International Journal of Cardiology 131 (2009) 265 – 295 www.elsevier.com/locate/ijcard
Letters to the Editor
Stress-induced (Takotsubo) cardiomyopathy: A transient disorder Turgay Celik a,⁎, Atila Iyisoy a , Cagdas Yuksel b a
Gulhane Military Medical Academy, School of Medicine, Department of Cardiology, Etlik-Ankara, Turkey b Sarikamis Army District Hospital, Department of Cardiology, Sarikamis, Turkey Received 12 June 2007; accepted 2 July 2007 Available online 25 July 2007
Abstract Once the diagnosis of Takotsubo cardiomyopathy has been made, treatment should be based upon the patient's overall clinical condition. Up to now, there has been no controlled data to guide the optimal medical regimen, but it is reasonable to treat these patients with standard medications for left ventricular systolic dysfunction during acute phase. This includes aspirin, beta-blockers, ACE-inhibitors, and diuretics as necessary for volume overload. Since this type of cardiomyopathy is a transient disorder, the appropriate duration of therapy is not known. Although the current study demonstrates that the use of beta-blockers, aspirin, ACE inhibitors and calcium channel blockers does not seem to be indicated for chronic treatment of Takotsubo cardiomyopathy, we strongly believe that we need to achieve the data which will be obtained from large scale prospective studies in the near future to assess the clinical significance of chronic medical treatment. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Takotsubo cardiomyopathy; Chronic medical treatment
In their recently published study, Fazio and coworkers have retrospectively looked at the benefits of treatment with angiotensin converting enzyme (ACE)-inhibitors, beta-blockers, aspirin and calcium channel blockers, started until the early phases of disease and continued for 30 days, in 36 patients suffering from Takotsubo cardiomyopathy [1]. They found that chronic treatment with beta-blockers, ACE-inhibitors, calcium channel blockers and aspirin does not provide any benefit in patients with Takotsubo cardiomyopathy. They concluded that early correct differential diagnosis is important to avoid any chronic treatment in these patients. Stress-induced cardiomyopathy, also called transient left ventricular (LV) apical ballooning, broken heart syndrome, and, in Japan, Takotsubo cardiomyopathy (‘fishing pot for trapping octopus’, because the left ventricle of a patient with this condition resembles that shape) is an increasingly recognized clinical syndrome characterized by transient dysfunction of the ⁎ Corresponding author. Department of Cardiology, Gulhane School of Medicine, 06018 Etlik-Ankara, Turkey. Tel.: +90 312 3044268; fax: +90 312 3044250. E-mail address:
[email protected] (T. Celik).
apical portion of the left ventricle, with compensatory hyperkinesis of the basal walls, producing ballooning of the apex with systole in the absence of significant coronary artery disease [2–6]. The data about the incidence and prevalence of Takotsubo cardiomyopathy are limited. Although it was initially considered to be not a common disorder, it is increasingly reported in the literature and recognized in daily routine practice. Some of the best available data come from four small series of consecutive patients presenting with a suspected acute coronary syndrome [6,7], which were included in a larger systematic review [2]. Each of these series included 10 to 16 patients with Takotsubo cardiomyopathy which accounts for 1.7 to 2.2% of cases. The onset of Takotsubo cardiomyopathy is typically triggered by acute medical illness or intense physical or emotional stress (e.g., catastrophic medical diagnoses, devastating financial or gambling losses, natural disasters death of relatives, particularly if unexpected, domestic abuse, arguments) [2,8]. The pathogenesis of this disorder is not well understood. Although the clinical presentation simulates that of an acute,
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Letters to the Editor
usually ST elevation, myocardial infarction, coronary arteriography shows no critical lesions [3,8]. A number of features of Takotsubo cardiomyopathy led the clinicians to suggest that this disorder may be caused by diffuse catecholamine-induced microvascular spasm or dysfunction, resulting in myocardial stunning [2]. Plasma catecholamines were significantly higher in patients with Takotsubo cardiomyopathy: epinephrine (1264 versus 376 pg/mL) and norepinephrine (2284 versus 1100 pg/mL). Why the left ventricular apex are predominantly affected is not known [5]. Several explanations have been proposed [3]. The apex is structurally vulnerable since it does not have a 3-layered myocardial configuration, it has limited elasticity reserve, it can easily become ischemic as a consequence of its relatively limited coronary circulation, and it is more responsive to adrenergic stimulation [9]. All of those factors may make the apex more sensitive to catecholamine-induced surge which were frequently encountered in Takotsubo cardiomyopathy. In the relatively small number of patients with Takotsubo cardiomyopathy undergoing endomyocardial biopsy, the findings have ranged from no evidence of myocarditis [10] to interstitial fibrosis with or without slight cellular infiltration [11] to mononuclear infiltrates with contraction band necrosis [12]. It has been reported that in-hospital mortality rates have ranged from 0 to 8% [3,4,8] and was 1% in the largest series of 88 patients in Japan [3]. Patients who survive the acute episode typically recover normal ventricular function within one to four weeks [3,8,10]. In two series, the mean LVEF increased from 29% at presentation to 63% at a mean of six days [8] and from a median of 20% at presentation to 60% at two to four weeks [12]. Although short-term clinical outcomes are excellent, with complete resolution in cases, there are limited data in the literature regarding long-term outcome in patients suffering from Takotsubo cardiomyopathy [2]. In occasional patients, late sudden death and recurrent disease have occurred [3,4,8]. In a report of 22 patients, all of whom survived the initial episode, 2 patients had a second similar episode triggered by psychologic stress at 3 and 10 months [8]. Both of the patients with a recurrent event were being treated with aspirin and a statin, and one was also taking a beta-blocker and an angiotensin converting enzyme inhibitor [8]. In conclusion, once the diagnosis of Takotsubo cardiomyopathy has been made, treatment should be based upon the patient's overall clinical condition. Up to now, there has been no controlled data to guide the optimal medical regimen, but it
0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.07.009
is reasonable to treat these patients with standard medications for left ventricular systolic dysfunction during acute phase. This includes aspirin, beta-blockers, ACE-inhibitors, and diuretics as necessary for volume overload. Since this type of cardiomyopathy is a transient disorder, the appropriate duration of therapy is not known. Although the current study demonstrates that use of beta-blockers, aspirin, ACE-inhibitors and calcium channel blockers does not seem to be indicated for chronic treatment of Takotsubo cardiomyopathy, we strongly believe that we need to achieve the data which will be obtained from large scale prospective studies in the near future to assess the clinical significance of chronic medical treatment. References [1] Fazio G, Pizzuto C, Barbaro G, et al. Chronic pharmacological treatment in takotsubo cardiomyopathy. Int J Cardiol 2008;127:121–3. [2] Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006;27:1523–9. [3] Tsuchihashi K, Ueshima K, Uchida T, 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. [4] Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [5] Dec GW. Recognition of the apical ballooning syndrome in the United States. Circulation 2005;111:388–90. [6] Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343–6. [7] Matsuoka K, Okubo S, Fujii E, et al. Evaluation of the arrhythmogenecity of stress-induced “Takotsubo cardiomyopathy” from the time course of the 12-lead surface electrocardiogram. Am J Cardiol 2003;92:230–3. [8] Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472–9. [9] Mori H, Ishikawa S, Kojima S, et al. Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli. Cardiovasc Res 1993;27:192–8. [10] Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448–55. [11] Abe Y, Kondo M, Matsuoka R, et al. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42. [12] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48.
