CRVASA-171; No. of Pages 8

Case report

Uncommon type of tako-tsubo cardiomyopathy – Case reportand current view

A. Qadeer Negahban a,*, Jan Máchal b, Roman Panovský a, Věra Feitová c

a Interní kardio-angiologická klinika, Fakultní nemocnice u svaté Anny v Brně, MU, ICRC, Czech RepublicbÚstav patologické fyziologie, Lékařská fakulta, MU, Czech RepubliccKlinika zobrazovacích metod, Fakultní nemocnice u svaté Anny v Brně, MU, ICRC, Czech Republic

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a r t i c l e i n f o

Article history:

Received 27 April 2013

Received in revised form

17 September 2013

Accepted 20 September 2013

Keywords:

Tako-tsubo cardiomyopathy

Myocardial stunning

Coronary angiography

Late gadolinium enhancement

a b s t r a c t

Tako-tsubo cardiomyopathy is a heart disease that imitates acute myocardial infarction.

Classical findings include apical and mid segment hypokinesia. However, it may have

different appearance than was originally described.

In our case report we describe a case of woman with tako-tsubo cardiomyopathy (TTC),

who was admitted to hospital after a stressful event because of chest pain, with normal

coronary angiogram and with mild elevation of Troponin-I level.

Electrocardiogram corresponded with non-Q myocardial infarction of inferior wall.

Following left ventriculography, echocardiography and magnetic resonance, impaired

contractility of the basal part of inferior wall was noticed, together with good global ejection

fraction. Full recovery was attained in five weeks after the onset.

This impairment of left ventricle is not typical for TTC. In our patient, the basal part of left

ventricle was affected, and not the apex as it is usually seen in TTC. This finding corresponds

to rare ‘‘inverted’’ form of TTC. Another atypical feature is segmental involvement that,

moreover, covered the inferior wall. This morphological pattern, according to our best

knowledge, has not yet been described in literature.

Pathophysiology, epidemiology and clinical significance are shortly reviewed in the paper.

# 2013 The Czech Society of Cardiology. Published by Elsevier Urban & Partner Sp. z o.o.

All rights reserved.

Available online at www.sciencedirect.com

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journal homepage: http://www.elsevier.com/locate/crvasa

Introduction

Tako-tsubo cardiomyopathy (TTC) is relatively recentlydescribed disease, which imitates clinical, laboratory andelectrocardiographical (ECG) findings in acute myocardial

* Correspondence to: Jugoslavska 18, 61300 Brno, Czech Republic. TeE-mail address: kadir@seznam.cz (A.Q. Negahban).

Please cite this article in press as: A.Q. Negahban et al., Uncommon typet Vasa (2014), http://dx.doi.org/10.1016/j.crvasa.2013.09.004

http://dx.doi.org/10.1016/j.crvasa.2013.09.0040010-8650/# 2013 The Czech Society of Cardiology. Published by Else

infarction (AMI). The disease was first described by Japaneseauthors in 1991 [1,2]. The term ‘‘tako-tsubo’’ corresponds tothe typical shape of left ventricle, which resembles totraditional Japanese octopus trap (‘‘tako’’=octopus, ‘‘tsubo’’=pot) [2]. Typically, it is characterized by ball-shaped ballooningof anterior wall and the apex. Low contractility in this area is

l.: +420 723715164.

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accompanied by hyperkinesia of the basal part of left ventricle[3–5]. In approximately one quarter of the patients, there isalso similar impairment of the right ventricle [6,7].

An emotional or physical stress is often initiating factor ofTTC [8], however, in many cases, immediate cause is notapparent. Most of the patients are women in post-menopausalage [3,8,9]. Potentially life-threatening complications includecardiogenic shock, arrhythmias or pulmonary oedema [4], in-hospital mortality is about 2% [10]. Long-term prognosis ismostly favourable with complete resolution [3,11].

The diagnostic criteria according to Mayo Clinic are asfollows:

1. New abnormalities on ECG (ST-segment elevation and/or T-wave inversion) and/or cardiac troponin elevation.

2. Transient (reversible) akinesia or dyskinesia of the leftventricular mid segments, eventually also with involve-ment of the apex, independently of vascular distribution.

3. Absence of obstructive coronary artery disease at coronaryangiography.

4. Absence of myocarditis or pheochromocytoma.

Original criteria also included an absence of head injuryor intracranial haemorrhage. However, the wall motionabnormalities in these cases, which are also known asneurogenic stunned myocardium (NSM), likely share thesame pathogenetic mechanisms with the classical form ofTTC [8,12].

