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Basal wall hypercontraction of Takotsubo cardiomyopathy in a patient who had been diagnosed with dilated cardiomyopathy: a case report
© The Author(s). 2017
Received: 24 April 2017
Accepted: 5 December 2017
Published: 12 December 2017
Takotsubo cardiomyopathy is characterized by the basal hypercontractility and apical ballooning of the left ventriculum and T-wave inversion in the electrocardiogram. It has been suggested that Takotsubo cardiomyopathy might underlie the pathogenesis of persistent cardiac dysfunction; however, few reports are present demonstrating the advent of Takotsubo cardiomyopathy in patients with idiopathic cardiomyopathy.
A 64-year-old women was admitted due to dyspnea on effort and lower extremity edema. She had been diagnosed with idiopathic dilated cardiomyopathy 2.5 years before owing to the reduced left ventricular ejection fraction (24%), normal coronary artery, and interstitial fibrosis of the myocardial samples. On admission, her electrocardiogram showed giant negative T wave in II, III, aVF, and precordial leads. Echocardiography showed dyskinesis of the left ventricular apex and hypercontraction of the basal wall, which had not been observed in the previous examinations. Coronary angiography showed normal coronary arteries, and apical ballooning and basal hypercontractility was confirmed by left ventriculography. On day 15 of admission, contraction of apical wall was recovered, and basal hypercontraction was disappeared.
The present case is the first report demonstrating appearance the transient basal wall hypercontraction along with the advent of Takotsubo cardiomyopathy in a patient diagnosed with dilated cardiomyopathy. Whether such findings are indicative of fair prognosis and have the utility of understanding the pathogenesis of dilated cardiomyopathy needs further investigation.
Takotsubo cardiomyopathy is characterized by transient left ventricular apical ballooning, which typically occurs in older women after emotional or physical stress . The pathophysiology of Takotsubo cardiomyopathy remains obscure, but it may occur after emotional or physical stress, so-called “triggering events”. In order to diagnose Takotsubo cardiomyopathy, several disorders that might show reversible abnormal cardiac contraction should be excluded, including obstructive coronary artery disease , subarachnoid hemorrhage, pheochromocytoma crisis, intracranial or subarachnoid bleeding myocarditis, tachycardia-induced cardiomyopathy, and hypertrophic cardiomyopathy [3–6]. On the other hand, the possibility exists that some of these conditions might present together with Takotsubo cardiomyopathy and underlie it as a triggering event [7, 8]. There have been few reports, until now, about Takotsubo cardiomyopathy in the dilated cardiomyopathic heart. We herein present a case of basal cardiac wall hypercontraction during the acute-phase of Takotsubo cardiomyopathy that occurred in a patient with idiopathic dilated cardiomyopathy.
Laboratory data on the current admission
Blood cell count
White blood cell count, ×103/μL
Red blood cell count, ×106/μL
Platelet count, ×103/μL
Total protein, mg/dL
serum creatinine, mg/dL
Creatine kinase, U/L
Creatine kinase MB, U/L
C-reactive protein, mg/dL
In the present case, we demonstrated the occurrence of Takotsubo cardiomyopathy in a patient who had been diagnosed with dilated cardiomyopathy. Of note, in the acute phase, the left ventricular basal wall showed hypercontraction together with the advent of apical ballooning, although these findings were transient and disappeared within 2 weeks. These findings indicated that basal wall hypercontraction can occur in patients diagnosed with dilated cardiomyopathy.
Whether there were any relationships between previously diagnosed idiopathic dilated cardiomyopathy and Takotsubo cardiomyopathy remains unclear; however, there are some possibilities. Although wall motion abnormality is, in general, transient in Takotsubo cardiomyopathy , several previous studies suggested that Takotsubo cardiomyopathy might be emerging as a chronic form , causing congestive heart failure and acute coronary syndrome-like symptoms. It is increasingly recognized that Takotsubo cardiomyopathy may not always be benign , and may cause left ventricular fibrosis  leading to appearance as a non-ischemic cardiomyopathy . In addition, presence of Takotsubo cardiomyopathy may not be able to be recognized or diagnosed when it is not associated with anginal chest pain .
Considering that our patient had T-wave inversion in her electrocardiogram 2.5 years before the current admission, and the chief complaint of the current admission was not chest pain, typical for Takotsubo cardiomyopathy, there is a possibility that dilated cardiomyopathy diagnosed 2.5 years before the current admission might have been attributed to the cardiac remodeling by chronic and recurrent Takotsubo cardiomyopathy.
It has been demonstrated that contractile reserve assessed by the administration of catecholamine predicts long-term prognosis in patients with dilated cardiomyopathy [16–18]. Therefore, whatever the etiology of cardiac dysfunction of our patient is, improved left basal contraction during the advent of Takotsubo cardiomyopathy, a potential intrinsic catecholamine-mediated cardiomyopathy, might indicate the fair prognosis of our patient, although circulating catecholamine levels are not always increased in Takotsubo cardiomyopathy .
We showed a case who had been diagnosed with dilated cardiomyopathy who demonstrated left ventricular basal hypercontraction at the advent of Takotsubo cardiomyopathy on the latest admission. Such findings might provide important information on the possibility of chronic or recurrent Takotsubo cardiomyopathy as the underlying cause of dilated cardiomyopathy in some patients.
The authors declare that there are no relationships with the company relating to employment, consultancy, patents, products in development or marketed products.
Availability of data and materials
Some, not all, original data may be able to be shown upon request, to a limited extent; however, some other data cannot be done so due to the confidentiality of the patient’s personal information.
NI (Ichihara), collected data, analyzed, and interpreted data. SF and YK, extracted the data and provided the clinical information. TF and MO, helped to interpret the data and draft the manuscript. NI (ishizaka) made substantial contributions to acquisition and interpretation of data and prepared the drafted the manuscript. All authors read and approved the final manuscript.
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The authors declare that they have no competing interests.
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