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Acute Coronary Syndrome: Non–Q-Wave (Non–ST-Elevation) MI, Emergency Medicine

Basics

Description

- Thrombus generation: - Platelet adhesion via glycoprotein (GP) Ia/IIa to collagen; GP Ib to vWF: - Platelet activation: Release of ADP, thromboxane A2, and serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstriction - Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen, cross-links platelets, forming local platelet plug

- Pain: - Pressure or tightness or heaviness - Substernal, epigastric - +/- radiation to arm, jaw, back - More likely nonpositional, nonpleuritic, nonreproducible on palpation

- Cardiac markers: - Troponins: Specific indicators of myocardial infarction, rises within 3-6 hr after MI, peaks at 9-10 days - Creatine kinase (CK): Rises within 4-8 hr, peaks at 18-24 hr, subsiding at 3-4 days; isoenzyme CK-MB more specific for cardiac origin - Myoglobin: Rises within 2-6 hr, returns to baseline within 24 hr, highly sensitive but very nonspecific - LDH: Rises within 24 hr, peaks at 3-6 days, returns to baseline at 8-12 days

  • Non-ST-elevation myocardial infarction (NSTEMI) is a part of a clinical syndrome that also includes unstable angina and ST-elevation MI (STEMI).
  • Caused by subtotal occlusion of coronary blood flow:Often indicates an incomplete ischemic event
  • Coronary plaque disruption:Endothelial disruption exposes subendothelial collagen and other platelet-adhering ligands, von Willebrand factor (vWF), and fibronectin.Release of tissue factors activates factor VII and extrinsic pathway.
  • Thrombus generation:Platelet adhesion via glycoprotein (GP) Ia/IIa to collagen; GP Ib to vWF:Platelet activation: Release of ADP, thromboxane A2, and serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstrictionPlatelet aggregation: GP IIb/IIIa receptor binds fibrinogen, cross-links platelets, forming local platelet plugPlatelet stabilization: Thrombin converts fibrinogen to fibrin, provides fibrin mesh, stabilizes platelet aggregate
  • Microembolization to downstream coronary arterioles may occur

Etiology

  • Coronary thrombosis
  • Coronary vasospasm, idiopathic or cocaine induced
  • In situ thrombosis/hypercoagulable states
  • Embolic event (e.g., endocarditis, paradoxical emboli through PFO)
  • Arteritis

Diagnosis

Signs and Symptoms

History

  • Pain:Pressure or tightness or heavinessSubsternal, epigastric+/- radiation to arm, jaw, backMore likely nonpositional, nonpleuritic, nonreproducible on palpation
  • Nausea, vomiting
  • Diaphoresis
  • Cough
  • Dyspnea
  • Anxiety
  • Light-headedness
  • Syncope
  • Recent cocaine or amphetamine use
  • Family history of coronary disease
  • Atypical presentations common, especially in women, diabetics, and the elderly

Geriatric patients may present with atypical symptoms or silent ischemia. пїЅ

Physical Exam

  • Pallor or diaphoresis
  • Hypertension or hypotension
  • Arrhythmias
  • S4 gallop
  • Physical exam is often normal

Essential Workup

ECG, cardiac biomarkers, CXR пїЅ

Diagnosis Tests & Interpretation

Lab

  • Cardiac markers:Troponins: Specific indicators of myocardial infarction, rises within 3-6 hr after MI, peaks at 9-10 daysCreatine kinase (CK): Rises within 4-8 hr, peaks at 18-24 hr, subsiding at 3-4 days; isoenzyme CK-MB more specific for cardiac originMyoglobin: Rises within 2-6 hr, returns to baseline within 24 hr, highly sensitive but very nonspecificLDH: Rises within 24 hr, peaks at 3-6 days, returns to baseline at 8-12 days
  • CBC
  • Serum electrolytes including magnesium
  • 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.
  • CXR:To assess heart size, pulmonary edema/congestion or identify other causes of chest pain
  • ECHO (generally not part of ED evaluation):To identify wall motion abnormalities and assess ventricular function
  • Radionuclide studies (if conservative management; generally not part of ED evaluation):Sestamibi scan: Identify viable myocardiumTechnetium 99: Identify recently infarcted myocardium

