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| CASE REPORT |
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| Year : 2019 | Volume
: 3
| Issue : 2 | Page : 70-72 |
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Emotional stress-induced takotsubo cardiomyopathy, acute heart failure, and atrial fibrillation in the same patient
Branislava Ivanovic1, Marijana Tadic2
1 Clinical Centre of Serbia, Clinic of Cardiology, Belgrade, Serbia
2 Department of Internal Medicine and Cardiology, Charité – Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany
| Date of Submission | 25-Aug-2019 |
| Date of Acceptance | 25-Sep-2019 |
| Date of Web Publication | 25-Nov-2019 |
Correspondence Address:
Prof. Marijana Tadic
Department of Internal Medicine and Cardiology, Charité – Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburgerplatz 1, Berlin 13353
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/hm.hm_41_19
Takotsubo cardiomyopathy is characterized by transient systolic dysfunction of apical and central parts of the left ventricle in the absence of obstructive coronary artery disease. Usually, it is triggered by intense emotional or physical stress. The prognosis tends to be good. Rare complications include heart failure, cardiogenic shock, left ventricular free wall rupture, and cardiac arrhythmia. We present a patient with takotsubo cardiomyopathy complicated by acute heart failure and atrial fibrillation. The symptoms appeared due to emotional stress. This case highlights acute emotional stress as a potent trigger for transient myocardial dysfunction with acute heart failure and rhythm disturbance.
Keywords: Atrial fibrillation, emotional stress, takotsubo cardiomyopathy
How to cite this article:
Ivanovic B, Tadic M. Emotional stress-induced takotsubo cardiomyopathy, acute heart failure, and atrial fibrillation in the same patient. Heart Mind 2019;3:70-2 |
| Introduction | |  |
Takotsubo cardiomyopathy is also called apical ballooning syndrome or stress-induced cardiomyopathy. It is characterized by transient systolic dysfunction of apical and central parts of the left ventricle in the absence of obstructive coronary artery disease.[1],[2],[3] The occurrence of chest pain is followed by different electrocardiogram (ECG) changes and a slightly increased level of cardiac enzymes. Sometimes, in the acute phase, some complications such as heart failure, cardiogenic shock, myocardial rupture, and cardiac arrhythmias may occur.
We present a female patient with takotsubo cardiomyopathy complicated by acute heart failure and in further course with the occurrence of atrial fibrillation.
| Case Report | | |
A 71-year-old Caucasian female was hospitalized for prolonged chest pain and shortness of breath. Symptoms appeared due to the stress caused by the death of a close family member. She had arterial hypertension and hyperlipidemia as risk factors in the development of cardiovascular disease.
On admission, the patient was with orthopnea, and the number of respiration was 24/min. There were basal bilateral crackles on chest examination. The examination also revealed gallop heart rhythm and systolic murmur on the apex, heart rate was 80 beats/min, and blood pressure was 190/90 mmHg. The ECG registered sinus rhythm with negative T-wave in D1 and aVL and minimal ST elevation in V5 and V6.
Troponin level was 2.97 (reference value is <0.5 μg/l). Echocardiography showed left ventricular dysfunction (ejection fraction 40%) with septo-apical akinesis, mid-anterolateral hypokinesis, and apical ballooning. Mitral annulus was sclerotic and moderate mitral regurgitation was detected in the enlarged left atrium.
After receiving an aspirin and clopidogrel, the patient was sent to cardiac catheterization that revealed normal coronary angiogram, but left ventriculography showed that apical and anterolateral segments were akinetic [Figure 1].
Twelve hours after admission, the patient complained about palpitations. Auscultation revealed irregular heart rhythm, whereas ECG confirmed atrial fibrillation. Successful pharmacological conversion in sinus rhythm was done with parenteral amiodarone.
Symptoms and signs of heart failure resolved after the diuretic therapy, angiotensin-converting enzyme inhibitors, and beta-blockers. On the 7th day of admission into the hospital, echocardiography showed a full recovery of left ventricular function.
| Discussion | | |
The diagnosis of takotsubo cardiomyopathy in our patient was based on the concomitant chest pain, ECG changes, increase of cardiac enzymes, transient dysfunction of medial and apical segments of the left ventricle, and normal coronary angiogram.
The pathophysiology of takotsubo cardiomyopathy is not clear, but it is certainly multifactorial.[4] The fact that emotional or physical stress is the precipitating factor in most patients with this cardiomyopathy led to the assumption that sympathetic hyperactivity had its role in the development of this disease. Wittstein et al. published their findings that the level of catecholamines in patients with Takotsubo cardiomyopathy was two- or threefold higher than in the patients with myocardial infarction complicated with left ventricular dysfunction.[3]
Direct toxic effects of catecholamines[2],[3],[4] are stated as a possible mechanism of takotsubo cardiomyopathy. These effects are achieved by the direct influence of free radicals and their increasing. Both mechanisms lead to the cell calcium overload. The histological contraction band necrosis which is seen in these patients could be used as the evidence for the hypothesis of a direct unfavorable action of catecholamines, which is also met in patients with pheochromocytoma and subarachnoid hemorrhage.[3],[4]
Microvascular dysfunction, which also occurs in response to sympathetic hyperactivity, is stated as an alternative mechanism for the development of takotsubo cardiomyopathy. The finding of abnormal myocardial perfusion registered in 69% of the patients with this entity supports this mechanism.[5]
It is assumed that the multivessel epicardial coronary artery spasm is one of the potential mechanisms in the development of takotsubo cardiomyopathy. This hypothesis is based on the findings of this pathophysiological mechanism in 70% of the patients exposed to provocative maneuvers in which ST elevation was registered.[3] This assumption, however, did not find serious scientific confirmation. In fact, it was determined that the ST segment in patients with takotsubo cardiomyopathy remains elevated even in the absence of spasm of epicardial vessels.[6]
The role of myocarditis in the development of takotsubo cardiomyopathy is not confirmed. Increased viral antibody titers were not found, and myocardial biopsy was not suggestive of myocarditis.