The condition of no coronary atherosclerosis has alsobeen put into question. The etiopathogenic mechanismsleading to TTC can be basically present regardless thepresence or absence of coronary atherosclerosis [13]. Fromthe diagnostic point of view, this can be compared forexample to coincidence of ischaemic heart disease anddilated cardiomyopathy: one disease, in principle, does notexclude the other.

The terms ‘‘tako-tsubo cardiomyopathy’’, as well asalternative name ‘‘apical ballooning syndrome’’ are being stillin use, in spite of many patients having abnormalities ofdifferent parts of heart wall than the apex [11,14]. Othersynonymous terms are ‘‘stress cardiomyopathy’’ or ‘‘broken-heart syndrome’’. The disease is responsible for 1–2% of casesdiagnosed as acute coronary syndrome [15], it is thusnecessary to bear it in mind in differential diagnostics ofacute chest pain with negative findings on coronary arterio-gram and impaired ejection fraction.

Case report

We present a case of 56 year old female with positive familyhistory of ischaemic heart disease, post hysterectomy andadnexectomy due to cervical carcinoma at 34 years; she hadmigraine with occasional attacks, but otherwise no disease.She was working as a secretary in public services, smoking 5–6cigarettes daily and drinking 2–3 cups of coffee per day, shedenied drinking alcohol.

The patient presented to the Emergency with chest painand hypertension after a car accident when she was annoyeddue to indecency of the second participant in this accident.

Please cite this article in press as: A.Q. Negahban et al., Uncommon typet Vasa (2014), http://dx.doi.org/10.1016/j.crvasa.2013.09.004

Paramedics were called by her husband, who measured theblood pressure of 180/120 mmHg, regular heart rate of 80 beatper minute, oxygen saturation of 97%. She was given captopril12.5 mg sublingually and diazepam 5 mg intravenously andshe was immediately transferred to the nearest hospital forfurther management.

Laboratory tests on admission showed slight elevation ofTroponin-I level of 0.48 micrograms per litre (mg/L) and reachedthe maximum of 0.72 mg/L within 24 h, while normal values donot exceed 0.014 mg/L. Neither creatine kinase (CK), nor itsisoenzyme CK MB was elevated, as there were no otherlaboratory abnormalities noticed on admission.

Transthoracic echocardiography (TTE) was performed onadmission (Fig. 1a and b) with the finding of posterobasalhypokinesis of the inferior wall and slightly decreased leftventricular systolic function with left ventricular ejectionfraction (LVEF) of 48%. Electrocardiogram on admissionshowed Q wave in lead III, aVF with negative T wave in leadI, III, aVF and in lead V5–V6 (Fig. 2a and b) with normal AVconduction. The patient was given clopidogrel, acetyl salicylicacid (ASA) and low molecular weight heparin and she wastransferred to the cath lab of St Anne's University Hospitalin Brno.

Coronary angiography was performed and no stenosis orother impairment of coronary arteries was detected (Fig. 3aand b). On ventriculography, posterobasal hypokinesis ofinferior wall was demonstrated (Fig. 3c and d), decreased leftventricular systolic function with LVEF of 45%. A suspicion foran atypical pattern of tako-tsubo cardiomyopathy wasexpressed. In differential diagnosis, thrombembolic AMI orAMI following coronary vasospasm could have been hypothe-sized.

Two days later the patient was discharged with followingmedication: metoprolol succinas 25 mg once daily and ASA100 mg once daily. ECG and TTE on discharge showed the samefinding as was seen on admission. Patient was followed up fornext 2 months.

Second TTE (Fig. 1c and d) was performed 2 weeks afterdischarge and it showed only slight posterobasal hypokinesisof inferior wall. In the same time, a cardiac magneticresonance imaging (Fig. 4a–d) was performed in order to getmore information about the myocardial muscle. The exami-nation confirmed the posterobasal hypokinesis of inferiorwall. No scar in the myocardium, as a sign of AMI, was found inthe late gadolinium enhancement.

Unfortunately the patient has not been agreeable toundergo the second MRI scan in order to assess if there areany new changes in the myocardium.

We assumed that if the late gadolinium enhancement hadnot shown any scar within the myocardium it is fairlyconvincing that there was no myocardial infarction.

The third TTE (Fig. 1e and f) was performed by the sameechocardiographer 5 weeks after discharge.

Normal segmental and global left ventricular function wasfound. ECG curve showed no Q wave or T wave inversion ininferior leads (Fig. 2c).

