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Recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction
Journal of Cardiology Cases (2010) 2, e37—e40
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction Masaki Izumo (MD) a,∗, Yoshihiro J. Akashi (MD) a, Kengo Suzuki (MD) a, Kazuto Omiya (MD) a, Fumihiko Miyake (MD, FJCC) a, Eiji Ohtaki (MD, FJCC) b a
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, 216-8511 Kawasaki, Kanagawa, Japan b Ohtaki Hearts Clinic, Bunkyo-ku, Tokyo, Japan Received 28 October 2009; received in revised form 11 January 2010; accepted 21 January 2010
KEYWORDS Apical ballooning; Heart failure; Invert; Stress; Takotsubo
Summary A 78-year-old man presented to our emergency department with dyspnea. The patient was diagnosed as having pneumonia from the chest X-ray which depicted mass-like opacity in the left lower lobe. On the 5th hospital day, electrocardiography showed giant negative T waves in pericardial leads and echocardiography demonstrated left ventricular apical akinesis and basal hyperkinesis. Accordingly, the patient was retrospectively diagnosed as having typical takotsubo cardiomyopathy. Two years later, the patient was admitted again to our hospital with pneumonia. On the 2nd hospital day, echocardiography showed left ventricular basal and mid-ventricular akinesis combined with normal apical wall motion. Ventricular wall motion was normalized within two months. The patient was finally diagnosed as having inverted takotsubo cardiomyopathy. Here, we report the patient who had recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction caused by repeated physical stress in two years. © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
Introduction Takotsubo cardiomyopathy is recognized as reversible ventricular dysfunction and characterized by transient left ventricular (LV) apical ballooning and electrocardiographic (ECG) changes that mimic acute myocardial infarction in the absence of obstructive coronary artery disease [1]. Various types of transient ventricular dysfunction have been
reported [1]. The mechanism of takotsubo cardiomyopathy is still a matter of debate, which varies according to the individual. Recurrent takotsubo cardiomyopathy is rare; only a handful of case reports have described the typical and atypical ventricular contractile patterns in the same patients [2]. Here, we report our encounter with recurrent takotsubo cardiomyopathy with variant forms of LV dysfunction which was caused by repeated physical stress.
Case report ∗
Corresponding author. Tel.: +81 44 977 8111ext3313; fax: +81 44 976 7093. E-mail address: [email protected] (M. Izumo).
A 78-year-old man presented to our emergency department with dyspnea. On admission, the pulse was 120 beats/min,
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.jccase.2010.01.009
e38
M. Izumo et al.
Figure 1 12-lead electrocardiogram. (a) On the 5th hospital day on the first admission, sinus rhythm (91 beats/min) with inverted T waves in V2-6 and abnormal Q in III, aVF, V1-3 was observed. (b) On the 1st day of the 2nd admission, sinus rhythm (64 beats/min) with abnormal Q wave formations in V1-4 and low voltage in limb leads was observed. (c) Before 1st admission, sinus rhythm (72 beats/min) with high voltage in V5, 6.
the blood pressure was 114/69 mmHg, and the body temperature was 37.0 ◦ C. The laboratory data showed leukocytes of 6200 × 109 /L, hemoglobin of 10.9 g/dL, platelets of 234 × 109 /L, creatine kinase of 133 U/L, and C-reactive protein of 21.3 mg/dL. Chest X-ray showed mass-like opacity in the left lower lobe; the patient was diagnosed as having pneumonia and immediately treated with antibiotic therapy. On the 5th hospital day, 12-lead ECG showed sinus rhythm (91 beats/min) with inverted T waves in leads V2 through V6 and abnormal Q formations in leads V1 through V3 (Fig. 1a). Echocardiography depicted LV akinesis except in
the basal region; however, no pericardial effusion, LV hypertrophy, or thrombus was found (Fig. 2a). Multi-detector computed tomography showed no significant obstruction in the coronary arteries. Accordingly, the patient was diagnosed as having takotsubo cardiomyopathy. On the 21st hospital day, 123 I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy showed decreased uptake in the apical area (Fig. 3a). The defect area was accentuated in the delayed image; the accelerated washout of 123 I-MIBG was observed in the apical area. The heart to mediastinum (H/M) ratio remarkably decreased both in the early (1.29) and delayed
Recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction
e39
(1.16) phases; the washout rate (WR) was 48%. All findings matched to the proposed diagnostic criteria for takotsubo cardiomyopathy. One month later, ECG showed completely normalized LV contraction and segmental wall motion. Two years later, the patient was admitted to our hospital again with pneumonia. On the 2nd hospital day, echocardiography was performed because of the previous history. ECG showed the inverted T waves were normalized (Fig. 1b); however, echocardiography showed LV basal akinesis and apical normokinesis (Fig. 2b). On the 37th hospital day, 123 IMIBG myocardial scintigraphy showed decreased uptake in the LV inferolateral wall (Fig. 3b). The patterns of 123 I-MIBG uptake in the myocardium were completely different in the first and second episodes (Fig. 3a). Although the H/M ratio of the second episode was preserved rather than that of the first episode, the H/M ratio in the second episode was still low in both the early (1.40) and delayed (1.30) phases. The WR was remarkably accelerated (52.4%). Two months later, echocardiography showed completely normalized LV wall motion. Accordingly, the patient was diagnosed as having inverted takotsubo cardiomyopathy.
