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European Journal of Echocardiography Advance Access published online on January 5, 2007
European Journal of Echocardiography, doi:10.1016/j.euje.2006.11.011
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Subaortic dynamic obstruction: a contributing factor to haemodynamic instability in tako-tsubo syndrome?

Adrian Ionescu*

Morriston Cardiac Centre, Swansea SA6 6NL, UK

Received 21 September 2006; accepted after revision 26 November 2006.

* Corresponding author. Tel: +44 01792703195; fax: +44 01792703522. E-mail address: adrian.ionescu{at}swansea-tr.wales.nhs.uk


   Abstract
Top
 Abstract
Introduction
 Presentation of case
 Discussion
 References
 
We present a case of transient apical ballooning with haemodynamic instability in a female patient with normal coronaries and a history of poorly controlled systemic arterial hypertension. There was dynamic obstruction of the outflow tract and moderate secondary mitral regurgitation at presentation. These were due to systolic anterior motion of the mitral valve, which normalised gradually with the recovery of left ventricular function, and to a ‘sigmoid’ septum. Mid-cavity obstruction is potentially an important contributory factor to the haemodynamic instability sometimes encountered in this syndrome.

Keywords: Apical ballooning; Sigmoid septum; Dynamic mitral regurgitation


   Introduction
Top
 Abstract
 Introduction
Presentation of case
 Discussion
 References
 
The pathophysiology of tako-tsubo syndrome (stress cardiomyopathy, apical left ventricular ballooning) is not fully characterised; recently, dynamic subaortic obstruction was reported.1 We describe a case of tako-tsubo where transient subaortic obstruction and mitral regurgitation led to haemodynamic instability. Abnormalities resolved over 3 months.


   Presentation of case
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 Abstract
 Introduction
 Presentation of case
Discussion
 References
 
A 65-year-old woman with a history of systemic arterial hypertension presented with epigastric discomfort and dizziness. Heart rate was 78 bpm in sinus and blood pressure was 60/40 mmHg. ECG showed non-specific ST/T wave changes in the anterior leads.

Four hours later a loud pansystolic murmur was reported. The patient was transferred to our tertiary centre with a diagnosis of cardiogenic shock and possible ischaemic VSD.

On arrival there was a loud systolic murmur over the precordium. There were negative T waves in V1–V6 on ECG and interstitial oedema and upper lobe venous diversion on the chest X-ray.

The echocardiogram obtained on arrival showed akinesis and thinning of the anterior ventricular septum, of the apex and of the anterior wall of the left ventricle, with normal contractions elsewhere. There was a septal bulge (‘sigmoid septum’ – Figure 1) and a false tendon in the outflow tract of the left ventricle. There was pansystolic anterior motion (SAM) of the mitral valve, with subaortic obstruction and a dynamic gradient > 60 mmHg (Figure 2), and with moderate, eccentric mitral regurgitation. With i.v. fluids, beta-blockers and diuretics the haemodynamics improved; second troponin came back elevated at 0.97 µg/ml (n < 0.03).


Figure 1
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  		Figure 1 Initial parasternal long axis systolic frame. The sigmoid septum (arrowheads) and the systolic anterior motion of the mitral valve (arrow) are visible. The apex is akinetic and bulges outwardly. LA, left atrium; LV, left ventricle.

 


Figure 2
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  		Figure 2 Subaortic systolic gradient at presentation.

 
A repeat echo 2 days later showed marked improvement of subaortic obstruction and the disappearance of mitral regurgitation, but unchanged anterior thinning and akinesis. Coronary angiography showed normal coronaries. Vasculitic, phaeochromocytoma and coagulation screens were normal. The discharge diagnosis was anterior infarct with angiographically normal coronaries.

Three months later LV function was normal (Figure 3), without SAM or MR; a retrospective diagnosis of tako-tsubo cardiomyopathy was made.


Figure 3
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  		Figure 3 Initial (left) and follow-up systolic frames in the apical 2-chamber view, demonstrating the resolution of the apical akinesis (arrowheads).

 

   Discussion
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 Abstract
 Introduction
 Presentation of case
 Discussion
References
 
The Mayo criteria for tako-tsubo are as follows: transient akinesis of the apical and mid-ventricular septum, no obstructive coronary artery disease, new ECG changes, and no coexisting systemic pathology (phaeochromocytoma, head trauma).2 Troponin, but not CK release, is almost universal.3 Females are predominantly affected and emotional or physical stress at onset is common. Cardiogenic shock requiring intra-aortic balloon counterpulsation is reported in 6–46% of cases.2 Plasma catecholamine levels can be markedly elevated.4

Merli et al.1 reported that all their patients had mid-septal thickening contributing to the development of subaortic obstruction. Low-dose dobutamine stress echo showed regional stunning. Intraventricular gradients are not universally present though,5 suggesting a complex, non-homogeneous pathophysiology. Widespread subendocardial ischaemia (from excess catecholamines and high intracavitary pressures, potentially exacerbated by relative or absolute hypovolaemia) may lead to loss of apical ventricular function, perhaps with a contribution from microvascular dysfunction.6 Our patient had a septal bulge (‘sigmoid septum’)7 and also a false tendon in the LVOT8 contributing to outflow obstruction. Systematic research into the anatomic and pathophysiological substrate of this condition appears warranted.


   References
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 Abstract
 Introduction
 Presentation of case
 Discussion
 References
 

  1. Merli E, Sutcliffe S, Gori M, Sutherland GR. Tako-tsubo cardiomyopathy: new insights into the possible role of underlying pathophysiology. Eur J Echocardiogr (2006) 7:53–61.[Abstract/Free Full Text]
  2. Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review transient left ventricular apical ballooning: a syndrome that mimics ST-elevation myocardial infarction. Ann Intern Med (2004) 141:858–65.[Abstract/Free Full Text]
  3. Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white human patients. Heart (2003) 89:1027–31.[Abstract/Free Full Text]
  4. Wittstein IS, Thiemann DR, Lima JAC, Baughman KL, Schulman SP, Gerstenblith G, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med (2005) 352:539–48.[Abstract/Free Full Text]
  5. Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol (2003) 41:737–42.[Abstract/Free Full Text]
  6. Malafronte C, Farina A, Tempesta A, Lobiati E, Galbiati R, Cantu E, et al. Tako-tsubo: a transitory impairment of microcirculation? A case report. Ital Heart J (2005) 6:933–8.[Medline]
  7. Shapiro LM, Howat AP, Crean PA, Westgate CJ. An echocardiographic study of localized subaortic hypertrophy. Eur Heart J (1986) 7:127–32.[Abstract/Free Full Text]
  8. Tamborini G, Pepi M, Celeste F, Muratori M, Susini F, Maltagliati A, et al. Incidence and characteristics of left ventricular false tendons and trabeculations in the normal and pathologic heart by second harmonic echocardiography. J Am Soc Echocardiogr (2004) 17:367–74.[CrossRef][Web of Science][Medline]

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