Acute Coronary Syndrome: Non-Q-Wave (Non-St-Elevation) Mi

Basics

Description

  • Non-ST-elevation myocardial infarction (NSTEMI) is within the acute coronary syndrome (ACS) category suggesting infarct/injury without STEMI ECG findings
  • Occlusion myocardial infarction (OMI): ACS with occlusive disease in a culprit artery that can present with subtle, classic, or without ECG changes. Newer term that suggests patients who may benefit from early reperfusion
  • Myocardial infarction can be classified as type 1 or type 2:
    • Type 1: Thrombotic coronary atherosclerotic plaque disruption or erosion (occlusive)
    • Type 2: Mismatch of oxygen supply and myocardial demand (atherosclerosis, vasospasm, dissection, increased cardiac demand, systemic causes, dysrhythmia)
  • Coronary plaque disruption:
    • Endothelial disruption exposes subendothelial tissue
    • Release of tissue factors generating thrombus, platelet adhesion, activation, aggregation, and stabilization of fibrin clot

Etiology

  • Coronary thrombosis
  • Coronary vasospasm (idiopathic or cocaine or other stimulant induced)
  • In situ thrombosis/hypercoagulable states
  • Embolic event (eg, endocarditis, paradoxical emboli through patent foramen ovale [PFO])
  • Arteritis

Diagnosis

Signs And Symptoms

History

  • Pain:
    • Pressure, crushing, tightness, or heaviness
    • Substernal, epigastric
    • +/− radiation to arm, jaw, back
    • More likely nonpositional, nonpleuritic, nonreproducible on palpation
  • Nausea, vomiting
  • Diaphoresis:
  • Dyspnea
  • Anxiety
  • Lightheadedness
  • Syncope or near syncope
  • Recent cocaine or amphetamine use
  • Family history of coronary disease
  • Atypical presentations:
    • Abdominal pain, burning epigastric discomfort
    • Common, especially in women, diabetics, and the elderly

Geriatric Considerations

Geriatric patients may present with atypical symptoms, altered mentation or silent ischemia

Physical Exam

  • Pallor or diaphoresis
  • Hypertension or hypotension
  • Dysrhythmia, bradycardia, irregular heart rate
  • S4 gallop
  • Physical exam is often normal

Essential Workup

ECG, cardiac biomarkers, CXR

Diagnostic Tests And Interpretation

Lab

  • Cardiac markers:
    • Troponins: Specific indicators of myocardial infarction, rise within 2–4 hr after MI, peak at 1–2 d, and return to normal in about 10 d
    • High sensitivity troponins: Preferred, increased sensitivity leading to rapid and reliable rule out of myocardial injury
    • Most hospitals have standard timing protocols and cutoff values for abnormal
    • CBC
  • Serum electrolytes including magnesium and phosphorus
  • PT/PTT/INR for patients on warfarin
  • NT-proBNP: Higher levels correlate with increased mortality in NSTEMI patients

Imaging

  • ECG:
    • ST-segment depression or transient elevation indicates increased risk
    • T-wave inversion in regional patterns does not increase risk but helps differentiate cardiac pain from noncardiac pain
    • Deep (>2 mm) precordial T-wave inversion suggests cardiac ischemia
    • Hyperacute T waves suggest ischemia
    • New conduction abnormality
  • CXR:
    • To assess heart size, pulmonary edema/congestion, or identify other causes of chest pain
  • Echo (often not part of ED evaluation):
    • To identify wall motion abnormalities and assess ventricular function
  • Radionuclide studies (if conservative management; often not part of ED evaluation)

Diagnostic Procedures/Surgery

Coronary angiography (+/– PCI), timing and decision making in conjunction with cardiology based on history, ECG, and troponin trends

Differential Diagnosis

  • STEMI (get serial ECGs more urgent PCI)
  • Pulmonary embolism
  • Aortic dissection
  • Acute pericarditis/myocarditis
  • Pericardial effusion/tamponade
  • Pneumothorax
  • Pancreatitis
  • Pneumonia
  • Esophageal spasm/gastroesophageal reflux
  • Esophageal rupture
  • Musculoskeletal pain/costochondritis