Discussion Figure 2 Echocardiography obtained from 4 chamber view. (a) Apical akinesis and basal hyperkinesis in the left ventricle without pericardial effusion and thrombus were observed, which showed the typical takotsubo contractile pattern. (b) On the 2nd admission, basal akinesis in the left ventricle and apical normokinesis were observed, which presented the inverted takotsubo pattern.
A typical feature of takotsubo cardiomyopathy is transient regional systolic dysfunction involving LV apical ballooning. However, recent studies have reported different patterns of this syndrome, including preserved apical contraction and impaired basal/lateral contractility [2], and the increasing incidence of recurrent takotsubo cardiomyopathy [3]. A number of etiologies are considered to be involved, such as vasospasm [4], catecholamine cardiotoxicity [5],
Figure 3 123 I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy. (a) On the 21st hospital day of the 1st admission, Bull’s eye map of 123 I-MIBG myocardial scintigraphy showed the decreased uptake especially in the apical area, which was remarkable in the delayed phase due to accelerated washout of MIBG. (b) On the 37th hospital day in the 2nd admission, the decreased uptakes in the apical area and in the inferolateral wall of the left ventricle were observed. MIBG washout of the lateral wall was accelerated compared to that of the anterior wall.
e40 and neurogenic myocardial stunning caused by several stresses [6]. The mechanism of transient ventricular dysfunction has not been fully clarified; however, neurogenic myocardial stunning is considered as a main cause of takotsubo cardiomyopathy [1]. The cardiac manifestation of takotsubo cardiomyopathy is similar to that of subarachnoid hemorrhage-associated LV dysfunction. Takotsubo cardiomyopathy also occurs in children with brain disease. Since clinical and histological similarities exist in these patients, intracranial changes may be deeply related to LV dysfunction. One study has proved the higher norepinephrine content and greater density of sympathetic nerves at the base of the heart than at the apex [7]. These factors do not directly induce excessive sympathetic sensitivity or reactivity in the myocardium, even though the distribution of sympathetic nerve in the myocardium is clearly indicated. Fripp et al. [8] conducted a study on rabbits and reported that isotropic responsiveness to norepinephrine was decreased by catecholamine-induced cardiomyopathy because of decreased -receptors in the myocardium. We previously encountered takotsubo patients whose plasma norepinephrine concentrations were not well increased [1]. It seems that the hyperreactivity of ␣- or -adrenoreceptors in the myocardium may be the possible underlying mechanism of LV dysfunction with normal norepinephrine concentrations [9]. Recent case reports have described takotsubo cardiomyopathy associated with suppression of basal contraction and apical sparing, a type of inverted takotsubo [10]. It has not been fully clarified whether ischemia caused by multivessel coronary vasospasm induces abnormal wall motion in inverted takotsubo patients. Various patterns of LV wall motion abnormalities seem to exist in takotsubo cardiomyopathy [2]. Transient LV apical ballooning is relatively more common, meanwhile, regional wall motion abnormalities in the other parts are less common. Abnormal LV wall motion in pheochromocytoma-related cardiomyopathy is similar to that in inverted takotsubo cardiomyopathy. The precise mechanism of the different contractile patterns is still unknown; however, we presume that the alternation of adrenoceptor sensitivity or reactivity in the same individual may trigger the different LV contractile patterns. In the present case report, catecholamine concentration was not measured at the acute phase in the first and second episodes. Catecholamine concentration might affect the specific region which showed abnormal ventricular wall motion.
