Acute Coronary Syndrome

Epidemiology

• >30% of all deaths in developed countries
• 3-6% of those thought to have an alternative cause for chest pain ultimately have short-term adverse cardiac events
  • Reserve diagnoses of non-cardiac chest pain to those with a very low likelihood of coronary artery disease (<1%) and clear evidence of alternative diagnoses only
• 1-6% of patients with a normal ECG will ultimately be diagnosed as NSTEMI + another 4% will have unstable angina
• Dynamic ECG changes confer
  • 84% risk of CAD with classical anginal symptoms
  • 85% risk of CAD with non-classic anginal symptoms

Definitions

• Rise and/or fall of troponin, with at least one value >99^th centile + one of:
  • Symptoms of myocardial ischaemia
  • New (or presumably new) ST/T wave changes or LBBB
  • Development of pathological Q waves (>40ms wide, >2mm deep (sometimes normal in III, aVR), >25% of QRS, leads V1-3 (always pathological)
  • New loss of viable myocardium or regional wall motion abnormality
  • Identification of coronary thrombus by angiography or autopsy

• Types of MI
  • Type I – Spontaneous due to plaque disruption
  • Type 2 – Imbalance O2 delivery/demand
  • Type 3 – MI resulting in death in absence of biomarkers
  • Type 4 – PCI–related MI
  • Type 5 – CABG-related MI

Unstable angina

• <4% of patients have normal biomarkers and ECG with altered pattern of previously stable angina
• New onset angina is considered unstable at first presentation
• Rest angina
  • Angina at rest that is usually >20 min duration (most common presentation of NSTEMI)
• New-onset angina
  • New-onset angina that markedly limits normal physical activity such as walking 1-2 blocks or climbing 1 flight of stairs or lighter activity
• Increasing angina
  • Previously diagnosed angina that has become more frequent, of longer duration or is lower in threshold, limiting ability to walk 1-2 blocks, climb 1 flight of stairs or perform lighter activity

Risk factors

Predict CAD over time not likelihood at specific point in time

• DM
• HTN
• Lipids
• FHx <50
• Male
• Obesity
• Previous MI
• Hormone replacement therapy
• Inactivity

NYHA Angina Classification

• Class 1 – Cardiac disease without limitation of activity
• Class 2 – Cardiac disease with slight limitation of activity
• Class 3 – Cardiac disease with marked limitation of activity
• Class 4 – Symptoms at rest or with any activity whatsoever

Risk stratification of confirmed ACS (NHF)

• Very high risk
  • Haemodynamic instability
  • Life-threatening arrhythmia or cardiac arrest
  • Recurrent or ongoing ischaemia or recurrent dynamic ST/T wave changes, especially:
    • Intermittent ST elevation
    • DeWinter’s T waves
    • Wellen’s syndrome
    • LMCA syndrome
    • Widespread ST elevation in 2 or more coronary territories
• High risk
  • Rise and/or fall in troponin consistent with MI
  • Persistent or dynamic ST segment and/or T wave changes with or without symptoms
  • GRACE score >140
• Intermediate risk
  • DM
  • Renal insufficiency
  • LVEF <40%
  • Prior CABG/PCI
  • GRACE 109-140
• Low risk
  • No recurrent symptoms
  • No risk criteria

Assessment of bleeding risk

• Important pre-thrombolysis
• CRUSADE score
  • HR
  • SBP
  • Haematocrit
  • Creatinine clearance
  • Sex
  • Signs of CCF
  • Hx of vascular disease
  • Hx of DM

STEMI criteria

• 2 or more contiguous leads
  • >2.5mm STE in V2/3 in males <40
  • >2.0mm STE in V2/3 in males >40
  • >1.5mm STE in V2/3 in females
  • >1.0mm STE in all other leads
• New LBBB considered STEMI equivalent and treated similarly (but not as predictive as once thought)
• Cameron suggests >2mm in any 2 contiguous praecordial leads and >1mm in any 2 contiguous limb leads

Up to 20% of STEMI are diagnosed on serial ECG!