The findings in cardiac MRI, as well as the completeresolution of ventricular wall motility and rearrangement ofthe ECG curve, were thus consistent with the first proposeddiagnosis, i.e. TTC.

e of tako-tsubo cardiomyopathy – Case report and current view, Cor

Fig. 1 – Echo figures: (a) Echocardiography on admission, parasternal short axis (PSAX) at the level of papillary muscles, end-diastole – area of hypokinesis (arrow); (b) Echocardiography on admission, PSAX at the level of papillary muscles, end-systole– area of hypokinesis (arrow); (c) Echocardiography, 2 weeks after discharge, PSAX at the level of papillary muscles, End-diastole – area of hypokinesis (arrow); (d) Echocardiography, 2 weeks after discharge, PSAX at the level of papillary muscles,end-systole – area of hypokinesis (arrow); (e) Echocardiography, 5 weeks after discharge, PSAX at the level of papillarymuscles, end-systole – no hypokinesis – complete recovery; (f) Echocardiography, 5 weeks after discharge, PSAX at the levelof papillary muscles, end-diastole – no hypokinesis – complete recovery.

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Discussion

This case study is interesting notably for an atypical localiza-tion of myocardial hypokinesis, where the basal part of leftventricle was involved. The form of TTC with basal involve-ment, usually together with apical hyperkinesia, is known as‘‘inverted tako-tsubo’’ and is only rarely described in theliterature [16]. In recent multi-centre study, published inJournal of the American Medical Association and comprising239 patients from 7 centres in Europe and North America, thisform was present only in 2 cases. Typical form with apicalinvolvement was present in 197 patients (82%), mid segmentinvolvement in 40 patients (17%) and right ventricle involve-ment in 81 patients (34%) [14]. In our case, there was ahypokinesia of the basal part of inferior wall. This feature isalso atypical, as in segmental involvement, the hypokinesia ofanterior wall is usually present [16]. Absence of apicalhyperkinesia could be explained by a delay between the onsetof chest pain and ventriculography, which was almost 48 h.

Appearance and disappearance of Q waves is common inTTC. In most cases, it involves chest leads V2–V4 and is causedby electrical hyperactivity of basal left ventricle compared tothe apex. In our case, when posterobasal segments wereaffected, the Q waves in III and aVF corresponded with relative

Please cite this article in press as: A.Q. Negahban et al., Uncommon typet Vasa (2014), http://dx.doi.org/10.1016/j.crvasa.2013.09.004

apical hyperactivity. Rapid disappearance of Q waves (in days),observed in our case, is unique for TTC and probablycorresponds with the normalization of electric stunning [17].

The cases of TTC were described e.g. during anaesthesia[18], in systemic lupus erythematodes [19], or during sepsiscaused by Pseudomonas aeruginosa [20]. The same picture canbe seen in some cases of NSM after subarachnoidealhaemorrhage, as well as in other diseases of central nervoussystem. This fact points to very fuzzy borderline and largeintersection between both diseases [12].

Exact pathophysiology of TTC is still a subject of discus-sions. First studies were proposing multivessel coronaryvasospasm as the most important mechanism. This, however,has not been confirmed by subsequent research [9]. Further-more, magnetic resonance findings do not show the presenceof necrosis, despite of elevated concentrations of cardiactroponin [21]. These results are in good accordance with ourcase, where the tissue saturation in late gadolinium enhance-ment was not apparent.

In present research, most of the authors favour catechol-amine overload as the key contributor to TTC development[22]. Lyon et al. [23] suggested that changes in post-receptorcascade of b2-adrenergic receptors should play the principalrole. Under normal conditions, after adrenaline binds theb2-receptor, adenylatecyklase is activated via Gs proteins. This

e of tako-tsubo cardiomyopathy – Case report and current view, Cor

Fig. 2 – ECG figures: (a) ECG on admission, extremity leads Q wave in III, aVF (arrows); (b) ECG on admission, chest leadsnegative T wave in V5–V6 (arrows); (c) ECG 5 weeks after discharge, all leads, no Q wave or T wave inversion apparent.

