Acute Coronary Syndrome: Myocardial Infarction

Basics

Description

  • Imbalance in myocardial blood supply and oxygen requirement
  • Acute coronary syndrome (ACS) encompasses a spectrum of disease processes:
    • Unstable angina pectoris
    • Acute myocardial infarction (AMI)
    • ST-elevation myocardial infarction (STEMI)
    • Non-STEMI

Etiology

  • Atherosclerotic narrowing of coronary vessels
  • Vasospasm (Prinzmetal or variant angina)
  • Microvascular angina or abnormal relaxation of vessels with diffuse vascular disease
  • Plaque disruption
  • Thrombosis
  • Arteritis:
    • Lupus
    • Takayasu disease
    • Kawasaki disease
    • Rheumatoid arthritis
  • Prolonged hypotension
  • Anemia/stress ischemia:
    • Hemoglobin <8 g/dL
  • Carbon monoxide/elevations in carboxyhemoglobin
  • Coronary artery gas embolus
  • Thyroid storm
  • Structural abnormalities of coronary arteries:
    • Radiation fibrosis
    • Aneurysms
    • Ectasia
  • Cocaine- or amphetamine-induced vasospasm
  • Cardiac risk factors include:
    • Hypercholesterolemia
    • DM
    • HTN
    • Smoking
    • Family history in a first-degree relative <55 yr old
    • Men, age >55 yr
    • Postmenopausal women

Diagnosis

Signs and Symptoms

  • Chest pain:
    • Most common presentation of MI
    • Substernal pressure
    • Heaviness
    • Squeezing
    • Burning sensation
    • Tightness
  • Anginal equivalents (MI without chest pain):
    • Abdominal pain
    • Syncope
    • Diaphoresis
    • Nausea or vomiting
    • Weakness
  • May localize or radiate to arms, shoulders, back, neck, or jaw
  • Associated symptoms:
    • Dyspnea
    • Syncope
    • Fatigue
    • Diaphoresis
    • Nausea
    • Vomiting
  • Symptoms are usually reproduced by exertion, eating, exposure to cold, or emotional stress
  • Symptoms commonly last 30 min or more
  • Symptoms may occur with rest or exertion
  • Often preceded by crescendo angina
  • May be improved/relieved with rest or nitroglycerin
  • Symptoms generally unchanged with position or inspiration
  • Positive Levine sign or clenched fist over chest is suggestive of angina
  • BP is usually elevated during symptoms

Physical Exam
  • Physical exam is usually unrevealing
  • Occasional physical findings include:
    • S3 or S4 due to left ventricular systolic or diastolic symptoms
    • Mitral regurgitation due to papillary muscle dysfunction
    • Diminished peripheral pulses
    • Physical findings of decompensated CHF

Essential Workup

History is critical in differentiating MI from noncardiac etiologies.

Diagnostic Tests and Interpretation

Lab
  • Electrolytes
  • Calcium, magnesium
  • Cardiac enzymes
  • Digoxin level

Imaging
  • CXR:
    • May identify cardiomyopathy or CHF
    • Often abnormal in aortic dissection

Diagnostic Procedures/Other
  • ECG:
    • Differentiate from nonischemic causes of ST elevation:
      • Pericarditis
      • Benign early repolarization
      • Left ventricular hypertrophy with strain
      • Prior MI with left ventricular aneurysm
      • Hyperkalemia
  • ECG criteria for STEMI:
    • New ST elevation at J point in at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of 1 mm (0.1 mV) in other contiguous chest leads or the limb leads
    • ST depression in leads V1–V2 may indicate posterior injury
    • New or presumably new left bundle branch block (LBBB) has been considered a STEMI equivalent. Most cases of LBBB at time of presentation are not old but prior ECG is unavailable
    • Modified Sgarbossa criteria for MI in LBBB or paced rhythm are diagnostic:
      • Concordant ST elevation >1 mm in leads with a positive QRS complex
      • Concordant ST depression >1 mm V1–V3 in leads with a negative QRS complex
      • Discordance of the ST segment (measured at the J point relative to the PR) with the R or S wave (whichever is larger, measured relative to the PR) in a ratio <−0.25
  • Echo:
    • May identify regional wall motion abnormalities or valvular dysfunction

