Unstable angina


  • Angina = chest pain or other equivalents (e.g. SOB) that occur due to myocardial ischemia
  • Considered unstable with 1 or more:
    • Occurs for 1st time
    • Occurs at rest
    • Accelerating frequency or severity

Clinical ACS Categories

  1. ST-segment elevation myocardial infarction (30%)
  2. Non-ST-elevation myocardial infarction (25%)
  3. Unstable Angina (UA) (38%)
    • The new title, “Non-ST-Elevation Acute Coronary Syndromes,” emphasizes the continuum between UA and NSTEMI[1]
    • NSTEMI myocardium is damaged enough to increase biomarkers, UA is not.

MI Types by Causation[2]

Myocardial Infarction types by causation
  • Type 1: Spontaneous Myocardial Infarction
    • Atherosclerotic plaque rupture or intraluminal thrombus in one or more of the coronary arteries
  • Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance
    • Condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand (e.g. coronary spasm, embolism, low or high blood pressures, anemia, or arrhythmias)
  • Type 3: Cardiac Death Due to Myocardial Infarction
    • Sudden cardiac death with symptoms suggestive of myocardial ischaemia without elevated biomarkers
  • Type 4: Myocardial Infarction Associated With Revascularization Procedure
    • 4a: Related to PCI
    • 4b: Related to Stent Thrombosis
  • Type 5: Myocardial Infarction Related to CABG Procedure

Clinical Features

Risk of ACS

Clinical factors that increase likelihood of ACS/AMI:[3][4]

Clinical factors that decrease likelihood of ACS/AMI:[5]

  • Pleuritic chest pain
  • Positional chest pain
  • Sharp, stabbing chest pain
  • Chest pain reproducible with palpation

Gender differences in ACS

  • Women with ACS:
    • Less likely to be treated with guideline-directed medical therapies[6]
    • Less likely to undergo cardiac catheterization[6]
    • Less likely to receive timely reperfusion therapy[6]
    • More likely to report fatigue, dyspnea, indigestion, nausea or vomiting, palpitations, or weakness,[6] although some studies have found fewer differences in presentation[7]
  • More likely to delay presentation[6]
  • Men with ACS:
    • More likely to report central chest pain

Factors associated with delayed presentation[6]

  • Female sex
  • Older age
  • Black or Hispanic race
  • Low educational achievement
  • Low socioeconomic status

Differential Diagnosis

Chest pain





Same as for NSTEMI

  • Dual antiplatelet therapy and antithrombotic therapy is mainstay of treatment
  • Medical management vs cath determined by level of risk for future cardiovascular events


  • Aspirin
    • Recommended dose is 325 mg chewed
    • Reduces death from MI by 12.5 → 6.4%
    • Should be used in all ACS unless contraindicated (eg Anaphylaxis)
    • In pts with true ASA allergies, substitute Clopidogrel[8]
  • Clopidogrel (see drug link for specific age and indication-related dosages)
    • Give in addition to ASA
    • Mortality benefit with NSTEMI (CURE trial: Decrease in cardiovascular death, MI, or stroke by 9.3-11.5%)
    • Main risk and contraindication is bleeding
  • GPIIb/IIIa Inhibitors


  • Give heparin or enoxaparin along with ASA (Class 1A evidence)
  • Enoxaparin (Lovenox)
    • 1mg/kg subq BID
    • AHA recommends for moderate & high risk Unstable angina/NSTEMI unless CABG within 24hr
    • Safer than UFH
    • ESSENCE trial showed 20% decrease in death, MI or urgent revascularization with LMWH
    • Adjust for CrCl<30ml and extremes of weight
    • No need to monitor labs
  • Unfractionated Heparin
    • Bolus 60-70u/kg (max 5000) followed by infusion of 12-15u/kg/hr (max 1000/hr), goal ptt 45-75s
    • Consider if patient likely to undergo PCI/CABG within 24hr of admission or in setting of renal failure
  • Hirudins
    • Approved only for patients with HIT


  • Oxygen
    • Use only if SpO2 <90%
  • Nitrates (decrease preload)
    • Administer sublingual nitroglycerin every 5 min x3 for continuing ischemic pain and then assess need for IV nitroglycerin (AHA ACA Level I)
    • Use cautiously in inferior MI or if on sildenafil
    • Not shown to decrease MACE
  • Analgesia
    • Morphine, Fentanyl, or other opioid (AHA ACA Level IIb)
    • Do not use NSAIDs other than ASA (AHA ACA Level III: Harm)
    • Complete absence of pain is likely not feasible - aim for pain level <5
  • β-blockers
    • Start PO dose within 24 hours (Do not give IV β-blocker in ED (AHA ACA Level III: Harm))
    • Goal HR is 50-60
    • Contraindicated if HR<50 or SBP<90, acute CHF, low flow state, or PR>240ms
    • Decreases inotropic and chronotropic response to catecholamines
    • Use diltiazem if cannot use beta-blocker (nifedipine clearly harmful)
  • ACE inhibitor
    • Start short-acting (captopril) within 24 hours of admission
    • Reduces RR of 30 day mortality by 7%
    • Those with recent MI (especially anterior) and LV dysfunction benefit most
  • Transfusion
    • Transfuse to keep hemoglobin >10
  • Thrombolytics
    • Not indicated (only useful for STEMI)

