Acute Coronary Syndrome

Introduction

Acute coronary syndromes (ACS) encompass clinical symptoms compatible with acute myocardial ischemia/injury. Typically, these include ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

ACS is categorized as STEMI when symptoms of myocardial ischemia are associated with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis. In the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB), ST elevation diagnosis is determined by new ST elevation at the 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. Most STEMI patients will also have ECG evidence of Q-wave infarction. New or presumably new LBBB is considered a STEMI equivalent.

ACS is categorized as NSTEMI in the absence of persistent ST-elevation, except in patients with true posterior myocardial infarction (MI). NSTEMI is further subdivided on the basis of cardiac biomarkers of necrosis. If cardiac biomarkers are elevated and the clinical context is appropriate, the patient is considered to have NSTEMI, otherwise a diagnosis of UA is made.

ACS typically represents a medical emergency, and outcomes are closely linked with the speed with which patients obtain appropriate care. The following notes provide physicians with a guide to the management of ACS, based on currently available treatment guidelines. The goal of this program is to assist physicians in rapidly making treatment decisions at crucial points during the management of patients with ACS.

Faculty

Eddy Lang, MDCM- CCFP(EM)-CSPQ
Michel Le May, BSc, MD
Mark Mensour, MD CCFP EM ANAES FCFP

Suspected Deep Vein Thrombosis

53 y/o male presents to ED with recent onset retrosternal chest discomfort; 20 min episode at rest on day of presentation; heaviness in chest while climbing stairs 2 wk ago; history of dyslipidemia, hypertension, and diabetes mellitus; Rx include statin, beta blocker, and metformin; no past cardiac history

Examination

BP 145/70 mmHg; HR 54 bpm; RR 18/min; SaTO2 96 % on RA; chest clear on auscultation; normal heart sounds, no S3, S4, or murmur

Serum creatinine: 90 μmol/L
HS troponin: 10 ng/L (ULN: 14 ng/L)
Chest X-ray: normal
ECG: Normal
GRACE score=53 (low risk: <1% probability of death in hospital and 6 months postdischarge)
TIMI score=2 (8% risk of all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization through 14 days)

Actions

Discussion:

  1. Classic history of new onset crescendo angina
    1. Chest discomfort initially provoked by exertion that culminated into pain at rest
  2. Multiple risk factors increase probability of ACS despite low-risk TIMI and GRACE scores

Treatment:

  1.  Aspirin: loading dose 160 mg chewable, then maintenance 81 mg daily
    1. chewable form available as 80 mg tablet; enteric coated form available as 81mg tablet
  2. Does not meet PLATO or CURE criteria, but consider empiric use of clopidogrel

Scenario 2: Intermediate-risk NSTEMI

62 y/o obese female presents to ED with 3 prolonged episodes (20-30min) of chest pain associated with SOB in past 12 hr; history of hypertension and prior MItreated with PCI 10 yr ago; Rx include antihypertensive and aspirin

Examination

BP 175/80 mmHg ; HR 80 bpm; RR 24/min; SaTO2 96% on RA; chest clear on auscultation; heart sounds normal; no murmur

HS troponin: 42 ng/L (ULN: 14 ng/L)
Chest X-ray: normal
ECG: ST segment depression
GRACE score=112 (intermediate risk: 1-3% probability of death in hospital and 3-8% risk of death 6 months postdischarge)
TIMI score=4 (19.9% risk of all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization through 14 days)

Actions

Discussion:

  1. Moderate- to high-risk ACS
  2. Evidence of NSTEMI based on elevated troponins
  3. Meets several PLATO criteria for use of dual-antiplatelet therapy
    1. Age >60, prior MI, positive biomarkers, ST segment deviation

Treatment:

  1. Aspirin: loading dose 160 mg chewable, then maintenance 81 mg daily
    1. Chewable form available as 80 mg tablet; enteric coated form available as 81mg tablet

Scenario 3: NSTEMI on oral anticoagulants

74 y/o female presents to ED with recurrent retrosternal chest discomfort radiating to left arm; history of AF on apixaban, hypertension, and dyslipidemia; Rx include beta-blocker and statin

Examination

BP 170/90 mmHg; HR 80 bmp and irregular; chest clear to auscultation; heart sounds normal, with no 3rd or 4th heart sounds; soft systolic murmur.

