527836 research-article2014

ACC0010.1177/2048872614527836European Heart Journal: Acute Cardiovascular CareGhadri et al.

EUROPEAN SOCIETY OF CARDIOLOGY ®

Clinical practice

First case of atypical takotsubo cardiomyopathy in a bilateral lungtransplanted patient due to acute respiratory failure

European Heart Journal: Acute Cardiovascular Care 2015, Vol. 4(5) 482­–485 © The European Society of Cardiology 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/2048872614527836 acc.sagepub.com

Jelena R Ghadri1, Roxana D Bataisou1, Johanna Diekmann1, Thomas F Lüscher1,2 and Christian Templin1

Abstract Takotsubo cardiomyopathy which is characterised by a transient left ventricular wall motion abnormality was first described in 1990. The disease is still not well known, and as such it is suggested that an emotional trigger is mandatory in this disease. We present the case of a 51-year old female patient seven years after bilateral lung transplantation, who developed acute respiratory distress syndrome and subsequently suffered from atypical takotsubo cardiomyopathy with transient severe reduction of ejection fraction and haemodynamic instability needing acute intensive care treatment. Acute respiratory failure has emerged as an important physical trigger factor in takotsubo cardiomyopathy. Little is known about the association of hypoxia and takotsubo cardiomyopathy which can elicit a life-threatening condition requiring acute intensive care. Therefore, experimental studies are needed to investigate the role of hypoxia in takotsubo cardiomyopathy. Keywords Takotsubo cardiomyopathy, heart failure, hypoxia, acute cardiac care Received: 30 September 2013; accepted: 22 February 2014

Introduction Takotsubo cardiomyopathy was first described in 1990 in the Japanese population and it has been shown that takotsubo cardiomyopathy is often associated with emotional triggers such as the death of a beloved one or extreme anger or frustration.1 Patients with takotsubo cardiomyopathy show a transient reversible wall motion pattern while, on coronary angiography, obstructive coronary artery disease is often not found. However, recently it has been shown that co-existence of coronary artery disease does not exclude the presence of takotsubo cardiomyopathy.2 During the last few years, more and more physical triggers have been reported to provoke takotsubo cardiomyopathy, however little is known about the association of acute respiratory failure and takotsubo cardiomyopathy. Furthermore, the acute stage of takotsubo cardiomyopathy can be life-threatening since arrhythmia, ventricular

rupture or even death have been reported – therefore there is a strong need for intensive care during the acute phase of this disease. Here, we report the case of a patient with respiratory failure who developed a midventricular takotsubo cardiomyopathy. As far as we know, this is the first case report on

1Department

of Cardiology, University Hospital Zurich, Switzerland for Integrative Human Physiology (ZIHP), University of Zurich, Switzerland

2Center

Corresponding author: Christian Templin, MD, PhD University Heart Center, Department of Cardiology, University Hospital Zurich, Ramistrasse 100, D-Rämi CH8091 Zurich, Switzerland. Email: [email protected]

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Figure 1.  (a) ECG on admission shows diffuse T-wave inversion in leads I, II, aVL, aVF, and V2-V6. (b) Coronary angiography shows patency of the left anterior descending artery, circumflex artery as well the right coronary artery. Left ventricular (LV) angiogram during diastole and systole (demonstrates akinesis of the midventricular myocardium with apical and basal sparing. This definies the pattern of a midventricular taktosubo type. Cardiac biomarkers on admission are modestly elevated. (c) Echocardiography on apical four-chamber view in systole and diastole one day after the acute takotsubo event revealed improvement of LV ejection fraction (38%) still with hypokinesis of the midventricular segments; one day after the acute event troponin decreased but proBNP increased to a maximum of 6130 ng/l. CK: creatine kinase; h-s Trop: high-sensitive troponin.

a patient with atypical takotsubo cardiomyopathy who has undergone bilateral lung transplantation.

Case report A 51-year-old female patient was referred to our hospital after she had an acute onset of respiratory distress requiring ventilator support. Seven years before she underwent bilateral lung transplantation due to systemic sclerosis with severe pulmonary arterial hypertension. On hospital admission she became haemodynamically unstable and required noradrenaline. Twelve-lead electrocardiogram (ECG) demonstrated diffuse T-wave inversion in leads I, II, aVL, aVF and V2–V6 (Figure 1(a)). On physical

examination she presented with signs of congestive heart failure which included audible rales bilaterally, elevated jugular venous distention and mild oedema in the lower extremities. Laboratory values showed an elevated highsensitive troponin (0.592 µg/l) but a normal creatine kinase (CK) (98 U/l) (Figure 1(b)). Due to a suspicion of acute myocardial infarction, an emergency coronary angiography was performed. Coronary arteries were normal revealing “Thrombolysis In Myocardial Infarction” (TIMI) III flow (Figure 1(b)), however, a left ventricular (LV) angiogram showed akinesis of the LV mid segments which extended beyond a single coronary vascular territory and a hyperdynamic contraction of the LV base and apex allusive of an atypical takotsubo type

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Figure 2.  ECG five days after admission shows a reduction of the diffuse T-wave inversions in comparison to the admission ECG.

