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258 EDITORIAL

DOI 10.4070 / kcj.2010.40.6.258

Print ISSN 1738-5520 / On-line ISSN 1738-5555 Copyright ⓒ 2010 The Korean Society of Cardiology

Open Access

Stress-Induced Cardiomyopathy:

A Need for Prospective Multicenter Trials

Kyung-Soon Hong, MD

Division of Cardiology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Chuncheon, Korea

Introduction

Stress-induced cardiomyopathy (also called Takotsubo cardiomyopathy, apical ballooning, or broken heart syn- drome) was first reported in 1991 as “myocardial stun- ning due to simultaneous multivessel coronary spasms:

a review of 5 cases” by Japanese doctors,

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and is well known disease entity now. This disease primarily affects postmenopausal women after psychological or physical stress.

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Clinical characteristics are a triad of sudden on- set of chest pain or dyspnea, electrocardiographic find- ings with ST segment elevation and evolutional T-wave changes, and a moderate elevation in cardiac enzymes mimicking acute myocardial infarction.

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As a precau- tion, coronary angiography is usually performed to dif- ferentiate from acute coronary syndrome. Even though many case and clinical study reports have been publi- shed, the mechanisms of stress-induced cardiomyopathy (SCM) are still unknown. The pathophysiology of SCM is includes vasospasm of coronary arteries; disturbance of microcirculation; obstruction of the left ventricular outflow obstruction; catecholamine-mediated myocar- dial stunning, which is an important link between emo- tional or physical stress and cardiac injury; hormonal interactions; and inflammation.

4-7)

Clinical Characteristics and Adverse Events

Lee et al.

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report some different clinical characteristics and prognoses of SCM in this issue.

In their study,

8)

they found that in 32 of 39 patients (82%), a major triggering factor is physical stress due to medical illness or procedure, that common presenting symptoms are dyspnea (18/39, 46%) rather than chest pain, and that the prevalence of cardiogenic shock (13/39, 33%) and mortality (3/39, 8%) are very high when com- pared with the data reported by Gianni et al.

9)

However, the data published recently by Song et al.

10)

on a study done in Korean subjects is very similar to the data of Lee et al.

3)

in clinical characteristics of SCM and the pre- valence of cardiogenic shock. Additionally, according to these findings, racial differences may be a factor. The sig- nificance of the interpretation of these studies is limited, however, because each has enrolled only a small num- bers of patients and been carried out in a single center.

Biomarkers in the Pathophysiology and Clinical Outcomes

A study by Dorfman and Iskandrian

11)

shows that se- rum b-type natriuretic peptide (NT-proBNP) and catecho- lamine level at presentation correlates with the Killip class of heart failure and associated complications, and low levels predict favorable outcomes. Madhavan et al.

12)

has suggested that marked systemic inflammatory res- ponse occurs in SCM, similar to those seen in acute myo- cardial infarction, despite the absence of significant myo- cardial injury. Morel et al.

7)

recently published a study that shows that elevated C-reactive protein (CRP) levels were correlated with baseline left ventricular ejection frac- tion (LVEF) and BNP levels, and that inflammatory st- atus in SCM was related to LVEF impairment and to the extent of neurohormonal activation. Lee et al.

3)

reported

Correspondence: Kyung-Soon Hong, MD, Division of Cardiology, Depart- ment of Internal Medicine, Hallym University Sacred Heart Hospital, 153 Gyo-dong, Chuncheon 200-704, Korea

Tel: 82-33-240-5275, Fax: 82-33-252-9275 E-mail: [email protected]

Refer to the page 277-282

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.

org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

cc

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Kyung-Soon Hong·

259

similar findings, showing that elevated high-sensitivity CRP (hs-CRP) and decreased left ventricular systolic func- tion at admission were related to death or cardiogenic shock.

Hence, as described above, various biomarkers and cli- nical parameters may act as prognostic and pathophy- siological markers for SCM, but causal relationships are as yet unkown. Hs-CRP is non-specific inflamma- tory marker, and many cases of SCM are triggered by physical stress such as a medical illness or surgical pro- cedure. High levels of hs-CRP can be due to severity of the associated disease. Therefore, cases with cardioge- nic shock or mortality should be reviewed for the se- verity of the associated underlying disease. Also, in the study reported by Lee et al.

3)

patients reported to have had cardiogenic shock should be reviewed and possible re-classified because the criteria for shock herein includ- ed all types of shock and the prevalence of cardiogenic shock is thus very high in this study when compared with data from other studies showing favorable prognoses.

In conclusion, a prospective, multicenter, large volume clinical study of SCM is needed. We have had many case reports and small, single-center study results and now know pathophysiology and clinical importance of SCM very well. Along with ongoing basic research on the car- diac reaction to psychological and physical stress, a mul- ticenter clinical trial would potentially show a straight- forward correlation between the pathophysiology and clinical outcomes of SCM, and direct clinicians toward specific treatments.

REFERENCES

1)

Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial

stunning due to simultaneous multivessel spasms: a review of five cases. J Cardiol 1991;21:203-14.

2)

Eshtehardi P, Koestner C, Adorjan P, et al. Transient apical bal- looning syndrome: clinical characteristics, ballooning pattern, and long-term follow-up in a Swiss population. Int J Cardiol 2009;

135:370-5.

3)

Lee H, Gwon H, Kim B, et al. Clinical manifestation of novel stress-induced cardiomyopathy mimicking acute myocardial in- farction: single center prospective registry. Korean Circ J 2002;32:

1054-63.

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Nef HM, Mollmann H, Akashi YJ, Hamm CW. Mechanisms of stress ( Takotsubo ) cardiomyopathy. Nat Rev Cardiol 2010;7:

187-93.

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Angelini P. Takotsubo cardiomyopathy: what is behind the oc- topus trap? Tex Heart Inst J 2010;37:85-7.

6)

Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral fea- tures of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539-48.

7)

Morel O, Sauer F, Imperiale A, et al. Importance of inflammation and neurohumoral activation in Takotsubo cardiomyopathy. J Card Fail 2009;15:206-13.

8)

Lee JW, Kim JY, Youn YJ, et al. Clinical characteristics and pro- gnostic factors of stress-induced cardiomyopathy. Korean Circ J 2010;40:277-82.

9)

Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E.

Apical ballooning syndrome or takotsubo cardiomyopathy: a sys- tematic review. Eur Heart J 2006;27:1523-9.

10)

Song BG, Park SJ, Noh HJ, et al. Clinical characteristics, and la- boratory and echocardiographic findings in takotsubo cardiomyo- pathy presenting as cardiogenic shock. J Crit Care 2010;25:329-35.

11)

Dorfman T, Iskandrian A. Takotsubo cardiomyopathy: state-of-the- art review. J Nucl Cardiol 2009;16:122-34.

12)

Madhavan M, Borlaug BA, Lerman A, Rihal CS, Prasad A. St-

ress hormone and circulating biomarker profile of apical bal-

looning syndrome ( Takotsubo cardiomyopathy ) : insights into the

clinical significance of B-type natriuretic peptide and troponin

levels. Heart 2009;95:1436-41.

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