Treatment

Prehospital

  • IV access
  • Oxygen administration (if SpO2 <90%)
  • 12-lead ECG, cardiac monitoring, and treatment of dysrhythmias
  • Aspirin, analgesia

Initial Stabilization/Therapy

  • Oxygen administration (if SpO2 <90%)
  • IV access
  • 12-lead ECG, cardiac monitoring, and treatment of unstable dysrhythmias

Ed Treatment/Procedures

  • Anti-ischemic therapy to reduce demand and increase supply of oxygen to myocardium:
    • Nitrates: Contraindicated with critical AS, suspicion of RV infarct, or recent use of phosphodiesterase inhibitors (eg, sildenafil). Useful in severe hypertension
    • Oxygen, if hypoxic
    • Morphine if in severe pain
    • β-Blockers: Help reduce myocardial oxygen demand by decreasing heart rate, blood pressure, and myocardial contractility. Consider providing an IV dose if severe hypertension with ongoing pain, ischemia, treatment of dysrhythmias. Avoid in acute decompensated heart failure, low output state, risk for cardiogenic shock
    • Calcium channel blockers (nondihydropyridines – eg, diltiazem, verapamil) may be used in patients with contraindications to β-blockade with ongoing ischemia, dysrhythmias in the absence of LV dysfunction or increased risk for cardiogenic shock
  • Dual antiplatelet therapy to decrease platelet aggregation:
    • Aspirin: Only withhold if prior anaphylaxis (substitute with clopidogrel)
    • ADP inhibitor: Clopidogrel, ticagrelor, or prasugrel (if low bleeding risk, CABG unlikely, no history of CVA, age <75 yr); these may be delayed until after angiography
  • GP IIb/IIIa inhibitors (eptifibatide, tirofiban):
    • Only if ongoing ischemia, positive cardiac markers and PCI planned; can defer to inpatient administration
    • May omit if loading dose of clopidogrel administered at least 6 hr prior to PCI or bivalirudin used for anticoagulation
  • Anticoagulation therapy to prevent thrombus propagation in patients planned for invasive treatment:
    • Unfractionated heparin and enoxaparin are 1st-line therapies
    • Fondaparinux (factor Xa inhibitor) is a reasonable alternative, may have reduced bleeding risk
    • Reserve bivalirudin (direct thrombin inhibitor) for patients with known heparin-induced thrombocytopenia
  • Anxiolytics if needed (may suppress sympathetic drive)

Medication

First Line

  • Aspirin 325 mg PO
  • β-Blockers:
    • Atenolol: Start 5 mg IV over 5 min, then 5 mg IV 10 min later, then 50–100 mg PO per day (1–2 hr after IV doses)
    • Esmolol: 100 mcg/kg/min IV infusion (titrate by increasing 50 mcg/kg/min q15min until effect – to max. dose 300 mcg/kg/min)
    • Metoprolol: Start 5 mg IV q5min × 3, after 15 min begin 25–50 mg PO q12h
    • Propranolol: 0.5–1 mg IV then 40–80 mg PO q6–8h
  • Clopidogrel: 300–600 mg PO × 1, then 75 mg/d
  • ADP blocker:
    • Ticagrelor: 180 mg PO × 1 as soon as possible, then 90 mg PO q12h
    • Prasugrel: 60 mg PO × 1 at time of PCI or no later than 1 hr post-PCI, then 10 mg/d
  • Heparins:
    • Enoxaparin: 1 mg/kg SC q12h
    • Unfractionated heparin: 60-units/kg IV bolus then 12-units/kg/hr infusion (max. bolus 4000 units, max. infusion rate 1000 U/hr) (goal is a PTT 50–75 s)
  • Morphine sulfate: 1–5 mg IV q5-30min PRN pain
  • Nitroglycerin: 0.3–0.6 mg SL or 0.4 mg by spray q5min followed by IV infusion beginning at 10–20 mcg/min if pain persists (max. dose 200 mcg/min)
  • GP IIb/IIIa inhibitors:
    • Eptifibatide: 180-mcg/kg IV bolus then 2-mcg/kg/min infusion for 72–96 hr
    • Tirofiban: 25 mcg/kg IV bolus over 3 min, then 0.15 mcg/kg/min infusion