Original Sgarbossa

• Concordant STE >1mm (5)
• Concordant ST depression >1mm in V1-3 (3)
• Discordant ST elevation >5mm (2)
• >= 3 = 90% specific for MI

Modified Sgarbossa

• Concordant STE >1mm
• Concordant ST depression >1mm in V1-3
• Discordant ST elevation >25% of preceding S wave amplitude
• If meet any of above criteria = activate cath lab (99% specific)
• Only 80% sensitive (therefore cannot rule out acute coronary occlusion)

Specific syndromes

Atypical chest pain

• 1/3 of MI’s have NO CHEST PAIN
• Often present with dyspnea alone or weakness, N&V, epigastric discomfort, palpitations, syncope or cardiac arrest
• Often diabetic, female, elderly

ST elevation

• In general, the higher the ST elevation and the more ST segments that are elevated, the more extensive the injury
• New ST elevation >= 1mm in two contiguous chest leads is seen in 50% of acute MI with PPV of 90%
• 50% of acute MI have normal or non-diagnostic ECG

Acute inferior MI

• 80-90% due to RCA occlusion; 10-20% LCx
• ST elevation in V4R and ST elevation III>II strongly predict RCA
• Reciprocal ST depression in V1/2 may suggest LCx (although in distal RCA occlusion without RV involvement can still get this)
• ST elevation in V4-6 appears equally prevalent in each
• V3:III ratio (ratio of ST depression in V3 relative to ST elevation in lead III)
  • <0.5 indicates proximal RCA
  • 0.5-1.2 indicates distal RCA occlusion
  • >1.2 indicates LCx
• Isoelectric or ST elevation in I/aVL suggests LCx

DeWinter’s T waves

• Tall, prominent, symmetric T waves in praecordial leads
• Upsloping ST segment depression >1mm in praecordial leads
• Absence of ST elevation in praecordial leads
• ST segment elevation 0.5-1mm in aVR
• Highly predictive of LAD occlusion

Wellen’s syndrome

• Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• Minimal STE
• No praecordial Q waves
• Recent history of angina
• ECG pattern evident when pain free
• Normal or slightly elevated troponin
• Critical stenosis of LAD

Left main coronary artery syndrome

• Widespread horizontal ST depression, most prominent in I, II and V4-6
• ST elevation in aVR >1mm
  • Also seen in proximal LAD, triple vessel, diffuse subendocardial ischaemia (i.e. following resuscitation from cardiac arrest – mismatch)
  • Predicts the need for CABG
  • >0.5mm = 4-fold increase in mortality
  • >1mm = 6-7 fold increase in mortality
  • >1.5mm = Mortality of 20-75%
• ST elevation in aVR > V1
  • Differentiates LMCA from proximal LAD occlusion

New or presumed new LBBB

• <10% have AMI but early studies of fibrinolytic therapy found increased mortality in this group and benefit from fibrinolysis
• Counts as STEMI in Heart Foundation guideline

Reciprocal ECG changes

• Due to subendocardial ischaemia and denote:
  • Larger area of injury risk
  • Increased severity of underlying CAD
  • More severe pump failure
  • Higher likelihood of cardiovascular complications
  • Increased mortality

Territories

Coronary anatomy

Angiography

• >95% sensitivity/specificity
  • Sensitivity improved by endovascular USS
• Normal angiogram rules out atherosclerosis
  • Coronary artery spasm or slow flow can still precipitate symptoms
• Complications
  • Arterial access – Haematoma, fistula, pseudoaneurysm
  • Major bleeding in 5%
  • Stroke 0.01%, ICH 0.05%
  • Nephropathy in 2%
  • VF in 4%
  • Re-stenosis (1%)
  • Dissection 1/1000

• Results
  • Severity of lesions and size of distal vessels can be underestimated
  • 75% reduction in cross-section = 50% diameter reduction
  • 90% reduction in cross-section = 67% diameter reduction
  • Severity
    • 50% stenosis likely to cause exertional pain
    • >70% stenosis likely to cause functional impairment
    • 90% stenosis likely to cause rest pain
    • >95% stenosis likely to completely occlude within days/weeks
  • Ulcerated lesions more likely to be thrombogenic
  • The larger the area supplied by the artery, the more significant the lesion

STEMI management

• Target SpO2 >93%
• Analgesia
• Antiemetic
• GTN (S/L, tab or infusion)
• Antiplatelet
  • Aspirin 300mg
  • PCI
    • Clopidogrel 600mg then 150mg daily
    • Ticagrelor 180mg load (unless immediate CABG possibility) preferred if diabetic, stent thrombosis, recurrent events on clopidogrel or high burden of disease on angiography
    • Ticagrelor should not be used if previous haemorrhage stroke or liver disease
  • Fibrinolysis
    • Clopidogrel 300mg
  • CABG
    • Nothing unless planned for a weeks time when ciagrelor preferred