M. Izumo et al.
Conclusions We encountered a takotsubo cardiomyopathy patient with variant forms of ventricular dysfunction which occurred in two years. The main causes of takotsubo cardiomyopathy might be adenoreceptor hypersensitivity and/or adrenergic stunning triggered by stress, resulting in regional hypersensitivity or hyperreactivity. We considered that the alternation of adrenoceptor sensitivity or reactivity was one of the causes for recurrent takotsubo cardiomyopathy.
References [1] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy; a new form of acute, reversible heart failure. Circulation 2008;118:2754—62. [2] Blessing E, Steen H, Rosenberg M, Katus H, Frey N. Recurrence of takotsubo cardiomyopathy with variant forms of left ventricular dysfunction. J Am Soc Echocardiogr 2007;20:439.e11-2. [3] Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 2007;50:448—52. [4] Sato H, Tateishi H, Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspect of myocardial injury: from ischemia to heart failure. Tokyo, Japan: Kagakuhyouronsha; 1990. p. 56—64. [5] Wittstein IS, Thiemann DR, Lima JAC, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539—48. [6] Benarroch EE. The central autonomic network: functional organization, dysfunction, and perspective. Mayo Clin Proc 1993;68:988—1001. [7] Kawano H, Okada R, Yano K. Histological study on the distribution of autonomic nerves in the human heart. Heart Vessels 2003;18:32—9. [8] Fripp RR, Lee JC, Downing SE. Inotropic responsiveness of the heart in catecholamine cardiomyopathy. Am Heart J 1981;101:17—21. [9] Madhavan M, Borlaug BA, Lerman A, Rihal CS, Prasad A. Stress hormone and circulating biomarker profile of apical ballooning syndrome (Takotsubo cardiomyopathy): insights into the clinical significance of B-type natriuretic peptide and troponin levels. Heart 2009;95:1436—41. [10] Kurowski V, Kaiser A, von Hof K, Killermann DP, Mayer B, Hartmann F, Schunkert H, Radke PW. Apical and midventricular transient left ventricular dysfunction syndrome (takotsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest 2007;132:809—16.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction Masaki Izumo (MD) a,∗, Yoshihiro J. Akashi (MD) a, Kengo Suzuki (MD) a, Kazuto Omiya (MD) a, Fumihiko Miyake (MD, FJCC) a, Eiji Ohtaki (MD, FJCC) b a
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, 216-8511 Kawasaki, Kanagawa, Japan b Ohtaki Hearts Clinic, Bunkyo-ku, Tokyo, Japan Received 28 October 2009; received in revised form 11 January 2010; accepted 21 January 2010
KEYWORDS Apical ballooning; Heart failure; Invert; Stress; Takotsubo
Summary A 78-year-old man presented to our emergency department with dyspnea. The patient was diagnosed as having pneumonia from the chest X-ray which depicted mass-like opacity in the left lower lobe. On the 5th hospital day, electrocardiography showed giant negative T waves in pericardial leads and echocardiography demonstrated left ventricular apical akinesis and basal hyperkinesis. Accordingly, the patient was retrospectively diagnosed as having typical takotsubo cardiomyopathy. Two years later, the patient was admitted again to our hospital with pneumonia. On the 2nd hospital day, echocardiography showed left ventricular basal and mid-ventricular akinesis combined with normal apical wall motion. Ventricular wall motion was normalized within two months. The patient was finally diagnosed as having inverted takotsubo cardiomyopathy. Here, we report the patient who had recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction caused by repeated physical stress in two years. © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
Introduction Takotsubo cardiomyopathy is recognized as reversible ventricular dysfunction and characterized by transient left ventricular (LV) apical ballooning and electrocardiographic (ECG) changes that mimic acute myocardial infarction in the absence of obstructive coronary artery disease [1]. Various types of transient ventricular dysfunction have been
reported [1]. The mechanism of takotsubo cardiomyopathy is still a matter of debate, which varies according to the individual. Recurrent takotsubo cardiomyopathy is rare; only a handful of case reports have described the typical and atypical ventricular contractile patterns in the same patients [2]. Here, we report our encounter with recurrent takotsubo cardiomyopathy with variant forms of LV dysfunction which was caused by repeated physical stress.