Differential Diagnosis

  • Aortic dissection
  • Anxiety
  • Biliary colic
  • Costochondritis
  • Esophageal spasm
  • Esophageal reflux
  • Herpes zoster
  • Hiatal hernia
  • Mitral valve prolapse
  • Peptic ulcer disease
  • Psychogenic symptoms
  • Panic disorder
  • Pericarditis
  • Pneumonia
  • Pulmonary embolus

Treatment

Pre Hospital

  • IV access
  • Aspirin
  • Oxygen
  • Cardiac monitoring
  • Sublingual nitroglycerin for symptom relief
  • 12-lead ECG, if possible, with transmission or results relayed to receiving hospital

Initial Stabilization/Therapy

  • IV access
  • Oxygen
  • Cardiac monitoring
  • Oxygen saturation
  • Continuous BP monitoring and pulse oximetry

Ed Treatment/Procedures

  • STEMI requires reperfusion therapy as soon as possible:
    • Percutaneous coronary intervention (PCI) is preferred diagnostic and therapeutic modality if available.
  • Goal is primary PCI within 90 min of first medical contact:
    • Thrombolytics should be given if PCI is not available within 120 min of first medical contact (see “Reperfusion Therapy, Cardiac”).
    • Patients arriving at a hospital without PCI should be transferred to a PCI-capable hospital within a door-in–door-out time under 30 min.
    • Patients who are resuscitated during out-of-hospital cardiac arrest whose initial ECG shows STEMI should receive immediate PCI.
  • Aspirin should be administered first to all patients with suspected MI unless known allergy
  • Glycoprotein IIb/IIIa inhibitors (e.g., abciximab) may be started at time of PCI
  • Prasugrel or clopidogrel should be started at the time of PCI
  • Prasugrel should not be given to patients with history of prior stroke or transient ischemic attack (TIA)
  • Clopidogrel is the recommended ADP receptor inhibitor for patients given fibrinolytics:
    • Dose is reduced (age <75 yr: 300 mg, >75 yr: 75 mg)
  • If BP is >90–100 mm Hg systolic, administer sublingual nitroglycerin, nitropaste, or IV nitroglycerin assuming no ECG criteria or clinical evidence of right ventricular infarct:
    • Symptoms that persist after 3 sublingual nitroglycerin tablets are strongly suggestive of AMI or noncardiac etiology.
  • β-Blockers should be initiated within first 24 hr if not contraindicated (e.g., if heart block, heart rate <60, signs of heart failure, hypotension, or obstructive pulmonary disease is present):
    • No benefit of administration prior to PCI or in ED
  • Morphine should be avoided unless pain does not respond to nitrates because it may delay the effects of antiplatelet agents
  • Fentanyl may be given as an alternative
  • Heparin (UFH) or bivalirudin should be used in patients undergoing primary PCI. Bivalirudin is indicated in patients at high risk for bleeding
  • In patients undergoing thrombolysis, heparin (UFH), enoxaparin, or fondaparinux is appropriate
  • If patient is in cardiogenic shock, patient should be transported to a cardiac catheterization laboratory for angioplasty and intra-aortic balloon pump as soon as possible (see “Congestive Heart Failure”)
  • Ventricular dysrhythmias:
  • Bradydysrhythmia associated with hypotension should be treated with atropine or external pacing
  • Conduction disturbances:
    • First-degree atrioventricular (AV) block and Mobitz I (Wenckebach) are often self-limited and do not require treatment.
    • Mobitz II, complete heart block, new right bundle branch block (RBBB) in anterior MI, RBBB plus left anterior branch block or left posterior fascicular block, LBBB plus first-degree AV block may require a temporary transvenous pacemaker.
  • Accelerated idioventricular rhythm (AIVR) may present after reperfusion, appearing as a ventricular rhythm with rate below 120 bpm:
    • Only if sustained treat with electrical cardioversion or sodium bicarbonate
    • Lidocaine and other antidysrhythmics may cause asystole

