Takotsubo Cardiomyopathy Case

 Extensive PMH
• Previous DU 1972 / 2002
• COPD
• Pernicious Anaemia
• CKD stage III
• Crohn’s Disease – previous right Hemicolectomy, underwent
laparotomy and excision of perforated recurrent ileal / ileocolic
Crohn’s plus loop ileostomy 31st August 2008
 Admitted under Medicine with nausea / vomiting / high stoma
output 17 Oct 2008
 Severe hyponatraemia (117mmol/L), Mg also low at 0.27, CRP
25, plts 758, Stool – giardial cysts!
 Initial diagnosis
• Dehydration with electrolyte imbalance secondary to
nausea and vomiting
• Incidental giardiasis
• Crohn’s flare-up

 Treated with IV fluids / oral magnesium / oral
metronidazole – initial good improvement
 Transferred under Gastroenterologists
 23 Oct 2009 – deteriorated with worsening diarrhoea /
signs of LRTI
 Pyrexial, Sinus tachycardia 120bpm, BP 120/64mmHg
 CRP 137, WCC 30.2, Mg 0.30, Ca 1.38
 CXR – Left pneumonic consolidation
 AXR – not diagnostic
 Rx PO metronidazole / IV Tazocin / Mg & Ca replacement
 CT Abdo – no worrying intra-abdominal pathology

 Made slow but steady recovery over next few weeks
 Due to be commenced on IV TPN 11 Nov 2009 to
improve nutritional status
 Had some pain / distress during central line insertion
11 Nov 2009, then developed sudden onset malaise /
feeling of impending doom
 Transient pre-syncopal episode – only lasted 1-2
mins
 HR 108bpm>140bpm – SR, BP 142/62mmHg
 No clinical signs of heart failure
 Hb 8.0 g/dl, Cr 100, Mg 0.67, Cr 2.12
 ECG

 Treated initially as Acute STEMI 11 Nov 2008
 Not thrombolysed as recent major surgery / absence
of chest pain
 Referred for bail-out PCI at Hull – was not accepted
due to comorbidities (main issue being significant
anaemia)
 Rx Aspirin / Clopidogrel / IV Nitrates / blood
transfusion / IV fluids
 Troponin I elevated at 12 hours at 1.06, then dropped
to 0.13 within 24 hours
 CK not elevated at any stage – 60 maximally
 No pain, but worsening dyspnoea / hypotension
despite above therapy
 Coronary angiogram organised for 14 Nov 2008

• Showed angiographically normal wide calibre
coronary arteries with no significant flow-limitation in
any arterial segment
• Left ventriculography showed substantial LV apical
ballooning with overall mild-moderate LV impairment
and elevated LVEDP

 Likely triggered by dramatically elevated
catecholamine levels caused by concurrent illness in
a post-menopausal woman
 Rx entirely supportive
 Commenced on beta-blocker / ACEI, continued on
Aspirin / SC prophylactic clexane
 IV TPN continued
 Continued to recover with GI supportive therapy
 No further cardiac complications
 Discharged home 08 Dec 2008
 ECHO end Dec 2008 – Normal LV systolic function
with resolution of apical ballooning

 No subsequent GI complications – stoma
stable with no further vomiting / stoma
problems
 No further cardiac complications – no
recurrence of chest pain / cardiac failure
 However, patient readmitted with
exacerbation of COPD secondary to
pseudomonal pneumonia 08 Jan 2009 –
developed Type II respiratory failure and died
in ITU 16 Jan 2009

Colin A J Farquharson
Consultant Cardiologist
Diana Princess of Wales
Hospital
Grimsby
United Kingdom

 Cardiomyopathy characterized by transient apical and
midventricular LV dysfunction in the absence of
significant coronary artery disease that is triggered by
emotional or physical stress.
• In setting of depressed/abnormal function of distal and apical LV
segments there is compensatory hyperkinesis of basal walls 
“ballooning” of apex during systole.
 Typically recover normal LV function in 1-4 weeks.
Colin Farquharson , Cardiologist , Grimsby UK

 1st described in Japan in 1990
 Named after the tako-tsubo,
which is an octopus trap
• Shape of the trap is similar
to the appearance of LV
apical ballooning noted in
patients with this form of
cardiomyopathy
 Was later described in many
other reports and was
subsequently recognised as a
distinct entity

Kurisu, S., et al. 2002. American Heart Journal. 143: 448-455.

NORMAL LEFT
VENTRICULAR
CONTRACTION
ABNORMAL
CONTRACTION
OF LV TAKING
THE SHAPE OF A
“TAKO-TSUBO”

 Takotsubo cardiomyopathy
 Stress-induced cardiomyopathy
 Transient left ventricular apical ballooning
syndrome
 Apical ballooning syndrome
 Broken heart syndrome
 Ampulla cardiomyopathy

 May account for up to 2% of suspected ACS
 In-hospital mortality ranges between 0-8%
 Much more common in women (~90%),
especially postmenopausal women (>80% of
cases)
 Mean age 58-75 years
 More common in industrialised nations
 Many recognised triggers: death of loved one,
other catastrophic news, devastating financial
losses, natural disasters, physical illness/ICU,
etc.

1. Transient a/dyskinesis of apical and midventricular
segments in association with regional wall motion
abnormalities that extend beyond the distribution of a
single epicardial vessel
2. Absence on angiography of obstructive coronary artery
disease or evidence of acute plaque rupture
3. New ST segment elevation or T wave inversions on
ECG
4. Absence of recent significant head trauma, intracranial
bleeding, phaeochromocytoma, myocarditis, or
hypertrophic cardiomyopathy
Proposed by Bybee, et al. 2004. Annals of Internal Medicine. 141: 858-865.