It is not clear why this cardiomyopathy occurs predominantly in postmenopausal women, as it was the case with our patient. It is possible that the lower level of estrogen which increases vulnerability to stress has an important role. The estrogen substitution attenuates sympathoadrenal activation and vagal inhibition, which supports this hypothesis.[7]
Acute heart failure presented in our case is not a rare complication in patients with takotsubo cardiomyopathy. Madhavan et al. have found that the incidence of heart failure in patients with takotsubo cardiomyopathy is 45%, and that one in five patients developed cardiogenic shock.[8] They found that the patients with takotsubo cardiomyopathy complicated with heart failure were older, under stress such as those in the surgery, and had higher levels of troponin and more often ST elevation than those without this complication. It is clear that endothelial dysfunction and diastolic dysfunction, characteristics of older population, and the level of myocardial damage are predictors of cardiac failure in patients with takotsubo cardiomyopathy.
As previously described, this syndrome may be associated with arrhythmias and conduction abnormalities: sinus bradycardia, atrioventricular block, atrial fibrillation, and ventricular tachycardia and fibrillation. Atrial fibrillation is seen in 6%–7% of cases in large multicentric series of cases.[9]
The occurrence of atrial fibrillation in patients with takotsubo cardiomyopathy can also be explained by excess catecholamines.[10] Catecholamines in human atrium may affect the electrophysiological mechanisms which can cause fluctuations in membrane potential by increasing calcium influx that contributes to the change of sodium-calcium exchange which results in an increase of automaticity of the myocardium.
Catecholamines may affect action potential and refractory period. They may also affect reentry waves by changing the excitability and conduction in human atrium. With the undoubted role of catecholamine excess in the development of atrial fibrillation in our patient, the larger left atrial volume cannot be ignored in the development of this complication.
| Conclusions | | |
The prognosis of patients with takotsubo cardiomyopathy is generally good. This kind of cardiomyopathy could have many different severe manifestations, such as congestive heart failure, cardiac rupture, left ventricular apical thrombosis, or malignant arrhythmias. Several possible mechanisms such as coronary microvascular dysfunction, multivessel coronary artery spasm, myocarditis, or catecholamine toxicity have been suggested to explain takotsubo cardiomyopathy. However, numerous questions about the etiology, therapy, and even pathophysiology of takotsubo cardiomyopathy are unanswered. It seems that catecholamine excess has a very important role in the development of takotsubo cardiomyopathy, acute heart failure, and atrial fibrillation.
Consent
Informed consent was obtained from the presented patient.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Vidi V, Rajesh V, Singh PP, Mukherjee JT, Lago RM, Venesy DM, et al. Clinical characteristics of tako-tsubo cardiomyopathy. Am J Cardiol 2009;104:578-82.  |
| 2. | Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-tsubo or stress cardiomyopathy): A mimic of acute myocardial infarction. Am Heart J 2008;155:408-17. |
| 3. | Wittstein IS, Thiemann DR, Lima JA, 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. |
| 4. | Hurst RT, Prasad A, Askew JW 3 rd, Sengupta PP, Tajik AJ. Takotsubo cardiomyopathy: A unique cardiomyopathy with variable ventricular morphology. JACC Cardiovasc Imaging 2010;3:641-9. |
| 5. | Elesber A, Lerman A, Bybee KA, Murphy JG, Barsness G, Singh M, et al. Myocardial perfusion in apical ballooning syndrome correlate of myocardial injury. Am Heart J 2006;152:469.e9-13. |
| 6. | Yamasa T, Ikeda S, Ninomiya A, Yoshinaga T, Hata S, Yakabe K, et al. Characteristic clinical findings of reversible left ventricular dysfunction. Intern Med 2002;41:789-92. |
| 7. | Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: A new form of acute, reversible heart failure. Circulation 2008;118:2754-62. |
| 8. | Madhavan M, Rihal CS, Lerman A, Prasad A. Acute heart failure in apical ballooning syndrome (TakoTsubo/stress cardiomyopathy): Clinical correlates and mayo clinic risk score. J Am Coll Cardiol 2011;57:1400-1. |
| 9. | Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: A novel heart syndrome mimicking acute myocardial infarction. Angina pectoris-myocardial infarction investigations in Japan. J Am Coll Cardiol 2001;38:11-8. |
| 10. | Bettoni M, Zimmermann M. Autonomic tone variations before the onset of paroxysmal atrial fibrillation. Circulation 2002;105:2753-9. |
[Figure 1]
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