• Anticoagulation
  • If undergoing PCI
    • Heparin bolus 60U/kg (max 4000IU) then heparin infusion 12U/kg/hr (max 1000IU/hr) or Enoxaparin 1mg/kg SC BD
  • If undergoing fibrinolysis
    • Enoxaparin 30mg IV bolus if under 75 THEN 1mg/kg (max 100mg) beginning 15 minutes after bolus) or 0.75mg/kg if over 75 yo
• Glycoprotein IIb/IIIa inhibitors
  • At time of PCI

• TRITON-TIMI 38
  • Prasugrel reduced composite (CV death, non-fatal MI or stroke) in clopidogrel-naïve patients undergoing PCI
  • Prasugrel contraindicated in prior stroke/TIA, age >75 or <60kg
• PLATO trial
  • Ticagrelor reduced composite (CV death, non-fatal MI and stroke) and reduced CV mortality in clopidogrel naïve with STEMI or moderate-high risk NSTEMI
  • Increased non-CABG-related bleeding risk vs. clopidogrel
  • Ticagrelor associated with dyspnoea (no harm) and asymptomatic bradycardia in first week of therapy
• Both CI in coagulopathy or liver disease
• Clopidogrel never been compared to placebo in setting of primary PCI but high-dose superior to low-dose in OASIS trial

• UFH vs. Enoxaparin
  • ATOLL trial
  • Enoxaparin had no increased risk of bleeding
  • Primary endpoint unchanged
  • Secondary composite endpoint improved with enoxaparin (death, recurrent MI, ACS) as well as cardiac arrest or complication of MI
  • Enoxaparin may be preferred
  • Should receive full-dose anticoagulants for at least 48 hours

• Timing of PCI
  • If clinical presentation of STEMI within 12 hours of symptom onset and persistent ST elevation or new/presumed new LBBB, immediate PCI
  • Consider if clinical/ECG evidence of ischaemia, even if symptoms started >12 hours ago
  • Unclear if immediate PCI warranted if >12 hours and no ongoing symptoms or ECG signs of ischaemia
    • Small RCT showed myocardial salvage and improved 4 year survival in this group
    • Larger meta-analysis of late re-canalisation of occluded infarct culprit artery showed no benefit
    • Current ECS guideline states consider if 12-24 hrs and not recommended if >24 hours

• PCI clearly superior to thrombolysis if:
  • Thrombolysis CI
  • Cardiogenic shock
  • Angiography required to confirmd diagnosis
• PCI generally preferred if:
  • First Medical Contact to Balloon (FMCTB) < 90min (or <120min if at non-PCI centre)
  • Door-to-balloon time (DTB) <90 min
  • High risk from STEMI: Age >75, extensive anterior, high bleeding risk, previous MI/CABG or Killip Class >=3
  • Symptom onset >3 hours ago

• Fibrinolysis generally preferred if:
  • <3 hour from symptom onset
  • PCI not available
  • Prolonged transport predicted
  • Door-to-balloon >90 minutes
  • FMCTB > 90 min (or >120min if at non-PCI centre)

• Tenecteplase dosing guide

• Absolute contraindications for thrombolysis
  • Active bleeding or bleeding diathesis (excluding menses)
  • Suspected aortic dissection
  • Significant closed head or facial trauma within 3 months
  • Any prior ICH
  • Ischaemic stroke within 3 months
  • Known cerebral vascular lesion
  • Known malignant intracranial neoplasm
  • ? Chest pain with new neurology

• Relative contraindications to thrombolysis
  • Current anticoagulation
  • Non-compressible vascular puncture
  • Recent major surgery <3 weeks
  • Traumatic or prolonged CPR >10 min
  • Recent internal bleeding (<4 weeks) or active peptic ulcer disease
  • Suspected pericarditis
  • Advanced liver disease or metastatic cancer
  • Hx of chronic, severe, poorly controlled HTN
  • Severe uncontrolled HTN on presentation (SBP >180; DBP >110)
  • Ischaemic stroke >3 months ago/known intracranial abnormality/Dementia
  • Pregnancy or within 1 week postpartum

