Acute Coronary Syndrome

From Life in the Fast Lane: ACS

• Type 1: Spontaneous MI
• Type 2: MI secondary to ischaemic imbalance
• Type 3: MI resulting in death when biomarker values are unavailable
• Type 4a: MI related to PCI
• Type 4a: MI related to stent thrombosis
• Type 5: MI related to CABG MI related to CABG

• Very High Risk
  • Haemodynamic instability:
    • Heart failure/ cardiogenic shock
    • Mechanical complications of myocardial infarction
  • Life-threatening arrhythmias or cardiac arrest
  • Recurrent or ongoing ischaemia (e.g. chest pain refractory to medical treatment) or recurrent dynamic ST segment and/or T wave changes, particularly with:
    • Intermittent ST segment elevation
    • de Winter T wave changes
    • Wellens syndrome (or LMCA syndrome)
    • Widespread ST elevation in two or more coronary territories
• High Risk
  • Rise and/or fall in troponin level consistent with myocardial infarction
  • Dynamic episode of ST segment and/or T wave changes with or without symptoms
  • GRACE score >140
• Intermediate Risk
  • Diabetes mellitus
  • Renal insufficiency (glomerular filtration rate < 60mL/min/1.73m2)
  • Left ventricular ejection fraction ≤ 40 %
  • Prior revascularization:
    • Percutaneous coronary intervention
    • Coronary artery bypass grafting
  • GRACE score >109 and <140
• Low Risk
  • Patients with NSTEACS who have both of:
    • no recurrent symptoms
    • no risk criteria (as listed above)

• High Risk Patients
  • those presenting with clinical symptoms consistent with ACS and any of the following high risk features:
  • Persistent or dynamic S-T segment changes on ECG:
    • S-T segment depression ≥ 0.5 mm
    • New T wave inversion ≥ 2.0 mm in more than 2 contiguous leads
    • Transient S-T segment elevation ≥ 0.5 mm in more than 2 contiguous leads
    • ECG changes consistent with critical coronary artery stenosis, e.g. Wellens Syndrome or LMCA stenosis syndrome.
  • Hemodynamic compromise
    • Systolic blood pressure ≤ 90 mmHg
    • Signs of poor peripheral perfusion
    • Signs of cardiac failure or frank pulmonary edema, (ie Killip class > 1)
    • New onset of mitral regurgitation
    • Syncope
  • Ongoing pain, or recurrent episodes of pain despite initial treatment whilst in the ED
  • Arrhythmias requiring treatment such as sustained ventricular tachycardia
  • Diaphoresis
  • Elevated serum troponin
  • High risk co-morbidities:
    • Left ventricular systolic dysfunction (ejection fraction < 0.4)
    • Past PCI or CAGS
    • Past myocardial infarction
  • Intermediate Risk Patients
    • those presenting with clinical symptoms consistent with ACS but do not have high risk or low risk criteria
  • Low Risk Patients
    • Age < 40 years
    • Symptoms that are atypical for angina
    • Remain symptom free
    • Absence of known CAD
    • Normal troponin levels
    • Normal ECG (including no transient changes)

INVESTIGATIONS

Laboratory

  FBC
  UEC/ glucose (especially K)
  Cardiac troponin I
      Normal levels are considered vary according to the exact assay that is being used
      In general terms a normal level is considered to be < 99th percentile for the assay
      may persist for 5-14 days post infarction
      Reinfarction can also be assessed via troponin levels (CK/CKMB is now obsolete and not required)
      Rising versus falling levels
          For the vast majority of patients being investigated for possible MI, a rising pattern is suggestive of the diagnosis of MI
          In patients who present late following MI, troponin elevations may have already peaked and in this context, a falling troponin pattern is significant
          Note that all troponin assays, regardless of their detection sensitivity do not rule out unstable angina or stable coronary ischemia

0 Clinical management decisions should not be based solely on troponin levels, but on thorough investigation and risk assessment that includes detailed clinical assessment, observation, repeated ECG tests, and where available functional testing

      An initial troponin level should be done on all cases of suspected ACS with a second level done at 6 hours (sensitive assay) or 3 hours (highly sensitive assay) from the onset of the chest pain.
          Note that some patients that fit specific low risk stratification criteria may be suitable for validated accelerated diagnostic pathways.

ECG

  All patients who present with a suspected ACS must have an ECG within 10 minutes of first acute clinical contact
  A clinician with ECG expertise should review the ECG
  The immediate decision pathway then involves the ECG stratification of STEMI, from NSTEACS
  STEMI minimum criteria:
      STEMI is defined as presentation with clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
          ≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
          ≥ 1.5 mm ST elevation in V2-3 in women
          ≥ 1 mm ST elevation in other leads
          New LBBB (LBBB should be considered new unless there is evidence otherwise)
  Findings in ACS
      may be normal
      classic changes in acute myocardial infarction
          peaked T waves with ST elevation
          gradual loss of R wave
          development of pathological Q wave and TWI
      anatomical localisation of ST elevation
          Anteroseptal = LAD
          Anterolateral = Cx
          Inferior = RCA
          Posterior = Cx or PDA (off RCA)
  Minimal S-T changes can be difficult to interpret, especially in those with pre-existing CAD or other significant CVS disease. In such cases:
      Comparison with old ECGs will be useful
      Modified Sgarbossa criteria can help if LBBB or paced:
          concordant ST elevation of > 1mm
          concordant ST depression of > 1mm in V1, V2 or V3
          discordant ST elevation of > 5mm
      In cases of LBBB urgent echocardiography may be useful, if readily available, to detect wall motion abnormalities (suggesting myocardial ischaemia) and hence assist in decision making

CXR

  This should not be allowed to delay any treatment measures, especially reperfusion therapies.
  If an x-ray is done this should be in the Resus bay, except for stable low risk patients who may be suitable to leave the department for their x-ray, this will need to be judged on a case by case basis.
  Look for cardiomegaly, cardiac failure and differentials of chest pain (e.g. PE, pneumonia, pneumothorax, esophageal rupture, aortic dissection)

Echocardiography (not a routine test in ACS, but may be considered on an urgent basis in selected cases)

  Confirmation of wall motion abnormalities when the diagnosis of ACS is unclear (pericarditis or myocarditis is being considered for example or in cases of LBBB)
  Cardiogenic shock
  Inferior infarction where evidence of right ventricular infarction is being sort
  If secondary complications are suspected, such as cardiac tamponade or valvular disruption

Coronary Angiography

  This is the definitive investigation for any patient with a STEMI who is to undergo a PCI
  Patients with high or very high risk NSTEACS should be referred to cardiology urgently for consideration of a urgent coronary angiogram.

MANAGEMENT

  STEMI management
  NSTEACS management

COMPLICATIONS OF ACUTE CORONARY SYNDROMES

  cardiac failure
  post-infarction ischaemia
  ventricular free wall rupture
      therapy: pericardiocentesis and repair
  ventricular septal rupture
      therapy: IABP, inotropes, surgery
  acute mitral regurgitation
      therapy: afterload reduction, IABP, inotropes, surgery ASAP
  right ventricular infarction
      therapy: IV fluids, inotropes, AV synchrony, IABP, reperfusion
  arrhythmias
      therapy: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)
  cardiogenic shock
      therapy: must get revascularisation (PCI or CABG) within 24 hours
  thromboembolism
      therapy: mural thrombus -> anticoagulate
  pericarditis and Dressler’s syndrome
  complications of therapy, e.g. haemorrhage, coronary artery dissection, stent thrombosis, surgical complications