Case Reports Of Takotsubo Cardiomyopathy Research Articles

Description of a Patient Suspected of Myocardial Infarction With Normal Coronary Artery: A Case Report of Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy (TC) is characterized by transient systolic dysfunction, presenting with electrocardiographic (ECG) changes and mimicking acute coronary syndrome (ACS). Studies have shown that 95% of patients have changes in ECG. ECG changes in TC syndrome may be similar to myocardial infarction )MI(. ECG changes can be seen in the form of ST-segment elevation or deep T-wave inversion. TC can be considered a special form of ACS. TC is not a benign entity, and conduction abnormalities can occur. The acute phase can be predicted based on decreased EF and arrhythmia. Different treatments are used in the acute phase of TC, depending on the hemodynamic condition. Our case elucidates the importance of age, female gender, symptoms, such as stress and emotion, clinical manifestations, ECG characteristics, and echocardiography in TC. This paper describes a case of TC from a hospital affiliated to Rafsanjan University of Medical Sciences. The case was a 75-year-old woman with no history of cardiovascular diseases who has been admitted to the hospital with myocardial infarction.

A case report of Takotsubo cardiomyopathy associated with pituitary apoplexy

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

A case report of takotsubo cardiomyopathy

Takotsubo cardiomyopathy (TC) is defined as the weakening of the left ventricle. It occurs exclusively in women, and it accounts for 1–2% of all cases of suspected acute myocardial infarction, its true prevalence is unknown due to underdiagnosis. It may present with a similar clinical picture mimicking acute myocardial infarction. We report the case of a 53-year-old woman who came to the emergency department with complaints of recurrent vomiting and decreased oral intake. After sometimes, the patient started complaining of chest pain, for which electrocardiography was done, which showed ST-segment elevation. Coronary angiography was done, which showed normal coronary arteries. Afterward, a stressor precipitant was identified. The patient was diagnosed with TC. TC is a great mimic of acute myocardial infarction due to its close resemblance to myocardial infarction in terms of clinical presentation and clinical course. It should be considered as one of the important differentials in patients presenting with acute chest pain.

Stress-induced cardiomyopathy after nephrectomy in a patient with a kidney cancer: a case report

Stress-induced (takotsubo) cardiomyopathy is a rare disease, which characterized by transient left ventricle dysfunction in response to a trigger factor (stress or severe somatic disease with surgical intervention) and is manifested by symptoms of acute coronary syndrome, but without significant coronary artery damage. In the population, the disease most often observes in postmenopausal women. Every year, more and more cases of takotsubo cardiomyopathy described in the literature, mainly after a severe stress. The presented article describes a case report of takotsubo cardiomyopathy after nephrectomy in a patient with comorbidity.

Takotsubo cardiomyopathy complicated by cardiac tamponade due to non-hemorrhagic pericardial effusion: a case report

BackgroundCardiac tamponade is a rare but serious complication of Takotsubo cardiomyopathy (TC). Two cases of cardiac tamponade subsequent to TC have been reported. The pericardial effusion in these cases was hemorrhagic and caused by ventricular rupture. Cardiac tamponade induced by an inflammatory effusion complicated with TC has not been reported. This is the first case report of TC, which developed cardiac tamponade during the recovery phase with a large volume non-hemorrhagic inflammatory effusion.Case presentationWe describe a case of an 81-year-old woman admitted to our hospital because of severe chest pain. Her symptoms began soon after her son’s hospitalization. We diagnosed her with TC based on results of an electrocardiogram, echocardiogram, and emergent coronary angiography. Her symptoms and left ventricular dysfunction improved gradually. She developed newly confirmed chest pain and dyspnea on day 9 after admission. A large pericardial effusion developed, resulting in cardiac tamponade. Her symptoms and hemodynamic status improved immediately after the pericardiocentesis. The effusion was non-hemorrhagic and exudative. No specific signs of infection, collagen disease, or malignant tumors were observed, except for TC.ConclusionsWe experienced a case of circulatory collapse induced by TC-related inflammatory pericardial effusion at recovery phase. This case emphasizes the importance of careful follow-up even after improved left ventricular dysfunction in a patient with TC.