• ‘Failed’ thrombolysis
  • Only judged definitively with angiography
  • All patients should be transferred to PCI facility after thrombolysis within 24 hours
  • If <50% ST recovery at 60-90 minutes or haemodynamic instability – t/f immediately
  • If failure of relief of chest pain/haemodynamic/electrical compromise – t/f immediately
• Minor infarctions (esp. inferior) and severe comorbidities, especially if risk factors for intracranial haemorrhage (age >75, female, smaller patients, prior stroke of any kind, SBP >160mmHg) should not be thrombolysed
• Less effective for inferior STEMI (NNT 10-120)

Non-STEMI management

• O2 if necessary
• Analgesia
• Antiemetic
• GTN
• Aspirin 300mg
• Withold P2Y12 receptor inhibitors if going for CABG
• Ticagrelor 180mg or clopidogrel 300mg if intermediate or high risk
  • Leave decision up to treating cardiologist as need to weigh bleeding risk with risk of recurrent ischaemia
• Clexane (or UFH if clexane CI) if intermediate or high risk
  • 1mg/kg SC BD (0.75mg/kg SC BD if elderly or renal impairment)
  • 60IU/kg load then 12IU/kg/hr infusion targeting APTT 45-70

• GPIIb/IIIa inhibitors at time of PCI
• PCI
  • For confirmed NSTEACS with intermediate/high and very high risk
    • Very high risk within 2 hours
    • High risk within 24 hours
    • Intermediate risk within 72 hours
    • Low risk – Selective invasive strategy guided by provocative testing
  • Invasive approach within 24-48 hours reduces composite of death, MI or recurrent ACS by 19% in women and 27% in men
  • More aggressive and earlier PCI in these patients is of no proven benefit

• Statin within 24 hours
  • Atorvastatin 40-80mg or Rosuvastatin 20-40mg
• Beta-blocker within 24 hours
• ACEi/ARB within 24 hours

Drug-eluting stents

• Decreased early vessel closure but increased delayed closure, particularly once antiplatelet agents (i.e. clopidogrel) is stopped

PCI vs. fibrinolysis

• PCI reduces cardiovascular complication rate
• The longer the duration of symptoms, the greater the benefit of primary PCI over fibrinolysis
• PCI more effective at establishing TIMI flow and reducing reocclusion
• PCI associated with decreased incidence of short- and long-term death, non-fatal reinfarction and ICH

Fibrinolysis

• Indicated for STEMI if time to treatment is <6 hours to 12 hours from symptom onset and ECG has at least 1mm of STE in two or more contiguous leads
• More beneficial if given earlier and for larger infarction
• More benefit for anterior than inferior or smaller infarctions
• 0.5-1% risk of ICH
• Fibrinolysis inherently exposes thrombin (potent platelet activator), which may explain limited benefit of thrombolysis and benefit of potent antiplatelet and antithrombin therapy given concurrently

Tenectaplase vs. alteplase

• Alteplase is recombinant tPA
• Tenectaplase is a variant of tPA with prolonged half-life (20 min), resistant to endogenous plasminogen-activator inhibitor 1 inactivation and has high fibrin specificity and binding with minimal systemic fibrinogen depletion
  • Single bolus administration and weight-based dosing

Pharmacoinvasive therapy

• TRANSFER-AMI trial showed benefit of transfer to PCI-capable centre after fibrinolysis within 6 hours
  • 6.2% absolute risk reduction in composite endpoint of death, reinfarction, recurrent ischaemia, new or worsening HF or cardiogenic shock at 30 days

Facilitated PCI

• Planned initial fibrinolysis followed by PCI not recommended
• ASSENT-4 trial showed no benefit and higher incidence of death, CCF or shock at 90 days

Antiplatelets

• GpIIb/IIIa inhibitors are more potent than aspirin as interrupt platelet activation regardless of stimulating agonist
• Aspirin only inhibits platelet aggregation stimulated through the thromboxane A2 pathway

Aspirin

• Inhibition lasts 8-12 day life of platelet as they cannot produce new cycloxygenase
• Relative reduction in mortality of 23% in STEMI alone
• NNT – 41 and NNH – 167 (non-dangerous bleeding) – ISIS2 (Lancet 1998)
• Do not withold from those with vague allergy, history of remote peptic ulcer or GI bleeding as benefit is massive
• Clopidogrel is a viable alternative if truly contraindicated