Unstable Angina - NSTEMI Guidelines

Summary of Class I Guidelines

  • Aspirin should be initiated as soon as possible and continued indefinitely in patients who tolerate it. (Level A)
  • Clopidogrel loading dose should be initiated as soon as possible in patients unable to tolerate aspirin. (Level B)
  • Medium/High risk patients in whom initial invasive strategy is planned should receive dual therapy (Level A) including aspirin (Level A) and:
    • Before PCI one of the following:
      • Clopidogrel (Level B)
      • An IV GP IIb/IIIa inhibitor (Level A) preferably eptifibatide or tirofiban.
    • Otherwise during PCI one of the following:
  • If an initial conservative (i.e. noninvasive) strategy is selected, clopidogrel should be added to ASA and anticoagulant therapy as soon as possible after admission. (Level B)
  • If an initial conservative strategy is selected and recurrent symptoms/ischemia, heart failure, or serious arrhythmias subsequently appear, then diagnostic angiography should be performed. (Level A). Either an IV GP IIb/IIIa inhibitor (Level A) or clopidogrel (Level B) should be added to ASA and anticoagulant therapy before diagnostic angiography. (Level C)

Summary of Class IIa Guidelines

  • If an initial conservative strategy is selected and patient has recurrent ischemic discomfort with clopidogrel, ASA, and anticoagulant therapy, it is reasonable to add a GP IIb/IIIa inhibitor before diagnostic angiography. (Level C)
  • If an initial invasive strategy is selected, it is reasonable to omit administration of an IV GP IIb/IIIa inhibitor if bivalirudin is selected as the anticoagulant and clopidogrel was administered at least 6 hours earlier than planned catheterization or PCI. (Level B)

Summary of Class IIb Guidelines

  • If an initial conservative strategy is selected, it may be reasonable to add eptifibatide or tirofiban to anticoagulant and oral antiplatelet therapy.19,20 (Level B)
  • Prasugrel may be considered for administration promptly upon presentation if PCI is planned, before definition of coronary anatomy if both the risk for bleeding is low and the need for CABG is considered unlikely. (Level C)
  • The use of GP IIb/IIIa inhibitors may be considered in high-risk patients already receiving ASA and a thienopyridine who are selected for an invasive strategy, such as those with elevated troponin levels, diabetes, or significant ST-segment depression, and who are not otherwise at high risk for

bleeding. (Level B)

  • In patients with definite UA/NSTEMI undergoing PCI, the use of a loading dose of clopidogrel of 600mg, followed by a higher maintenance dose of 150mg daily for 6 days, then 75mg daily may be reasonable in patients not considered at high risk for bleeding. (Level B)

Summary of Class IIb Guidelines

  • Abciximab should not be administered to patients in whom PCI is not planned. (Level A)
  • Low risk patients for ischemic events (TIMI risk score 2) or at high risk of bleeding and who are already receiving ASA and clopidogrel, upstream GP IIb/IIIa inhibitors are not recommended. (Level B)

Summary of Class III Guidelines

  • In UA/NSTEMI patients with a prior history of stroke or TIA for whom PCI is planned, prasugrel is potentially harmful as part of a dual-antiplatelet therapy regimen.(Level B)

External Links

See Also


  1. AHA ACA - NSTEMI ACS Guidelines 2014 View Online
  2. Third Universal Definition of Myocardial Infarction http://circ.ahajournals.org/content/126/16/2020.full.pdf
  3. Body R, Carley S, Wibberley C, et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010;81(3):281–286. PMID: 20036454
  4. Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263. PMID: 9786377
  5. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629. PMID: 16304077
  6. 6.0 6.1 6.2 6.3 6.4 6.5 Mehta LS, et al. Acute myocardial infarction in women: A scientific statement from the American Heart Association. Circulation. 2016; 133:916-947.
  7. Gimenez MR, et al. Sex-specific chest pain characteristics in the early diagnosis of acute myocardial infarction. JAMA Intern Med. 2014; 174(2):241-249.
  8. CAPRIE Steering Committee.. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet. 1996 Nov 16;348(9038):1329-39.