Case report ∗
Corresponding author. Tel.: +81 44 977 8111ext3313; fax: +81 44 976 7093. E-mail address: [email protected] (M. Izumo).
A 78-year-old man presented to our emergency department with dyspnea. On admission, the pulse was 120 beats/min,
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.jccase.2010.01.009
e38
M. Izumo et al.
Figure 1 12-lead electrocardiogram. (a) On the 5th hospital day on the first admission, sinus rhythm (91 beats/min) with inverted T waves in V2-6 and abnormal Q in III, aVF, V1-3 was observed. (b) On the 1st day of the 2nd admission, sinus rhythm (64 beats/min) with abnormal Q wave formations in V1-4 and low voltage in limb leads was observed. (c) Before 1st admission, sinus rhythm (72 beats/min) with high voltage in V5, 6.
the blood pressure was 114/69 mmHg, and the body temperature was 37.0 ◦ C. The laboratory data showed leukocytes of 6200 × 109 /L, hemoglobin of 10.9 g/dL, platelets of 234 × 109 /L, creatine kinase of 133 U/L, and C-reactive protein of 21.3 mg/dL. Chest X-ray showed mass-like opacity in the left lower lobe; the patient was diagnosed as having pneumonia and immediately treated with antibiotic therapy. On the 5th hospital day, 12-lead ECG showed sinus rhythm (91 beats/min) with inverted T waves in leads V2 through V6 and abnormal Q formations in leads V1 through V3 (Fig. 1a). Echocardiography depicted LV akinesis except in
the basal region; however, no pericardial effusion, LV hypertrophy, or thrombus was found (Fig. 2a). Multi-detector computed tomography showed no significant obstruction in the coronary arteries. Accordingly, the patient was diagnosed as having takotsubo cardiomyopathy. On the 21st hospital day, 123 I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy showed decreased uptake in the apical area (Fig. 3a). The defect area was accentuated in the delayed image; the accelerated washout of 123 I-MIBG was observed in the apical area. The heart to mediastinum (H/M) ratio remarkably decreased both in the early (1.29) and delayed
Recurrent takotsubo cardiomyopathy with variant forms of left ventricular dysfunction
e39
(1.16) phases; the washout rate (WR) was 48%. All findings matched to the proposed diagnostic criteria for takotsubo cardiomyopathy. One month later, ECG showed completely normalized LV contraction and segmental wall motion. Two years later, the patient was admitted to our hospital again with pneumonia. On the 2nd hospital day, echocardiography was performed because of the previous history. ECG showed the inverted T waves were normalized (Fig. 1b); however, echocardiography showed LV basal akinesis and apical normokinesis (Fig. 2b). On the 37th hospital day, 123 IMIBG myocardial scintigraphy showed decreased uptake in the LV inferolateral wall (Fig. 3b). The patterns of 123 I-MIBG uptake in the myocardium were completely different in the first and second episodes (Fig. 3a). Although the H/M ratio of the second episode was preserved rather than that of the first episode, the H/M ratio in the second episode was still low in both the early (1.40) and delayed (1.30) phases. The WR was remarkably accelerated (52.4%). Two months later, echocardiography showed completely normalized LV wall motion. Accordingly, the patient was diagnosed as having inverted takotsubo cardiomyopathy.
Discussion Figure 2 Echocardiography obtained from 4 chamber view. (a) Apical akinesis and basal hyperkinesis in the left ventricle without pericardial effusion and thrombus were observed, which showed the typical takotsubo contractile pattern. (b) On the 2nd admission, basal akinesis in the left ventricle and apical normokinesis were observed, which presented the inverted takotsubo pattern.
A typical feature of takotsubo cardiomyopathy is transient regional systolic dysfunction involving LV apical ballooning. However, recent studies have reported different patterns of this syndrome, including preserved apical contraction and impaired basal/lateral contractility [2], and the increasing incidence of recurrent takotsubo cardiomyopathy [3]. A number of etiologies are considered to be involved, such as vasospasm [4], catecholamine cardiotoxicity [5],
Figure 3 123 I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy. (a) On the 21st hospital day of the 1st admission, Bull’s eye map of 123 I-MIBG myocardial scintigraphy showed the decreased uptake especially in the apical area, which was remarkable in the delayed phase due to accelerated washout of MIBG. (b) On the 37th hospital day in the 2nd admission, the decreased uptakes in the apical area and in the inferolateral wall of the left ventricle were observed. MIBG washout of the lateral wall was accelerated compared to that of the anterior wall.