Ticagrelor

• Reversible P2Y12 receptor antagonist
• Effect lasts 3 days
• PLATO study compared ticagrelor to clopidogrel in all ACS patients
• 1.9% absolute RR of composite endpoint
  • No increase in bleeding risk
  • In those with STEMI undergoing PCI, increased risk of stroke 1.7 vs 1%

Clopidogrel

• Addition to aspirin and antithrombin therapy in those undergoing fibrinolysis improves cardiovascular outcomes as shown in CLARITY-TIMI 28 trial and COMMIT trial
  • Improves hospital and 30-day outcomes
• NSTEMI/unstable angina
  • Addition to aspirin reduces composite outcome of death, AMI and stroke
  • CURE trial showed 20% reduction in death, AMI or stroke between 3 and 12 months
  • Did increase bleeding risk but was reduced in patients receiving lower dose aspirin
• For those undergoing urgent PCI, 600mg is preferred to 300mg to prevent post-procedure MI but does increase bleeding risk
• Consider alternatives in:
  • Patients on omeprazole have 50% reduction in antiplatelet effect
  • Patient with CYP2C19 variant gene have reduced ability to active prodrug and increased risk of stent thromboses and recurrent ischaemia

GPIIb/IIIa inhibitors

• Abciximab chimeric antibody binds irreversibly
• Eptifibatide binds reversibly
• Tirofiban binds reversibly
• All require IV infusion for sustained benefit
• Initiation prior to PCI has not shown benefit as compared to delivery at time of PCI
• 40% reduced risk of death or AMI in 30 days (13% over 3 years)
• Very minimal benefit in unstable angina/NSTEMI (especially if not undergoing early PCI)

Anticoagulation

UFH

• Reduces risk of AMI and death in unstable angina when combined with aspirin by 56%
  • This benefit is almost certainly dominated by aspirin
• Enoxaparin preferred as more reliable clinical effect (unless primary PCI for STEMI, in which case heparin preferred)
  • 0.9% reduction in death or recurrent AMI vs. UFH
• SYNERGY trial showed consistent therapy with a single antithrombin agent had improved outcomes and less bleeding
• Cochrane (2014)
  • Heparin for NSTEMI vs. placebo
    • No change in mortality
    • No change in revascularisation
    • No change in recurrent angina
    • Small decrease in non-fatal MI
    • Small increase in major bleeding
• Heparin for STEMI going for PCI without thrombolytics
  • Recommended but no evidence for this
• Heparin for STEMI treated with thrombolytics
  • 3 RCT showed no benefit
  • AMI-SK showed small benefit in non-fatal MI balanced by small increase in major bleeding
  • CREATE study showed LMWH had 0.9% mortality benefit over UFH but partially balanced against increased risk of major bleeding

Fondaparinux

• Binds to antithrombin III to form an antithrombin complex very specific for Factor Xa inhibition
• Similar efficacy to UFH in STEMI
• Recommended to be used with UFH or bivalirudin before PCI
• Recommended by European Socitety of Cardiology over enoxaparin for unstable angina/NSTEMI if conservative management regime employed

Bivalirudin

• Direct thrombin inhibitor
• Reduces short-term risk of post-ischaemic complications relative to UFH in patients undergoing PCI
• Safe and effective for intermediate-to-high risk NSTEMI/unstable angina patients undergoing PCI
• Reduced bleeding for STEMI going for primary PCI than UFH + GPIIb/IIIa inhibitors

Other medications

Nitrates

• Also inhibit platelet aggregation
• When used in patients not treated with thrombolytics they reduce infarct size, improves regional function and decreases rate of cardiovascular complications
• 35% reduction in mortality
• In most studies, IV GTN used to reduce MAP by 10% (in normotensive patients) or 30% in hypertensive patients rather than titrated to symptom resolution = THIS IS WHAT YOU AIM FOR
• Data is confounded in those receiving thrombolytics
• IV GTN recommended for STEMI with recurrent ischaemia, CCF or hypertension for 24-48 hours
• IV GTN recommended for NSTEMI if not responsive to S/L GTN
• Avoid use for 24 hours after sildenafil and 48 hours of tadalafil