Medication

  • Aspirin: 162–325 mg PO
  • ADP receptor inhibitors:
    • Clopidogrel (Plavix): 600 mg PO
    • Prasugrel (Effient): 60 mg PO
    • Ticagrelor (Brilinta): 180 mg PO
  • Bivalirudin: 0.75-mg/kg IV bolus, then 1.75 mg/kg/hr infusion
  • Enoxaparin (Lovenox): 1 mg/kg SC q12h
    • Fondaparinux: 2.5 mg SC
  • Glycoprotein IIb/IIIa inhibitors:
    • Abciximab (ReoPro) for use prior to PCI only: 0.25-mg/kg IV bolus
    • Eptifibatide (Integrilin): 180 mcg/kg IV over 1–2 min, then 2 mcg/kg/min up to 72 hr
    • Tirofiban (Aggrastat): 0.4 mcg/kg/min for 30 min, then 0.1 mcg/kg/min for 48–108 hr
  • Heparin: 60-U/kg IV bolus (max. 4,000 units), then 12 U/kg/hr (max. 1,000 U/hr)
  • Metoprolol: 5 mg IV q5–15min followed by 25–50 mg PO starting dose as tolerated (Note: β-blockers contraindicated in cocaine chest pain)
  • Morphine: 2 mg IV, may titrate upward in 2-mg increments for relief of pain assuming no respiratory deterioration and SBP >90 mm Hg
  • Fentanyl: 25–50 mcg IV, may titrate upward in 25-mcg doses given respiratory and hemodynamic response
  • Nitroglycerin: 0.4 mg sublingual q5min for max. 3 doses
  • Nitroglycerin: IV drip at 5–10 mcg/min, USE NON-PVD tubing
  • Nitropaste: 1–2 in transdermal, less favored due to inconsistent absorption
  • Thrombolytics: See “Reperfusion Therapy, Cardiac,” for dosing

Ongoing Care

Disposition

Admission Criteria
  • Patients with an AMI require hospital admission.
  • If the diagnosis is unclear, admission to the hospital or an ED observation unit may be useful for serial cardiac enzymes, ECGs, and exercise stress testing and/or cardiac catheterization if needed.

Discharge Criteria
No patient with an AMI should be discharged from the ED.

Issues for Referral
  • If PCI is unavailable at the treating institution, particularly if the patient is in cardiogenic shock, he should be transported to another hospital if PCI can be initiated within 120 min of first medical contact.
  • Patients with failed reperfusion should be transported urgently to a PCI-capable facility.
  • Patients undergoing reperfusion therapy may benefit from transfer to a PCI-capable facility within 3–24 hr as part of an invasive strategy.

Pearls and Pitfalls

  • Goal of thrombolytic therapy is a 30-min door to needle time if PCI not possible.
  • New or presumably new LBBB at presentation occurs infrequently, and should not be considered diagnostic of AMI in isolation.

Additional Reading

  • Filippo C, Giovanna L. Pathogenesis of acute coronary syndromes. J Am Coll Cardiol. 2013;61:1–11.
  • Jneid H, Addison D, Bhatt DL, et al. 2017 AHA/ACC clinical performance and quality measures for adults with ST-elevation and non-ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. J Am Coll Cardiol. 2017;70:2048–2090.
  • Meyers HP, Limkakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170:1255–1264.
  • O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425.
  • Parodi G, Bellandi B, Xanthopoulou I, et al. Morphine is associated with a delayed activity of oral antiplatelet agents in patients with ST-elevation acute myocardial infarction undergoing primary percutaneous coronary intervention. Circ Cardiovasc Interv. 2015;8:1–7.

See Also

Authors

Joshua W. Joseph
Shamai A. Grossman


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