a game changer…

The case.

A 76 year old female presents to ED after being repeated assaulted by her aggressive, demented husband, including punches, kicks and attempted strangulation. She has a past medical history of hypertension & GORD and takes telmisartan, amlodipine & pantoprazole.

On examination, she is alert and oriented with a patent airway, complaining of central chest pain and jaw pain. There are ligature marks over the anterior neck, but no haematoma, subcutaneous emphysema or hoarseness of voice. She has significant bruising (of various ages) over her maxilla, mandible, chest wall and thigh.

E-FAST reveals trace free-fluid in the Pouch of Douglas only, so with her normal vital signs she is booked for a CT pan-scan….

Whilst you are writing your notes, the Resus nurse hands you her ECG…

… it appears to be a game-changer ! Suddenly your team questions everything !!

[DDET What’s your interpretation ?!]

• Sinus rhythm at 88 bpm. 1x junctional ectopic (5th complex).
• Normal axis.
• PR 200msec, QRS 80-90msec, QTc 485msec (Bazett)
• Widespread ST-segment elevation
  • Concave up.
  • Predominately inferolateral leads (V4-6, I, II, III, aVF – up to 4.5mm)
  • Associated ST depression & PR elevation aVR. Suggestion of PR depression along rhythm strip (II).

Differential Diagnoses.

• Acute Coronary Syndrome (STEMI).
• Pericarditis
• Myocardial injury/contusion ?

[/DDET]

[DDET What else should we consider ??]

Differential Diagnosis of ST-Segment Elevation

• Acute Coronary Syndrome / AMI
• Acute Pericarditis
• Bundle Branch Block (left & right)
• Benign Early Repolarisation
• Ventricular escape/paced rhythm.
• LVH
• LV aneurysm.
• Cardiomyopathy / Myocarditis
• Myocardial contusion.
• Post-defibrillation
• Hyperkalaemia
• Hypothermia (Osborn J-waves)
• Channelopathies (eg. Brugada)
• Preexcitation Syndrome (eg. WPW)
• Intracranial/CNS Injury (eg. SAH)

[/DDET]

[DDET What do you do next ?!]

• Bedside ECHO:
  • No pericardial effusion.
  • LV apex is hypokinetic.
• Do you give aspirin ?? What about other ischaemic meds ??
  • Is this a true AMI ??
  • She could have traumatic intracranial pathology.

[/DDET]

[DDET The story continues…]

Whilst the team is concerned about her ECG changes, it is decided that she should have her neuroimaging prior to administration of antiplatelet therapy. She is rushed off to CT…

The findings;

• CT Brain – Small acute left subdural haematoma with minimal mass effect with tiny focus of subarachnoid blood in the left parietal lobe.
  • Remainder of CT is negative for traumatic pathology.
• HS-Troponin is elevated @ 1161 ng/L (delta Trop returns at 1365 !!)
• Formal Cardiology ECHO (1150pm!!) shows moderate systolic impairment with apical & periapical hypokinesis.
• Decision made to give 300mg of aspirin and head to the CATH lab for angiography…
• Angiogram showed only minor coronary disease. No culprit lesion identified. No ventriculogram performed.

[/DDET]

[DDET The Diagnosis???]

TAKOTSUBO CARDIOMYOPATHY

aka. Stress-induced cardiomyopathy, Apical ballooning syndrome, Broken-heart syndrome.

 

The Basics.

• An increasingly reported syndrome.
  • May account for ~2% of suspected STEMIs.
• Characterised by transient systolic dysfunction of the apical &/or mid-segments of the left ventricle.
  • “Takotsubo” – Japanese for an octopus trap, the shape resembling that of the apical ballooning configuration of the left ventricle.
• Mimics acute myocardial infarction, but there is absent obstructive CAD.
• Most common in post-menopausal women.

 

The Pathophysiology.