Beta-blockers

• No benefit from early use (<24 hours) in recent trials
• Recommendation is to start PO beta-blockers within 24 hours if none of the following:
  • Signs of HF
  • Evidence of low CO state
  • Increased risk of cardiogenic shock: Age >70, SBP <120, sinus tachycardia >110 or bradycardia <60 and longer duratino of STEMI symptoms before diagnosis and treatment
  • PR >0.24 seconds, 2^nd/3^rd degree AV block, active asthma, reactive airways disease

ACEi

• Reduce LV dysfunction and LV dilatation and slow development of CHF after AMI
• Oral ACEi lower mortality after AMI
• STEMI or heart failure patients should receive ACEi within 24 hours
• NSTEMI/unstable angina patients should receive ACEi within 24 hours if pulmonary congestion or LVEF <40% in the absence of hypotension or contraindications
• Contraindications include hypotension, bilateral RAS, renal failure or history of cough/angioedema from ACEi

Magnesium

• Correct documented hypomagnesaemia and give for torsades-type VT with prolonged QT interval
• No clear evidence outside of torsades

CCB

• Do not reduce mortality after AMI and may be harmful
• Verapamil and diltiazem may have a role in ongoing ischaemia or AF with RVR if no CCF, LV dysfunction, AV block and beta-blockers are contraindicated

Complications of ACS

• Dysrhythmias seen in 72-100% of AMI patients admitted to CCU
• Consequences include reduced haemodynamic performance, compromised myocardial viability, increased myocardial demand and predisposition to more serious arrhythmias due to reduced VF threshold
• Loss of atrial kick in healthy heart reduces SV by 10-20% and up to 35% in those with reduced LV compliance
• Pump failure may lead to sympathetically driven sinus tachycardia, AF/flutter and SVT
• Cardiogenic shock seen in 6-7% of AMI with 80% mortality

Early dysrhythmias

• Bradydysrhythmias
  • Sinus brady 35-40%
  • 1^st degree block 4-15%
  • Type 1 second-degree 4-10%
  • Type 2 second-degree 0.5-1%
  • 3^rd degree 5-8%
  • Asystole 1-5%

• Tachydysrhythmias
  • Sinus tachy 30-35%
  • Atrial premature contractions 50%
  • SVT 2-9%
  • AF 4-10%
  • A flutter 1-2%
  • Ventricular premature beats 99%
  • Accelerated idioventricular rhythm 50-70%
  • Non-sustained VT 60-69%
  • Sustained VT 2-6%
  • VF 4-7%

• Sinus tachy
  • Prominent in anterior MI and associated with a poor prognosis due to increased O2 demand
  • Seek cause (anxiety, pain, LV failure, fever, pericarditis, hypovolaemia, atrial infarction, PE or medications) and treat if possible
• AF
  • Mostly in first 24 hours and usually transient
  • Warrants anticoagulation
  • Treatment depends on clinical status and previous anticoagulation

• Sinus bradycardia
  • If no hypotension, does not carry mortality risk
  • Atropine indicated if hypotensive, ischaemia or ventricular escape rhythms OR treatment of AV nodal block (e.g. type 1 second-degree)
  • In the setting of AMI, atropine may induce infarct extension, VF and excessive myocardial O2 demand so use with caution
• Complete heart block
  • Seen in anterior and inferior MI as AV conduction system receives blood supply from AV branch of RCA and septal perforating branch of LAD
  • In absence of RV involvement, mortality is 15%. In the setting of RV involvement, mortality is >30%
  • Complete heart block in anterior MI portends a grave prognosis
• Mortality in heart block in AMI is related to extensive infarction rather than heart block itself and as such, pacing does not confer a mortality benefit but is still recommended to prevent/treat hypotension, acute ischaemia or ventricular dysrhythmias

Indications for temporary pacing

• Transcutaneous
  • Unresponsive symptomatic bradycardia
  • Mobitz II or higher AV blocks
  • New LBBB and bifascicular blocks
  • RBBB or LBBB with first-degree block
  • Stable bradycardia and new or presumed new BBB (sometimes)
• Transvenous
  • Asystole
  • Unresponsive symptomatic bradycardia
  • Mobitz II or higher AV bocks
  • New or presumed-new LBBB
  • Alternating BBB
  • RBBB or LBBB with first-degree block
  • Consider in RBBB with LAFB or LPFB
  • Overdrive pacing in unresponsive VT
  • Unresponsive recurrent sinus pauses (>3s)