Diagnostic Procedures/Surgery

Coronary angiography (+/- PCI), typically as an inpatient, depending on patients risk profile and comorbidities пїЅ

Differential Diagnosis

  • STEMI
  • Pulmonary embolus
  • Aortic dissection
  • Acute pericarditis/myocarditis
  • Pneumothorax
  • Pancreatitis
  • Pneumonia
  • Esophageal spasm/gastroesophageal reflux
  • Esophageal rupture
  • Musculoskeletal pain/costochondritis

Treatment

Pre-Hospital

  • IV access
  • Oxygen administration
  • 12-lead EKG, cardiac monitoring, and treatment of arrhythmias
  • Aspirin, analgesia, anxiolytics

Initial Stabilization/Therapy

  • Oxygen administration
  • IV access
  • 12-lead EKG, cardiac monitoring, and treatment of arrhythmias

Ed Treatment/Procedures

  • Anti-ischemic therapy to reduce demand and increase supply of oxygen to myocardium:β-blockers: IV only if hypertensive with ongoing pain, else use orally within 24 hr; contraindicated in heart failureNitrates: Contraindicated with critical AS, suspicion of RV infarct or recent use of phosphodiesterase inhibitors (e.g., sildenafil)OxygenMorphine sulfateCalcium-channel blockers (nondihydropyridines-e.g., diltiazem, verapamil) may be used in patients with ongoing ischemia and contraindications to β-blockade. Contraindicated in heart failure
  • Dual antiplatelet therapy to decrease platelet aggregation:Aspirin: Only withhold if prior anaphylaxisADP Inhibitor: Clopidogrel (substitute for ASA if hypersensitivity), ticagrelor or prasugrel (if low bleeding risk, CABG unlikely, no history of CVA, age <75 yr)
  • GP IIb/IIIa inhibitors (eptifibatide, tirofiban):Only if ongoing ischemia, positive cardiac markers and PCI planned; can defer to inpatient administrationMay omit if loading dose of clopidgrel administered at least 6 hr prior to PCI or bivalirudin used for anticoagulation
  • Anticoagulation therapy to prevent thrombus propagation:Unfractionated heparin or enoxaparin are 1st-line therapies.Fondaparinux (factor Xa inhibitor) is a reasonable alternative, especially for medically managed patients; may have reduced bleeding risk.Reserve bivalirudin (direct thrombin inhibitor) for patients with known heparin-induced thrombocytopenia
  • Anxiolytics to suppress sympathomimetic release

Medication

First Line

  • Aspirin 162-325 mg PO per day
  • 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 Ојg/kg/min IV infusion (titrate by increasing 50 Ојg/kg/min q15min until effect-to max. dose 300 Ојg/kg/min)Metoprolol: Start 5 mg IV q5min пїЅ 3, after 15 min begin 25-50 mg PO BIDPropranolol: 0.5-1 mg IV then 40-80 mg PO q6-8h
  • Clopidogrel: 300-600 mg PO пїЅ 1, then 75 mg/d
  • Heparins:Enoxaparin: 1 mg/kg SC q12h, can give 30 mg IV bolus before SC dose (beware of enoxaparin in patients with renal dysfunction) orUnfractionated heparin: 60 U/kg IV bolus then 12 U/kg/hr infusion (max. bolus 4,000 U, max. infusion rate 1,000 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 Ојg/min if pain persists (max. dose 200 Ојg/min)
  • GP IIb/IIIa inhibitors:Eptifibatide: 180 Ојg/kg IV bolus then 2 Ојg/kg/min infusion for 72-96 hrTirofiban: 0.4 Ојg/kg/min IV пїЅ 30 min, then 0.1 Ојg/kg/min infusion for 12-24h