• Poorly understood.
  • Suggested mechanisms include; catecholamine excess, coronary artery spasm or microvascular dysfunction.
  • Potential role for plaque rupture & coronary thrombosis (with spontaneous thrombolysis).
• Frequently but not always triggered by an acute medical illness or intense, emotional or physical stress [unexpected family death, domestic violence, financial stress, natural disasters].
• Physical or emotional stress.
  • ?Diffuse catecholamine-induced microvascular spasm [“myocardial stunning”]
  • ?Direct catecholamine-associated myocardial toxicity.
• Critical illness.
  • A “not uncommon” diagnosis in the medical ICU population, even among patients with non-cardiac diagnoses and no prior history of cardiac disease.

Clinical Features.

• The presentation is similar to that of AMI.
• Most common symptom is acute, substernal chest pain.
  • Associated dyspnoea, syncope, shock and ECG abnormalities.
• Acute complications include;
  • Heart failure
    • More common when age > 70, physical stressor present & LVEF < 40%
  • Tachy & bradydysrhythmias
  • Mitral regurgitation
    • Secondary to acute LV outflow tract obstruction (a result of LV basal hyperkinesis)
  • Cardiogenic shock

Investigations.

• ECG abnormalities include;
  • ST-segment elevation (most common in precordial leads)
  • Deep T-wave inversion
  • Prolonged QT
  • Abnormal Q-waves
  • Can be normal…
• Troponin.
  • Usually elevated (typically mild).
• ECHO & Ventriculography.
  • Characteristic apical ballooning with akinesis/dyskinesis of the apical 1/2 to 2/3’s of the LV.
  • Systolic function is reduced.
  • Wall motion abnormalities may involve the distribution of more than one coronary artery.

Diagnosis.

• This should be suspected in postmenopausal women who present with ACS following intense psychological stress in whom clinical and ECG abnormalities are out of proportion to the degrees of troponin elevation.
• Coronary angiography typically shows either normal vessels or mild-moderate coronary atherosclerosis.
• Cardiac MRI can provide additional information.
• The Mayo Clinic diagnostic criteria require all of the following to make the diagnosis.
  • Transient hypokinesis, akinesis or dyskinesis of the LV mid-segments with or without apical involvement.
  • Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
  • New ECG abnormalities (ST-elevation or TWI) or modest troponin elevation.
  • Absence of phaeochromocytoma or myocarditis.

Management.

• A patient with chest pain and ST-elevation should be managed as though they have acute myocardial ischaemia.
  • Cardiac catheterisation if available, otherwise suspicion of stress-induced cardiomyopathy is not a sufficient reason to withhold fibrinolytic therapy.
• Takotsubo cardiomyopathy is a transient disorder managed with supportive therapy.
• Standard therapy for patients with LV impairment have been suggested.
  • Eg. ACE inhibitors, beta-blockers and diuretics.
  • Typically continued until there is resolution of LV function (usu. 1-4 weeks).
• Aspirin for those with co-existing coronary atherosclerosis.
• Hypotension/Shock.
  • Urgent ECHO for LVOT obstruction.
    • Treated w/ beta-blockers & fluid resuscitation.
  • Absence of LVOT obstruction.
    • Cautious use of inotropic agents (remember this is a condition of catecholamine excess).
  • Consideration of IABP counterpulsation.
• Thromboembolic prophylaxis.
  • Intraventricular thrombus formation and embolisation are potential sequelae.
  • Data is limited on use of anticoagulation.
    • Suggested for those with identified LV thrombus, or for those with severe LV dysfunction (until akinesis/hypokinesis resolves).

[/DDET]

[DDET The finale…]

• Troponin peaked 6 hours into admission.
• Further headache during day one of admission with CT showing slight progression of SDH. She did not require neurosurgical intervention.
• She remained haemodynamically stable and was started on bisoprolol and ramipril. Subsequent ECHOs showed some improved in LV function.
• She was discharged home on Day 10 with outpatient Cardiology followup.

[/DDET]

[DDET References.]

1. UpToDate. “Stress-induced (takotsubo) cardiomyopathy”
2. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

[/DDET]