Other dysrhythmias

• Accelerated idioventricular rhythms in those with AMI do not affect prognosis or require treatment
• Primary VT (soon after symptom onset) does not confer poor prognosis
  • Late VT is usually associated with transmural infarction and LV dysfunction, induces haemodynamic deterioration and is associated with a mortality of around 50%
• Primary VF (soon after symptom onset) does not have a large effect on mortality and prognosis, as long as it is quickly treated
  • Delayed or secondary VF during hospitalisation is associated with severe ventricular dysfunction and carries 75% in-hospital mortality

• New RBBB
  • Seen in 2% of AMI (mostly anteroseptal MI)
  • The first branch off the LAD supplies the right bundle so indicates proximal LAD occlusion
  • Associated with increased mortality and complete HB
• New LBBB
  • <10% of patients with AMI and associated with higher mortality
  • Left posterior fascicle is larger than anterior and subsequently left posterior hemifascicular block carries higher mortality as represents larger area of infarction
  • Bifascicular block (RBBB + LAFP/LPFB) has increased likelihood of progression to complete heart block and represents a large infarction, more frequent pump failure and higher mortality

Heart failure

• 15-20% of AMI patients have some degree of heart failure
  • 1/3 of these have shock
• The greater the LV dysfunction, the greater the mortality
• Mortality for AMI
  • No HF – 10%
  • Mild HF 15-20%
  • Frank pulmonary oedema 40%
  • Cardiogenic shock 50-80%
• Raised BNP early on portends worse 30-day outcome

Mechanical complications

• Ventricular free wall rupture
  • 10% of AMI fatalities
  • Usually 1-5 days after infarction
  • Rupture of LV free wall = >90% lead to tamponade and death
  • Tearing or sudden severe pain
  • Surgical therapy required
• Rupture of IV septum
  • Size of defect determines degree of shunt and prognosis
  • Presents with chest pain, dyspnoea, new holosystolic murmur with palpable thrill and heart best at lower left sternal border
  • Most common in anterior MI and extensive three-vessel CAD
  • Surgical therapy required

• Papillary muscle rupture
  • 1% of AMI and mostly inferior MI
  • Usually 3-5 days post-MI
  • Often occurs with small to medium sized infarcts (as opposed to free wall or IV septal rupture)
  • Present with acute dyspnoea, worsening heart failure and new holosystolic murmur consistent with MR
  • Posteromedial papillary muscle is most commonly ruptured as it receives blood supply from only one coronary artery, usually the RCA

Pericarditis

• Early post-AMI pericarditis seen in <5% (previously 20% prior to PCI)
• More common with transmural AMI or delayed presentations
• Usually 2-4 days post-MI
• Resorption rate of any pericardial effusion (if even present) is many months
• Treatment is symptomatic with aspirin or colchicine
• Dressler’s syndrome
  • Late post-AMI syndrome seen 2-10 weeks after AMI with chest pain, fever and pleuropericarditis

Right ventricular infarction

• Isolated RV infarction is rare but is seen as part of 1/3 of inferior MI
• Significant increase in mortality and cardiovascular complications
• RV infarction with concurrent LV dysfunction has a particularly devastating effect on haemodynamic function
  • Pulmonary congestion already exists with raised PAP
  • Each contraction of the LV causes the IV septum to move into the RV and expel blood into the pulmonary circulation
  • Pre-morbid CO already reduced and further diminished by reduced LV filling pressures

• Factors that reduce preload, increase RV afterload (LV failure) or impair atrial function (AF/flutter, atrial infarction) all lead to significant haemodynamic derangements
• Treatment consists of increasing preload, avoiding nitrates, reducing RV afterload and early inotropic support (dobutamine if 1-2L of crystalloid fails to show improvement)
• High-degree AV block is common and restitution of AV synchrony is crucial and may require AV sequential pacing

Other complications

• LV thrombus
• Arterial embolisation
• VTE
• Post-infarction angina
• Infarct extension

Recurrent or refractory ischaemia

• Options include continued medical management (e.g. GTN infusions), rescue angioplasty, CABG
• Warrants cath and antithrombin/antiplatelet therapy
• If haemodynamically unstable or cath not immediately available, intra-aortic balloon pump counterpulsation may be used to improve coronary flow and cardiac output, thereby decreasing oxygen demand and myocardial ischaemia