The importance of systematic point-of-care ultrasound for chest pain with ST-segment elevation: A case report of takotsubo cardiomyopathy precipitated by spontaneous pneumothorax

Introduction: Patients with chest pain and concomitant ST-segment elevation on an electrocardiogram should be identified as having suspected ST-segment elevation myocardial infarction. However, various etiologies cause ST-segment elevation other than ST-segment elevation myocardial infarction, such as takotsubo cardiomyopathy. Case presentation: Here we report the case of a 77-year-old man who requested transport by helicopter emergency medical service for ST-segment elevation myocardial infarction but was consequently diagnosed with takotsubo cardiomyopathy due to spontaneous pneumothorax. En route, findings of electrocardiogram as well as focused cardiac point-of-care ultrasound could not distinguish takotsubo cardiomyopathy from ST-segment elevation myocardial infarction, but a subsequent point-of-care ultrasound could reveal occult pneumothorax, which ultimately revealed to be the culprit stress factor of takotsubo cardiomyopathy causing ST-segment elevation myocardial infarction–alike presentation. After treatment with a closed thoracostomy, he recovered from the takotsubo cardiomyopathy and pneumothorax and was discharged without any complications. Discussion and conclusion: We should consider takotsubo cardiomyopathy a disease with ST-segment elevation and spontaneous pneumothorax as one of its precipitating stressors. To clarify the diagnosis, point-of-care ultrasound using a systematic rather than region-of-interest approach may be a useful method in the emergency department.

Tako-tsubo Cardiomyopathy on the First Day After Renal Transplantation — Case Report and Literature Review

BackgroundThe etiology of tako-tsubo cardiomyopathy, defined as a transient left ventricular dysfunction in the absence of significant coronary artery stenosis, still remains unclear. This syndrome mainly occurs in postmenopausal women and is often associated with emotional stress or miscellaneous diagnostic and therapeutic procedures. Estimated prevalence of tako-tsubo cardiomyopathy is found in 1% to 2% of patients presenting with suspected acute coronary syndrome. So far there has been only one case report of tako-tsubo cardiomyopathy in a renal transplant recipient. Case reportWe describe the case of a 68-year-old woman with a history of coronary artery disease and coronary artery bypass grafting in whom unspecific transient chest pain and hypotension were observed on the first day after renal transplantation. After transplantation, the patient was anuric with pulmonary congestion and toxic tacrolimus concentrations were observed. Electrocardiogram showed sinus rhythm with left bundle branch block (LBBB) that has not been described before. Plasma cardiac necrosis markers troponin I and creatine kinase MB were mildly elevated. Echocardiography showed severe left ventricular function impairment with characteristic shape of left ventricle. Subsequent cardiac catheterization revealed the absence of angiographic evidence of acute plaque rupture within both coronary arteries and bypass grafts. During the next few days there was marked clinical improvement with resolution of LBBB and full recovery of all biochemical parameters. On discharge, full functional recovery of the left ventricle in echocardiography was observed. Postulated mechanisms of tako-tsubo cardiomyopathy include catecholamine excess, coronary artery spasm, and microvascular dysfunction. On the other hand calcineurin inhibitors are known factors causing coronary epicardial endothelial dysfunction and negatively affecting vasomotor function. ConclusionsTako-tsubo cardiomyopathy in patients after renal transplantation may be at least in part a manifestation of calcineurin inhibitor cardiotoxicity.

トラスツズマブ投与中にたこつぼ型心筋症を発症した1例

トラスツズマブ投与中にたこつぼ型心筋症を発症した1例

PP-260 MELPHALAN INDUCED TAKOTSUBO CARDIOMYOPATHY

Case: A 53 year old women presented to the outpatient clinic with dyspnea and chest pain. She also complained about burning sensation in both arms. Her medical history included a cardiac surgery for secundum type atrial septal defect 25 years ago and a recent lower respiratory tract infection. She had also neurological diseases such as migreine and restless leg syndrome. Her ECG showed negative T waves in all leads with a mild QT prolongation (QTc =460ms). Laboratory examination showed increased troponin I levels (0.6 ng/ml). Coronary angiography showed normal coronary arteries, but ventriculography was demonstrative for an apical ballooning (Figure 1). Transthoracic echocardiography approved the mid-apical akinesia with basal hyperkinesia (Figure 2). Hence the possible diagnosis was takotsubo cardiomyopathy (TC), the patient was went on serial echocardiographic evaluation. On the 10th day of admission echocardiography showed nearly complete normalization of left ventricular dysfunction (Figure 3). When the patient was further questioned for possible triggers of TC, although there was no emotional or physical stres, a recent history of polymedication including antimigreine drugs and antibiotics was evident. The patient received clarithromycin 1000mg/day for the last 14 days which was prescribed for lower respiratory tract infection. She also received ergotamine tartarate 1.5mg /day for the last 5 days owing to her increased migreine headache. She was already on therapy for restless leg syndrome including pramipexole 0.25mg/day and fluoxetine 20mg/day. When the drugs she used were analyzed, ergotamine toxicity was seen as a possible etiology. Ergotamine, because of its a-adrenergic effects and extensive first pass metabolism via cytochrome p450–3A4 isoenzyme, could possibly cause such a condition in presence of concomitant use of clarithromycin and fluoxetine which were powerful inhibitors of CYP450. The proposed mechanisms of TC; coronary microvasculature vasospasm and catecholamine excess could readily be a consequence of ergotamine toxicity. Ergotamine tartrate and clarithromycin were stopped during the hospital stay. Clinical follow up was uneventful for the next 6 months with totally normal left ventricular functions. TC is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine and 5 fluorouracil [1]. To the best of our knowledge the peresent case is the first defining an association between ergotamin toxicity and TC.