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 releaseVerapamil: Start 5-10 mg IV, repeat after 30 min if needed, then 80-160 mg PO q8h: immediate release
  • ADP blocker:Ticagrelor 180 mg PO пїЅ 1 at time PCI or no later than 1 hr post-PCI then 90 mg PO BIDPrasugrel 60 mg PO пїЅ 1 at time of PCI or no later than 1 hr post-PCI then 10 mg/d
  • Lorazepam: 1-2 mg IV PRN anxiety
  • Anticoagulation (instead of unfractionated heparin or enoxaparin):Fondaparinux: 2.5 mg SC once a day orBivalirudin (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

  • All patients with positive cardiac biomarkers, high risk for adverse outcomes by clinical prediction rules (TIMI, GRACE, PURSUIT), or significant clinical probability of acute coronary syndrome undergoing consideration for urgent or early invasive management 12-24 hr after presentation.
  • Intensive care unit for monitoring unstable patients

Discharge Criteria

Only those who are ruled out for acute coronary syndrome/non-Q-wave infarction can be safely sent home. пїЅ

Followup Recommendations

Only patients ruled out for acute coronary syndrome can be safely discharged: пїЅ

  • Discharged patients should follow up in 1-2 days with their primary care physician or cardiologist.
  • Outpatient stress tests should be done within 72 hr.

Pearls and Pitfalls

  • EKG should be done in all patients with chest pain on arrival to the ED, preferably within 10 min.
  • Early medical therapy can reduce mortality in NSTEMI.
  • Pitfalls:Do not rule out infarction based on initial or single set of cardiac markers, 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 Reading

  • Anderson пїЅJL, Adams пїЅCD, Antman пїЅEM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:e1-e157.
  • Bonaca пїЅMP, Steg пїЅPG, Feldman пїЅLJ, et al. Antithrombotics in acute coronary syndromes. J Am Coll Cardiol. 2009;54(11):969-984.
  • Braunwald пїЅE. Unstable angina and non-ST elevation myocardial infarction. Concise clinical review. Am J Resp Crit Care Med. 2012;185:924-932.
  • DeFilippi пїЅCR. Evaluating the chest pain patient. Scope of the problem. Cardiol Clin. 1999;17(2): 307-326.
  • Doshi пїЅAA, Iskyan пїЅK, O'Neill пїЅJM, et al. Evaluation and management of non-ST-segment elevation acute coronary syndromes in the emergency department. Emerg Med Pract. 2010;12(1):1-26.
  • Fesmire пїЅFM, Decker пїЅWW, Diercks пїЅDB, et al. Clinical policy: Critical issues in the evaluation and management of adult patient with non-ST-segment elevation acute coronary syndromes. Ann Emerg Med. 2006;48(3):270-301.
  • Pollack пїЅCV Jr, Braunwald пїЅE. 2007 Update to the ACC/AHA Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction: Implications for emergency department practice. Ann Emerg Med. 2008;51(5):591-606.
  • Wackers пїЅFJ. Chest pain in the emergency department: Role of cardiac imaging. Heart. 2009;95(12):1023-1030.
  • Wright пїЅRS, Anderson пїЅJL, Adams пїЅCD, et al. ACC/AHA 2011 focused update incorporated into the ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST elevation myocardial infarction. J Am Coll Cardiol. 2011;57(19):e21-e181.

See Also (Topic, Algorithm, Electronic Media Element)

  • Acute Coronary Syndromes
  • Cardiac Testing
  • Chest Pain

Codes

ICD9

  • 410.70 Subendocardial infarction, episode of care unspecified
  • 410.71 Subendocardial infarction, initial episode of care
  • 410.72 Subendocardial infarction, subsequent episode of care
  • 411.1 Intermediate coronary syndrome
  • 410.7 Subendocardial infarction

ICD10

  • I21.4 Non-ST elevation (NSTEMI) myocardial infarction
  • I24.9 Acute ischemic heart disease, unspecified

SNOMED

  • 401314000 Acute non-ST segment elevation myocardial infarction (disorder)
  • 314207007 Non-Q wave myocardial infarction (disorder)
  • 307140009 acute non-Q wave infarction (disorder)
  • 394659003 Acute coronary syndrome (disorder)