 Emotional stress
 Death or severe illness or injury of family
member, friend, pet
 Receiving bad news – diagnosis of major illness,
family divorce, spouse leaving for war
 Severe argument
 Fear of public speaking
 Involvement of legal proceedings
 Financial loss – business / gambling
 Car accident
 Surprise party
 Moving to new house

 Non-cardiac surgery / procedure – e.g.
cholecystectomy / hysterectomy
 Severe illness – asthma / COPD, connective
tissue disorders, inflammatory bowel disease
 Illnesses that cause pain – fracture, renal colic,
pneumothorax, PE
 Recovery from general anaesthesia
 Cocaine abuse
 Opiate withdrawal
 Stress testing – dobutamine stress echo / MPS
 Thyrotoxicosis

 New England Journal of Medicine 2005;352:539-548

New England Journal of Medicine
2005;352:539-548

 Catecholamine excess
• Norepinephrine levels are very elevated in ~75% in some studies
• Plasma catecholamines significantly higher than in cases of MI
• May induce microvascular spasm or dysfunction myocardial
stunning or direct myocardial toxicity
• Limited endomyocardial biopsy data c/w histologic signs of
catecholamine toxicity
 Coronary artery spasm or microvascular spasm
 Myocarditis
 Post-menopausal downregulation of oestrogen
receptors
 Dense distribution of cardiac adrenoceptors in LV
apex of women > men

 Substernal chest pain (but not always)
 ECG abnormalities
• ST elevation (usually anterior leads)- 82%
• ST depression
• T wave inversion
• QT prolongation
• Abnormal Q waves
 Elevated cardiac biomarkers
 Dyspnoea
 Shock – similar haemodynamically to cardiogenic shock
 Syncope / feeling of “doom”

 Tachyarrhythmias, bradyarrhythmias
 Pulmonary oedema
 Cardiogenic shock
 Transient LV outflow tract obstruction
 Mitral valve dysfunction
 Acute thrombus formation and stroke
 Death

 Because presentation is similar to ACS, management is
usually similar in initial stages.
 LV ventriculogram and/or echocardiography can both be
used to visualize apical ballooning with a/dyskinesis of
apical ½ to ⅔ of the LV.
• Average LV EF range 20-49%
• Can have “atypical” ballooning of the middle or basal portions of
the LV (much less common)
• Wall motion abnormalities typically involve the distribution of more
than one coronary artery
 Ventriculography and echocardiography also allow
evaluation for LV outflow tract obstruction (~16%).
 Cardiac catheterization reveals lack of flow limiting
coronary lesions or evidence of plaque rupture.Colin Farquharson , Cardiologist , Grimsby UK

 Supportive, conservative therapy
• Hydrate, remove / reduce stress (if possible)
 Treat LV dysfunction with standard heart failure
regimen- including beta blocker, ACE inhibitor,
diuretics (if volume overloaded), aspirin
• Usually treated for ~6 months
 For pts who are hypotensive with shock, perform
echo to evaluate for LVOT obstruction.
• No LVOT obstruction inotropes, IABP if needed
• +LVOT obstruction NO inotropes (can worsen obstruction), use
beta blockers (+/- α-agonist phenylephrine), IABP if needed
• +/- fluid resuscitation (evaluate pulmonary status)

 0-8% in-hospital mortality, likely closer to 1-2% if
optimally treated
 Recovery of LV function, typically in 1-4 weeks
 Late sudden death (rare) and recurrent disease
(<10%) have been reported
Overall, good prognosis. If
patient survives the acute
phase, long-term prognosis
is excellent.

ABNORMAL LV
CONTRACTION
ON DAY 1 OF
CHEST PAIN
ADMISSION
RECOVERY OF
NORMAL LV
CONTRACTION 3
MONTHS AFTER
ADMISSION

New England Journal of Medicine 2005;352:539-548

 Takotsubo cardiomyopathy is a syndrome of transient
dysfunction of apical/midventricular left ventricle with
compensatory hyperkinesis of basal segment resulting in
apical ballooning.
 It is always triggered by significant emotional or physical
stress.
 It is much more common in post-menopausal women.
 Presentation is similar to MI (symptoms, ECG changes,
and biomarker elevations). Probably accounts for ~1-2%
of suspected ACS cases
 No significant coronary artery disease or evidence of
plaque rupture can be identified on coronary angio
 LV function usually recovers - typically within 4 weeks.

 Brenner, Z. R. and J. Powers. Takotsubo cardiomyopathy. 2008.
Heart & Lung. 37: 1-7.
 Bybee, K. A., et al. Systematic Review: Transient Left Ventricular
Apical Ballooning: A Syndrome That Mimics ST-Segment Elevation
Myocardial Infarction. 2004. Annals of Internal Medicine. 141: 858-
865.
 Celik, T., et al. Stress-induced (Takotsubo) cardiomyopathy: A
transient disorder. 2007. International Journal of Cardiology. (epub)
 Prasad, A., et al. Apical ballooning syndrome (Tako-Tsubo or stress
cardiomyopathy): A mimic of acute myocardial infarction. 2008.
American Heart Journal. 155: 408-17.
 Reeder, Guy S. Stress-induced (takotsubo) cardiomyopathy. 2007.
www.uptodate.com and references herein
 Wittstein, I. S., et al. Neurohumoral Features of Myocardial Stunning
Due to Sudden Emotional Stress. 2005. New England Journal of
Medicine. 352(6): 539-48.

Takotsubo Cardiomyopathy Case

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