Post-procedure chest pain

• Assume abrupt vessel closure until proven otherwise
• Seen in 4% of patients 2-14 days after stent placement
• Bare metal more likely to re-stenose in short term and drug-eluting more likely to re-stenose at 9-12 months after clopidogrel ceased
• Can be confused with post-MI pericarditis

Amphetamine-induced ACS

• AMI occurs in 6% of patients with chest pain after cocaine use
• Beta-blockers are contraindicated in first 24 hours after cocaine use but otherwise treatment is the same
• Cocaine-associated STEMI still warrants PCI
• Benzodiazepines are effective in addition to usual therapy

Acute medical disorders and ACS

• GI bleeding, stroke and severe infection carry risk of AMI
• GI bleeders admitted to ICU have 13% risk of MI and may have increased risk of death (33 vs 8% in one study of all GI bleeders, not just ICU admits)
• 17% of acute stroke have raised troponin, associated with 3.2 relative risk of death
• Conversely, risk of stroke post-MI is 0.6-1.8% but carries 17-27% risk of in-hospital mortality
• SAH shows elevated troponins in 28% and transient ECG changes + LV dysfunction but simultaneous STEMI is very uncommon
• AMI occurs in 5.3% of admitted CAP patients and 15% of those with severe pneumonia

OMI Manifesto

• Aims to change paradigm from STEMI vs. NSTEMI to 
  • Occlusion Myocardial Infarction (OMI) vs. Non-occlusion Myocardial Infarction (NOMI)

• History of reperfusion
  • Fibrinolytic therapy trialists (FTT) in 1994 showed in 60 000 patients randomized to thrombolysis vs. placebo a NNT of 56 for mortality benefit
    • 4 out of 9 included trials had no ECG criteria
    • 1/3 of patients had no ST elevation appreciable
    • Subgroup analysis of ST elevation NNT improved to 43 for mortality
      • ST depression and normal subgroup analysis found no benefit to thrombolysis and these terms were not defined
    • Primary indicator for thrombolysis was concerning story and undefined ECG findings
    • Did not have any angiographic confirmation of acute coronary occlusion or not

• Schmitt et al. 2001
  • 25-30% of ‘NSTEMI’ have acute coronary occlusion
  • 50% of these misses were left circumflex territory
• Wang et al. 2009
  • 27% of NSTEMI had acute coronary occlusion
  • Coronary occlusion group had higher 6-month risk-adjusted mortality
• Pride et al. 2010
  • 26% of anterior ST segment depressions had occluded culprit arteries despite not meeting STEMI criteria
  • 50% of these were LCx lesions

• Khan et al. 2007
  • Meta-analysis showed ¼ of NSTEMI had acute occlusion with increased all-cause mortality in short and long term

Early vs. delayed angiography for NSTEMI

• Mehta et al. TIMACS 2009
  • Early <=24 hrs vs. delayed >= 36 hrs
  • Mean time 14 vs. 50 hours (not actually early)
  • Early is considered <2 hours
  • No difference in death, MI or stroke

• Hoedemaker et al. ICTUS 2017
  • Early within 24-48 hours vs. selective invasive 
  • No difference in 1-year mortality or spontaneous MI
  • No difference at 10 year mortality or spontaneous MI
  • Patients excluded if refractory ischaemia, haemodynamic instability or congestive heart failure

• Van’t Hof et al. ELISA 2003
  • Early vs. late – Mean 6 vs. 50 hours
  • No difference at 30 days
  • Refractory ischaemia excluded
  • Still not early (<2 hours)

• Thiele et al. LIPSIA-NSTEMI 2012
  • Immediate <2 hours vs. 10-48 hours (Mean 18 hours)
  • No difference in MI or death at 6 months
  • Excluded refractory ischaemia
  • Most likely explanation is that those with refractory ischaemia also had acute occlusion and so were excluded from study

• Montelascot et al. JAMA 2009
  • Refractory ischaemia excluded
  • Immediate or next working day
  • 70min vs. 21 hours
  • No difference in TnT, death, MI or revascularization at 1 month
  • Likely no difference due to refractory ischaemia exclusion (= OMI)

Last Updated on September 21, 2022 by Andrew Crofton