- Avoid IV administration in patients with risk factors for cardiogenic shock 2
- Contraindications include: signs of heart failure, low-output state, heart rate <60 bpm, systolic BP <100 mmHg, PR interval >0.24 seconds, second or third degree heart block, active asthma or reactive airway disease 1, 4, 2
Morphine
- Administer morphine sulfate 2-4 mg IV with increments of 2-8 mg at 5-15 minute intervals for refractory chest pain uncontrolled by nitroglycerin 1, 4, 2
ACE Inhibitors/ARBs
- Administer an ACE inhibitor orally within the first 24 hours if pulmonary congestion or LVEF ≤0.40 is present, provided systolic BP ≥100 mmHg 4
- Use an ARB if the patient is intolerant of ACE inhibitors and has clinical or radiological signs of heart failure or LVEF ≤0.40 4
Risk Stratification and Timing of Invasive Strategy
Immediate Invasive Approach (Within 2 Hours)
Proceed to immediate coronary angiography for: 1, 2, 3
- Refractory angina despite maximal medical therapy
- Hemodynamic instability or cardiogenic shock
- Life-threatening ventricular arrhythmias
- Mechanical complications
- Recurrent angina with ST-segment depression ≥0.05 mV or new bundle branch block
- Acute heart failure
Early Invasive Strategy (Within 12-24 Hours)
Recommended for high-risk patients with: 2, 3
- GRACE score >140 or TIMI risk score >4
- Elevated troponin levels
- Dynamic ST-segment or T-wave changes
- LVEF <40%
- Diabetes mellitus
- Prior PCI or CABG
Conservative Strategy
- For low-risk patients without high-risk features, perform stress testing before discharge or within 72 hours as outpatient 1
- If stress testing reveals high-risk features, proceed to diagnostic angiography 1
Laboratory and Diagnostic Testing
Cardiac Biomarkers
- Obtain high-sensitivity cardiac troponin T or I at presentation 1
- Repeat troponin measurements at 1-3 hours if high-sensitivity assays are used, or at 3-6 hours with standard assays 1, 2
- Results should be available within 60 minutes 1
- Serial troponin measurements help distinguish NSTEMI (elevated biomarkers) from unstable angina (no biomarker elevation) 1
Additional Blood Work
- Serum creatinine, hemoglobin, hematocrit, platelet count, blood glucose 1
- INR in patients on warfarin 1
- Lipid profile should be assessed in the early phase of admission 1
Echocardiography
- Assess LV function with echocardiography during hospitalization to guide therapy with ACE inhibitors, beta-blockers, and aldosterone antagonists 4
- Consider immediate echocardiography in patients with ongoing chest pain and inconclusive ECG to exclude alternative diagnoses (pulmonary embolism, pericarditis, aortic dissection) 1
Critical Pitfalls to Avoid
- Never administer fibrinolytic therapy in NSTEMI patients—multiple trials demonstrated no benefit and potential harm 2
- Do not routinely use GP IIb/IIIa inhibitors upstream; reserve for high-risk patients undergoing PCI 2
- Do not delay angiography for "cooling off" period—early approach (median 2.4 hours) reduces death/MI compared to prolonged medical stabilization (median 86 hours) 2
- Avoid NSAIDs, as both COX-2 selective and nonselective agents increase mortality, reinfarction, and myocardial rupture risk 2
- Do not discontinue antiplatelet therapy prematurely, particularly in the first few weeks after ACS, as this increases risk of subsequent cardiovascular events 5
Distinguishing NSTEMI from Type 2 MI
NSTEMI typically results from acute atherothrombotic plaque rupture (Type 1 MI), but can also occur from oxygen supply-demand mismatch (Type 2 MI) 4, 6
- For Type 2 MI (e.g., secondary to respiratory failure, sepsis, anemia), an early invasive strategy is NOT automatically indicated 4
- Focus on treating the underlying precipitant rather than immediate coronary angiography 4
- Consider invasive approach only if evidence suggests concurrent Type 1 MI or patient becomes unstable with refractory ischemia 4