(Figure 1(c)). Global LV function was markedly reduced (ejection fraction, 30%) and left ventricular end diastolic pressure was elevated (23 mm Hg). The patient was transferred to the intensive care unit for further monitoring and treatment. Only 17 h later the patient was successfully weaned and extubated. Echocardiography study on the next day revealed an improvement of LV ejection fraction (38%) still with hypokinesis of the midventricular segments. Total CK values were normal during complete hospitalisation; however probrain-natriuretic-peptide (BNP) was raised to a maximal value of 6130 ng/l on the second day after admission (Figure 1(c)). On the third day of hospitalisation the patient developed a prolonged QTc interval of 508 ms and demonstrated negative T-waves in the precordial leads and after five days T-wave inversions slightly improved with normalisation of QTc time (Figure 2). No arrhythmia occurred. The patient was treated with an angiotensin converting enzyme inhibitor, diuretic and later on with a beta-blocker, as the latter is suggested to reduce activity in the sympathetic nervous system and thereby potentially prevent a takotsubo cardiomyopathy. The patient did physically well, had recovered fast and was discharged. Eight weeks later at follow-up study, the ECG had returned to completely normal without any T-wave inversion pattern (Figure 3(a)) and echocardiography evaluation demonstrated a complete resolution of LV ejection fraction (63%) with only discrete hypokinesis in the midventricular inferior and inferoseptal walls (Figure 3(b)).

Discussion Usually emotional triggers are a hallmark of takotsubo cardiomyopathy. During the last decade more physical stressors have been identified to be associated with takotsubo cardiomyopathy such as acute respiratory distress syndrome which has emerged as a physical stressor and patients with pulmonary disease are at increased risk of

Figure 3.  (a) Complete normalisation of ECG with upright of T-wave inversion. (b) Echocardiography on follow-up study on apical four-chamber view in systole and diastole and shows normalisation of the left ventricular ejection fraction and almost complete recovery of the wall motion abnormality.

hypoxia. However, the exact role of hypoxia in takotsubo cardiomyopathy has not been established nor systematically investigated. We suggest that severe hypoxia which is a life-threatening condition, might lead to an activated sympathetic drive through a chemoreflex response. Peripheral chemoreceptors are located in the carotid bodies and show a very sensitive response to hypoxia while the central chemoreceptors are responding to hypercapnia. Both systems may lead to an enhanced sympathetic drive. In addition, experimental studies have shown that hypercapnia, for instance, appeared as a strong stimulus for noradrenalin synthesis3 which is known to be increased in patients with takotsubo cardiomyopathy during the acute stage,4 as is hypoxia.5 In patients with acute respiratory failure associated with T-wave inversion and mild troponin elevation there is a strong need for suspicion of takotsubo cardiomyopathy which is a life-threatening condition. Furthermore, experimental studies are needed to investigate the potential role of hypoxia, hypercapnia and the chemoreflex response in takotsubo cardiomyopathy.

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Ghadri et al. Conflict of interest None declared.

Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

References 1. Bossone E, Savarese G, Ferrara F, et al. Takotsubo cardiomyopathy: Overview. Heart Fail Clin 2013; 9: 249– 266.

2. Parodi G, Citro R, Bellandi B, et al. Tako-tsubo cardiomyopathy and coronary artery disease: A possible association. Coron Artery Dis 2013; 24: 527–533. 3. Leitner LM. Dopamine metabolism in the rabbit carotid body in vitro: effect of hypoxia and hypercapnia. Leitner LM. Adv Exp Med Biol. 1993;337:183–90. 4. Wittstein IS, Thiemann DR, Lima JAC, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005; 352: 539–548. 5. Noll G, Wenzel RR and Luscher TF. Increased activation of sympathetic nervous system and endothelin by mental stress in normotensive offspring of hypertensive patients response. Circulation 1997; 93: 866–869.

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First case of atypical takotsubo cardiomyopathy in a bilateral lung-transplanted patient due to acute respiratory failure.

Takotsubo cardiomyopathy which is characterised by a transient left ventricular wall motion abnormality was first described in 1990. The disease is st...
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