PP-259 ERGOTAMINE INDUCED TAKOTSUBO CARDIOMYOPATHY

Case: A 53 year old women presented to the outpatient clinic with dyspnea and chest pain. She also complained about burning sensation in both arms. Her medical history included a cardiac surgery for secundum type atrial septal defect 25 years ago and a recent lower respiratory tract infection. She had also neurological diseases such as migreine and restless leg syndrome. Her ECG showed negative T waves in all leads with a mild QT prolongation (QTc =460ms). Laboratory examination showed increased troponin I levels (0.6 ng/ml). Coronary angiography showed normal coronary arteries, but ventriculography was demonstrative for an apical ballooning (Figure 1). Transthoracic echocardiography approved the mid-apical akinesia with basal hyperkinesia (Figure 2). Hence the possible diagnosis was takotsubo cardiomyopathy (TC), the patient was went on serial echocardiographic evaluation. On the 10th day of admission echocardiography showed nearly complete normalization of left ventricular dysfunction (Figure 3). When the patient was further questioned for possible triggers of TC, although there was no emotional or physical stres, a recent history of polymedication including antimigreine drugs and antibiotics was evident. The patient received clarithromycin 1000mg/day for the last 14 days which was prescribed for lower respiratory tract infection. She also received ergotamine tartarate 1.5mg /day for the last 5 days owing to her increased migreine headache. She was already on therapy for restless leg syndrome including pramipexole 0.25mg/day and fluoxetine 20mg/day. When the drugs she used were analyzed, ergotamine toxicity was seen as a possible etiology. Ergotamine, because of its a-adrenergic effects and extensive first pass metabolism via cytochrome p450–3A4 isoenzyme, could possibly cause such a condition in presence of concomitant use of clarithromycin and fluoxetine which were powerful inhibitors of CYP450. The proposed mechanisms of TC; coronary microvasculature vasospasm and catecholamine excess could readily be a consequence of ergotamine toxicity. Ergotamine tartrate and clarithromycin were stopped during the hospital stay. Clinical follow up was uneventful for the next 6 months with totally normal left ventricular functions. TC is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine and 5 fluorouracil [1]. To the best of our knowledge the peresent case is the first defining an association between ergotamin toxicity and TC.

A Case Report of Takotsubo Cardiomyopathy Complicated by Torsades de Pointes, Which Was Successfully Treated with Amiodarone

Takotsubo cardiomyopathy (TCM) is characterized by transient left ventricular dysfunction and intact coronary artery. Although TCM almost always prolongs QT interval, torsade de pointes (TDP) is rarely associated with TCM. Little is known of the mechanism and the treatment of TCM-associated TDP. We experienced a case of TCM-associated TDP. Eighty one year-old woman who admitted for heart failure suffered from TCM-associated TDP. Preceding TDP, electrocardiography showed dramatic QT prolongation and T wave inversion as compared with those at admission. The tachycardia was refractory with magnesium sulfate, cathecolamines, and lidocaine, required repetitious electrical cardioversion, and was successfully treated with amiodarone.

Takotsubo Cardiomyopathy After Electroconvulsive Therapy

Takotsubo cardiomyopathy is a novel acute cardiac syndrome characterized by transient regional systolic dysfunction of the left-ventricular apex and mid-ventricle, with hyperkinesis of the basal left ventricular segments, which has been associated with severe emotional or physical stress. This is the second published case report of takotsubo cardiomyopathy occurring in the setting of electroconvulsive therapy (ECT). The patient, a 52-year-old woman, experienced chest pain and discomfort shortly after ECT treatment. She was shown to have moderate left-ventricular dysfunction, with mid-cavity left-ventricular hypo- to akinesis, and hyperkinesis in the basilar region, consistent with a diagnosis of takotsubo cardiomyopathy. There was full resolution of her symptoms within 48 hours of the initial event. This report highlights a previously undocumented complication of ECT and adds to the growing list of stressors responsible for cases of takotsubo cardiomyopathy. The prognosis is favorable, and recovery is generally complete, especially with early recognition of the syndrome and proper supportive treatment.