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results into production of cAMP, which mediates positivelyinotropic effect of catecholamins. On the other hand, in high,‘‘supraphysiological’’ concentrations of adrenaline, the nega-tively inotropic effect via Gi proteins prevails [24]. The reasonof this ‘‘switch’’ is probably the phosphorylation of b2-receptor

Please cite this article in press as: A.Q. Negahban et al., Uncommon typet Vasa (2014), http://dx.doi.org/10.1016/j.crvasa.2013.09.004

by protein kinase A [25]. This process can primarily serve asprotection against pro-apoptotic effects of catecholaminesmediated by b1-receptors [26]. b1-mediated apoptosis ofcardiomyocytes could be responsible for elevated troponinlevels in the blood.

e of tako-tsubo cardiomyopathy – Case report and current view, Cor

Fig. 3 – Coronarography figures: (a) Selective left coronary angiogram, LAD and RC without stenosis; (b) Selective rightcoronary angiogram, ACD without stenosis; (c) Retrograde left ventriculography, diastole; (d) Retrograde leftventriculography, systole, posterobasal hypokinesis of the inferior wall.

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This mechanism may also be responsible for characteristiclocalization of myocardial contractility involvement withapical ballooning. In basal area, there are more sympatheticnerve endings compared to the apex [27]. The same distribu-tion is present also in dog hearts, where higher concentrationof b-receptors in the apex compared to the base has beenfound [28]. During adrenaline overload, this could lead tohigher response of apical parts of the heart. On the other hand,recently published study comparing b-receptor density inpatients after AMI and healthy subjects pointed to their lowerconcentration in the apex [29]. In all cases, none of thementioned studies distinguished between b1 and b2 receptors.

Another possible mechanism could be microvascularvasoconstriction. This effect is mediated by both a1 and a2-adrenergic receptors [30]. In TTC patients, abnormal Throm-bolysis In Myocardial Infarction (TIMI) frame count was found,indicating impaired microcirculatory flow [31]. There is also anevidence of impaired myocardial perfusion in contrastechocardiography [32] and reversible impairment of coronary

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flow reserve in positron emission tomography [33]. Indirectsupport of this mechanism comes from an experiment withanimal model of TTC, where the administration of both b-, anda-blockers was necessary to prevent pathological changes [34].It is thus probable that in TTC development, both mechanismsare relevant.

A typical feature of TTC is unequal distribution ofincidence between both sexes. About 90% of patients withTTC are women, and postmenopausal women are at highestrisk [3,8,9]. This fact continues to be a subject of investigation.Most likely, variable catecholamine concentration duringwomen's life takes place here. Young women have loweradrenaline and noradrenaline plasmatic concentration com-pared to men, but its increase with age is higher [35]. Lowerlevels of oestrogens after the menopause that are linked tohigher sympathetic activity, may play the role [36]. However,in other study, the increase of catecholamine levels with agewas independent on menopausal status [35]. Moreover,oestrogens protect the myocardium against high doses of

e of tako-tsubo cardiomyopathy – Case report and current view, Cor

Fig. 4 – MRI figures: (a) Cardiac magnetic resonance image (CMRI), T2 SSFP (TrueFISP), short axis view (SAX), area ofhypokinesis (arrow); (b) CMRI, T1 IR (inversion recovery) sequence after injection of contrast medium (gadolinium), short axisview (SAX), no late gadolinium enhancement finding; (c) CMRI, T2 SSFP (TrueFISP), three chamber view, end-diastole, area ofhypokinesis (arrow); (d) CMRI, T2 SSFP (TrueFISP), three chamber view, end-systole, area of hypokinesis (arrow); (e) CMRI, T1IR (inversion recovery) sequence after injection of contrast medium (gadolinium), three chamber view, no late gadoliniumenhancement finding.

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catecholamins by various mechanisms, and lack of oestro-gens in postmenopausal age may lead into its hypersensitivi-ty for adrenergic stimulation [37]. It can be expected, thatsimilar mechanism might be employed also in other forms ofcatecholamine-induced stunned myocardium, as in patientswith subarachnoideal haemorrhage, where lower plasmaticlevel of oestrogens was associated with impaired myocardialcontractility [38].

Conclusion

In our case report we describe a case of unusual, inverted formof tako-tsubo cardiomyopathy with the impairment of basalpart of inferior wall. It is a rare form of often overlookeddisease, that may imitate clinical, electrocardiographicallyand laboratory findings in acute myocardial infarction.

Conflict of interest

The authors state no conflict of interest.

Please cite this article in press as: A.Q. Negahban et al., Uncommon typet Vasa (2014), http://dx.doi.org/10.1016/j.crvasa.2013.09.004

Funding body

The study was funded by Regional Development Fund – ProjectFNUSA–ICRC (No. CZ.1.05/414 1.1.00/02.0123).

Ethical statement

The research was done according to ethical standards.

Informed consent

Informed consent was obtained from the patient.

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