e40 and neurogenic myocardial stunning caused by several stresses [6]. The mechanism of transient ventricular dysfunction has not been fully clarified; however, neurogenic myocardial stunning is considered as a main cause of takotsubo cardiomyopathy [1]. The cardiac manifestation of takotsubo cardiomyopathy is similar to that of subarachnoid hemorrhage-associated LV dysfunction. Takotsubo cardiomyopathy also occurs in children with brain disease. Since clinical and histological similarities exist in these patients, intracranial changes may be deeply related to LV dysfunction. One study has proved the higher norepinephrine content and greater density of sympathetic nerves at the base of the heart than at the apex [7]. These factors do not directly induce excessive sympathetic sensitivity or reactivity in the myocardium, even though the distribution of sympathetic nerve in the myocardium is clearly indicated. Fripp et al. [8] conducted a study on rabbits and reported that isotropic responsiveness to norepinephrine was decreased by catecholamine-induced cardiomyopathy because of decreased -receptors in the myocardium. We previously encountered takotsubo patients whose plasma norepinephrine concentrations were not well increased [1]. It seems that the hyperreactivity of ␣- or -adrenoreceptors in the myocardium may be the possible underlying mechanism of LV dysfunction with normal norepinephrine concentrations [9]. Recent case reports have described takotsubo cardiomyopathy associated with suppression of basal contraction and apical sparing, a type of inverted takotsubo [10]. It has not been fully clarified whether ischemia caused by multivessel coronary vasospasm induces abnormal wall motion in inverted takotsubo patients. Various patterns of LV wall motion abnormalities seem to exist in takotsubo cardiomyopathy [2]. Transient LV apical ballooning is relatively more common, meanwhile, regional wall motion abnormalities in the other parts are less common. Abnormal LV wall motion in pheochromocytoma-related cardiomyopathy is similar to that in inverted takotsubo cardiomyopathy. The precise mechanism of the different contractile patterns is still unknown; however, we presume that the alternation of adrenoceptor sensitivity or reactivity in the same individual may trigger the different LV contractile patterns. In the present case report, catecholamine concentration was not measured at the acute phase in the first and second episodes. Catecholamine concentration might affect the specific region which showed abnormal ventricular wall motion.
M. Izumo et al.
Conclusions We encountered a takotsubo cardiomyopathy patient with variant forms of ventricular dysfunction which occurred in two years. The main causes of takotsubo cardiomyopathy might be adenoreceptor hypersensitivity and/or adrenergic stunning triggered by stress, resulting in regional hypersensitivity or hyperreactivity. We considered that the alternation of adrenoceptor sensitivity or reactivity was one of the causes for recurrent takotsubo cardiomyopathy.
References [1] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy; a new form of acute, reversible heart failure. Circulation 2008;118:2754—62. [2] Blessing E, Steen H, Rosenberg M, Katus H, Frey N. Recurrence of takotsubo cardiomyopathy with variant forms of left ventricular dysfunction. J Am Soc Echocardiogr 2007;20:439.e11-2. [3] Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 2007;50:448—52. [4] Sato H, Tateishi H, Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspect of myocardial injury: from ischemia to heart failure. Tokyo, Japan: Kagakuhyouronsha; 1990. p. 56—64. [5] Wittstein IS, Thiemann DR, Lima JAC, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539—48. [6] Benarroch EE. The central autonomic network: functional organization, dysfunction, and perspective. Mayo Clin Proc 1993;68:988—1001. [7] Kawano H, Okada R, Yano K. Histological study on the distribution of autonomic nerves in the human heart. Heart Vessels 2003;18:32—9. [8] Fripp RR, Lee JC, Downing SE. Inotropic responsiveness of the heart in catecholamine cardiomyopathy. Am Heart J 1981;101:17—21. [9] Madhavan M, Borlaug BA, Lerman A, Rihal CS, Prasad A. Stress hormone and circulating biomarker profile of apical ballooning syndrome (Takotsubo cardiomyopathy): insights into the clinical significance of B-type natriuretic peptide and troponin levels. Heart 2009;95:1436—41. [10] Kurowski V, Kaiser A, von Hof K, Killermann DP, Mayer B, Hartmann F, Schunkert H, Radke PW. Apical and midventricular transient left ventricular dysfunction syndrome (takotsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest 2007;132:809—16.