Second Line

  • Calcium channel blockers:
    • Diltiazem: Start 0.25 mg/kg IV bolus, then 0.35 mg/kg IV after 15 min if needed then 30 mg PO q6h: Immediate release
    • Verapamil: Start 5–10 mg IV, repeat after 30 min if needed, then 80–160 mg PO q8h: Immediate release
  • Lorazepam: 1–2 mg IV PRN anxiety
  • Anticoagulation (instead of unfractionated heparin or enoxaparin):
    • Fondaparinux: 2.5 mg SC once a day or
    • Bivalirudin (only prior to PCI): 0.75 mg/kg IV bolus, then 1.75 mg/kg/hr IV for up to 4 hr, then 0.2 mg/kg/hr IV for up to 20 hr

Follow-Up

Disposition

Admission Criteria

  • Significant troponin elevation, recurrent chest pain, dynamic ECG changes:
    • Admit all patients who are high risk for adverse outcomes by clinical prediction rules (EDACS, TIMI, GRACE, PURSUIT, HEART), or significant clinical probability of ACS undergoing consideration for urgent or early invasive management 12–24 hr after presentation
  • Stress testing and Coronary CTA often used for assessment in stable patients
  • Intensive care unit for monitoring unstable patients

Discharge Criteria

Only those who are ruled out for ACS/non-Q-wave infarction can be safely sent home. Patients with the diagnosis of acute NSTEMI or meet NSTEMI criteria, which largely includes abnormal troponin, should not be discharged

Follow-Up Recommendations

  • Discharged patients should follow up in 1 wk with their primary care physician or cardiologist
  • Outpatient stress tests should be done
  • If low risk, there is no evidence that stress testing within 30 d of index ED visit improves outcomes

Pearls And Pitfalls

  • ECG should be done in all patients with chest pain on arrival to the ED, preferably within 10 min. Frequent repeat ECG can be very helpful distinguishing NSTEMI vs STEMI or subtle changes of acute progressing ischemia
  • Early medical therapy can reduce mortality in select NSTEMI – discuss with cardiology
  • Pitfalls:
    • Do not rule out infarction based on initial or single troponin, particularly if the time from symptom onset is <4–6 hr
    • Do not fail to ask about amphetamine or cocaine use
    • Do not fail to ask about use of sildenafil, vardenafil, or tadalafil before giving nitroglycerin

Additional Readings

  1. DeFillippis AP, Chapman AR, Mills NL, et al. Assessment and treatment of patients with Type 2 myocardial infarction and acute nonischemic myocardial injury. Circulation. 2019;140(20):1661–1678.
  2. Gulati M, Levy PD, Mukherjee D, et al. AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;144:e368–e454.
  3. Kofoed KF, Kelbaek H, Hansen PR, et al. Early versus standard care invasive examination and treatment of patients with Non-ST-Segment elevation acute coronary syndrome. Circulation. 2018;138:2741–2750  [PMID:30565996]
  4. Meyers HP, Bracey A, Lee D, et al. Comparison of the ST-Elevation Myocardial Infarction (STEMI) vs. NSTEMI and Occlusion MI (OMI) vs. NOMI Paradigms of Acute MI. J Emerg Med. 2021;60(3):273–284.  [PMID:33308915]

See Also (Topic, Algorithm, Electronic Media Element)

The authors gratefully acknowledge Nathaniel Mann and Daniel Brown for their contributions to the previous edition of this chapter

Authors

Alan John

Deborah Diercks

Mark Courtney