Acute Coronary Syndromes – From LITFL

Acute Coronary Syndromes

OVERVIEW

  • coronary artery disease accounts for > 30% of death in West

CLASSIFICATION

  • unstable angina: ischaemic pain that is more severe, frequent or prolonged than normal
  • MI: ischaemic symptoms + raised biomarkers (NSTE-ACS and STE-ACS)

ASSESSMENT

HISTORY

  • take pain history
  • assess severity
  • recent MI
  • previous thrombolysis, stent or CABG
  • CHF symptoms
  • functional ability (MET’s)
  • medications

Canadian Cardiovascular Angina Scale

I – ordinary physical activity doesn’t cause angina (> 4 METS)
II – slight limitation or ordinary activity (2-4 METS)
III – marked limitation of ordinary activity (1-2 METS)
IV – inability to carry out any physical activity (angina @ rest)

EXAMINATION

  • standard CVS examination
  • may be nothing to find
  • look for CCF (S3/S4, APO, edema)

RISK FACTORS

These are of little diagnostic use in the acute setting.

  • DM
  • HT
  • lipids
  • family history
  • male
  • obesity
  • previous MI
  • hormone replacement for menopause
  • inactivity

INVESTIGATIONS

CARDIAC BIOMARKERS

ECG

  • acute AMI changes: peaked T waves with ST elevation -> gradual loss of R wave -> development of pathological Q wave and TWI
  • Anteroseptal = LAD
  • Anterolateral = Cx
  • Inferior = RCA
  • Posterior = Cx or PDA (off RCA)
  • MI localisation

 

  • criteria for AMI in LBBB:

(1) new LBBB
(2) concordant ST elevation of > 1mm
(3) concordant ST depression of > 1mm in V1, V2 or V3
(4) discordant ST elevation of > 5mm

ETT

  • gives an assessment of functional capacity
  • looking for; ST depression, hypotension, arrhythmias

CPX Testing

  • bike or hand ergometer
  • under exercise O2 consumption is a linear function of Q and thus LV function
  • aerobic threshold of >11mL/min/kg is able to predict survival after major abdominal surgery accurately

Dobutamine Stress Echo

  • those that can’t exercise
  • up to 40mcg/kg/min
  • looks @ regional wall motion as an indicator of impaired perfusion
  • > 4 wall motion abnormalities = high risk

Nuclear Medicine Scan – Dipyridamole thallium scintography, SESTAMIBI, SPECT MPI, PET

  • coronary vasodilator (dipyridamole) and radio isotope (thallium) which is up taken into perfused myocardium
  • impaired perfusion shows up as reversible perfusion defects caused by dipyridamole causing a steel phenonmena
  • non-perfused areas show up as permanent perfusion defects
  • key findings one is looking for = reversible perfusion defects, permanent perfusion defects and cavity dilation
  • negative test is very reassuring

CT Coronary Angiogram

  • quantification of the amount of Ca2+ in the coronary arteries
  • massive dose of radiation
  • useful when wanting to completely rule out CAD burden

Dobutamine stress MRI

  • elegant up and coming form of stress testing
  • identifies wall motion abnormalities
  • highly accurate
  • safe

Coronary arteriography

  • delineates who needs PCI, CABG or medical management
  • anatomical nature of lesions
  • can stent but has issues relevant to surgery (see AHA 2007 Guidelines)

MANAGEMENT

STEACS

Reperfusion therapy

  • options: thrombolysis, PCI or CABG
  • aim for PCI within 90 minutes of initial presentation (arrival time)
  • if cannot transfer to PCI center such that PCI will be performed <120 minutes from initial presentation, then perform thrombolysis within 30 minutes
  • thrombolysis contraindications:
    absolute – active bleeding or bleeding diathesis (not menses), closed head injury or facial trauma in 3 months, suspected aortic dissection, prior ICH, suspected intracranial malignancy, known structural cerebral vascular lesion, ischemic stroke < 3months
    relative – anticoagulation, non-compressible vascular puncture, recent major surgery ❤ weeks, > 10 minutes of CPR, internal bleeding < 4 weeks, active peptic ulcer, poorly controlled HT, ischaemic CVA > 3 months, dementia or known intracranial abnormality (not covered above), pregnancy, advanced metastatic cancer

Anti-platelet therapy

  • aspirin 300mg (reduces risk of death or MI by 50% in USAP or NSTEMI)
  • clopidogrel 600mg (all those that require a stent, withhold if needs a CABG)
  • glycoprotein IIb/IIIa inhibitors (post NSTEMI and PCI)

Antithrombin therapy

  • PCI: UFH
  • thrombolysis: UFH or LMWH

Nitrates

  • symptomatic relief
  • use in CCF
  • no mortality advantage however

Beta-blockers

  • IV or PO
  • reduce mortality

ACE-I

  • use in patients with low EF, AMI and those who are vasculopaths

Statins

  • decreases risk of ischaemic events

NSTEACS

Risk stratification

  • high: repetitive or prolonged pain, elevated TNT, persistent or dynamic ECG changes, transient ST elevation, cardiogenic shock, VT, syncope, EF < 40%, prior CABG, PCI within 6 months, DM, CRF
  •  intermediate: rest or prolonged pain, age > 65, known IHD, 2 or more IHD risk factors, CRF, prior aspirin use
  • low: none of the above

Management

  • high: aggressive medical management (including LMWH) and coronary angiography
  • intermediate: inpatient monitoring and provocation testing
  • low: discharged and followed up

PERIOPERATIVE MANAGEMENT

  • early consultation with cardiology
  • keep cardiac medications going
  • avoid tachycardia, hypotension, hypoxia, hypercarbia
  • good analgesia
  • keep Hb > 90g/L
  • high index of suspicion for perioperative MI
  • 12 lead ECG post op day 1, 2 and 3
  • TNT if high risk day 2 and 3
  • keep anti-platelets going
  • if develops ST elevation -> urgent angiogram
  • treat angina and CHF aggressively

COMPLICATIONS

  • cardiac failure
  • post-infarction ischaemia
  • ventricular free wall rupture: pericardiocentesis and repair
  • ventricular septal rupture: IABP, inotropes, surgery
  • acute MR: afterload reduction, IABP, inotropes, surgery ASAP
  • right ventricular infarction: IV fluids, inotropes, AV synchrony, IABP, reperfusion
  • arrhythmias: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)
  • cardiogenic shock: must get revascularisation (PCI or CABG) within 24 hours
  • thromboembolism: mural thrombus -> anticoagulate
  • post-MI syndrome (Dressler’s) and pericarditis

References and Links

  • Delewi R, Zijlstra F, Piek JJ. Left ventricular thrombus formation after acute myocardial infarction. Heart. 2012 Dec;98(23):1743-9. doi: 10.1136/heartjnl-2012-301962. Review. PubMed PMID: 23151669; PubMed Central PMCID: PMC3505867.
  • StEmlyns — New STEMI Guidelines (2013)
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