Serum creatinine: 134 μmol/L
HS troponin: 60 ng/L (ULN: 14 ng/L)
Chest X-ray: Slight increase in cardiac silhouette; no evidence of pulmonary congestion
ECG: AF and deep T wave inversion in the inferior leads
Bedside ultrasound: Negative for pericardial effusion; adequate myocardial function

Actions

Discussion:

  1.  Moderate- to high-risk NSTEMI ACS
    1. New ECG changes, elevated biomarkers, AF on oral anticoagulants
  2. Meets PLATO criteria for ticagrelor, but contraindicated by oral anticoagulant use
    1. Use clopidogrel as alternative

Treatment:

  1. Aspirin: loading dose 160 mg chewable, then maintenance 81 mg daily (chewable form available as 80 mg tablet; enteric coated form available as 81mg tablet)

Scenario 4: High-risk NSTEMI

76 y/o male presents to ED with intense chest pain, nausea, and shortness of breath; ongoing chest discomfort in ED that does not respond to sublingual nitroglycerin x3; pain present for 30 min and unchanged; history of 2 prior MIs treated with PCI (12 and 6 yr apart), dyslipidemia, hypertension, and type 2 diabetes mellitus; Rx include beta-blocker, ARB, aspirin, metformin, statin, and insulin; smoker

Examination

BP 120/60 mmHg; HR 110 bpm; RR 30/min; SaTO2 93% on RA; bilateral crepitations on auscultation

HS troponin: 280 ng/L (ULN: 14 ng/L)
ECG: Sinus tachycardia with 3mm ST depression in V1 to V3
GRACE: 210 (high risk: >3% probability of death in hospital and >8% risk of death 6 months postdischarge)
TIMI: 6 (40.9% risk of all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization through 14 days)

Actions

Discussion:

  1.  High-risk ACS
    1. ST depression, positive biomarkers
    2. Ongoing chest discomfort suggests ongoing myocardial ischemia and myocardial necrosis
    3. O2 desaturation suggests heart failure

Treatment:

  1. Aspirin: loading dose 160 mg chewable then maintenance 81 mg daily
    1. Chewable form available as 80 mg tablet; enteric coated form available as 81mg tablet

Scenario 5: STEMI

65 y/o male presents to ED with crushing chest pain, nausea, and vomiting; pain began 45 min previously, while he was shoveling snow.

Examination

BP 145/70 mmHg; HR 54; RR 18; SaTO2 96 % on RA

ECG: 3mm ST elevation in leads 2, 3, and AVF

Actions

Treatment scenario 1: presents to a rural hospital where nearest cath lab is 3 hr away (cannot meet recommended door-to-balloon time of ≤ 120 min)

  1. Fibrinolytic therapy
    1. Tenecteplase (TNK) 5 sec bolus AND
    2. Aspirin 160 mg chewable AND
    3. Clopidogrel 300 mg if < 75yr-of-age;75 mg if ≥75 yr-of-age (CLARITY study) AND
    4. Heparin, to prevent reocclusion
      1. UFH 60 IU/kg bolus with max 4,000 IU and initial infusion 12 IU/kg/h, with a max 1,000 IU/h
  2. Immediate transfer to receiving PCI centre
  3. Re-assessment at PCI centre
    1. Rescue angioplasty if failure of reperfusion (i.e., persistent ST elevation >50% of baseline ECG, and/or chest discomfort)
    2. If reperfusion successful, cardiac catheterization 3-24 hr from the time of fibrinolytic therapy

Treatment scenario 2: presents to suburban/regional center, where on-site lytic vs. transfer for PCI could be debated

In the current design of a STEMI system, it is probably better to identify a center as a primary PCI hospital or a pharmaco invasive hospital. Pinto’s article (See reference below) can be used to define benefit vs distance/time and type of MI with symptom related delay for each patients location). This is because hesitation and debate lead to longer time to reperfusion.

Reference:
Pinto DS, Kirtane AJ, Nallamothu BK, Murphy SA, Cohen DJ, Laham RJ, Cutlip DE, Bates ER, Frederick PD, Miller DP, Carrozza JP Jr, Antman EM, Cannon CP, Gibson CM. Hospital delays in reperfusion for ST-elevation myocardial infarction: implications when selecting areperfusion strategy. Circulation. 2006;114:2019–2025

Disclaimer

CAEP Notes includes clinical tools and resources intended for use by healthcare professionals. These tools do not give professional advice; physicians and other healthcare professionals who use these tools or databases should exercise their own clinical judgment as to the information they provide. The contents of the CAEP Notes tool, such as text, graphics and images are for informational purposes only. While information on this site has been obtained from sources believed to be reliable, CAEP and its partners do not warrant the accuracy of the information contained on this site.

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