14 Case Report of Takotsubo Cardiomyopathy and a Review of Literatures

14 Case Report of Takotsubo Cardiomyopathy and a Review of Literatures

Myocarditis mimicking Takotsubo cardiomyopathy or Takotsubo cardiomyopathy with secondary inflammation?: reply

We read with great interest the letter from Eitel et al. We would like to reemphasize that in the reported case of Takotsubo cardiomyopathy (TTC), endomyocardial biopsy (EMB), the diagnostic gold standard for myocarditis, had not been systematically performed, in spite of the fact that Mayo Criteria specify that myocarditis should be excluded in all cases of suspected TTC.1,2 As mentioned by Eitel, there are case reports of TTC that appear to be caused by myocarditis, in keeping with our findings.1 Our patient was virus-negative, thus the issue of virus pathogenicity is not relevant.3–5 In relation to Eitel's provocative proposal that our case may be a TTC with secondary inflammation, we think this is highly unlikely. Active myocarditis is not simply characterized by sparse mononuclear cell infiltrates, as suggested by Eitel et al., but is defined (Dallas criteria), as an inflammatory infiltrate of the myocardium with necrosis and/or degenerative changes of adjacent myocytes not typical of infarction.6 Our case fulfils state-of-the-art WHO histological (active myocarditis by the Dallas criteria), immunological (serum anti-heart autoantibodies), immunohistochemical (infiltrating activated lymphocytes and macrophages), and molecular (absence of viral genomes) diagnostic criteria of a virus-negative, immune-mediated form of acute myocarditis masquerading as TTC.3–6 Further, in our case the ‘stressful event’ dated back 3 months, thus the onset was not strictly time-related with clinical presentation; autoimmune myocarditis is more likely to occur in females, as other autoimmune diseases; the rapid resolution of cardiac dysfunction is a clinical hallmark of myocarditis.3,5 Last but not least, lymphocytic myocarditis can occur in relation to hypercatecholaminergic states, but it is not a feature known to be associated with microvascular ischaemia.5 Thus, a proportion of TTC patients with sympathetic overdrive may have an underlying virus-negative toxic myocarditis, explaining the reversible systolic dysfunction, chest pain and non-ischaemic troponin release. We propose1 in agreement with Eitel et al. that the role of inflammation in the pathogenesis of TTC merits further study, to differentiate myocarditis mimicking TTC from ‘idiopathic’ TTC, and/or to have a better understanding of the frequency of (viral, immune-mediated, or toxic) myocarditis in TTC. Takotsubo cardiomyopathy may be a syndrome, rather than a distinct pathological entity. Regarding Eitel's proposal that EMB is not an adequate method for the diagnosis of myocarditis, we disagree. First, EMB sensitivity is higher using immunohistochemistry.3–5,7 Secondly, EMB is safe with a complication rate that is similar to that of standard coronary angiography,3,7,8 which is always performed in TTC. Thirdly, myocarditis is challenging to identify clinically,3–5,7,8 and current validation studies of cardiac magnetic resonance imaging (CMR) are mainly based upon clinical presentation.9 Finally, CMR is unable to differentiate viral from non-viral myocarditis.9 Viral genome10 and chronic inflammation may have independent prognostic value in distinct subsets of patients.7 EMB, with adjunct immunohistology and molecular detection of the viral genome is the mainstay to achieve confirmation or exclusion of myocarditis3,5,9,10 as well as identify its aetiopathogenetic forms and aetiology-based therapies.3,5

Report of Takotsubo Cardiomyopathy Occurring During Cardiopulmonary Bypass

On weaning from cardiopulmonary bypass, a 59-yearold Japanese woman with mitral valve plasty suddenly showed a greatly increased heart rate, and an electrocardiogram revealed elevated ST-segments. There was also abnormal wall motion in the inferior region and apical ballooning of the left ventricle. We diagnosed the condition as takotsubo cardiomyopathy (acute left ventricle apical ballooning syndrome), possibly caused by catecholamine release and regional stress-induced ischemia. We believe this to be the first case report of takotsubo cardiomyopathy observed during heart surgery. We hypothesize that the condition was mediated by regional myocardial stunning and that it could be prevented by administration of angiotensin converting enzyme inhibitors before surgery and by the use of superior biocompatible cardiopulmonary bypass components. Once takotsubo cardiomyopathy occurs, we recommend mechanical circulatory assistance during weaning from the bypass.

A Case Report of Takotsubo Cardiomyopathy in the Emergency Department

A Case Report of Takotsubo Cardiomyopathy in the Emergency Department

A Case Report of Takotsubo Cardiomyopathy in the Emergency Department

A Case Report of Takotsubo Cardiomyopathy in the Emergency Department