Cause Of Takotsubo Cardiomyopathy Research Articles

Takotsubo cardiomyopathy following pacemaker insertion complicated with polymorphic ventricular tachycardia: a case report

BackgroundTakotsubo cardiomyopathy is a novel form of rapidly reversible heart failure occurring secondary to a stressor that mimics an acute coronary event. The underlying etiology of the stressor is highly variable and can include medical procedures. Pacemaker insertion is an infrequent cause of Takotsubo cardiomyopathy.Case presentationAn 86-year-old Caucasian woman underwent an uncomplicated pacemaker insertion for symptomatic complete heart block in the background of slow atrial fibrillation. A transient episode of polymorphic ventricular tachycardia was noted on day 1 following the procedure; however, her pacemaker was checked and, as she remained stable, she was discharged home. She presented again 5 days later with symptomatic heart failure. Chest X-ray confirmed pulmonary edema. Echocardiography confirmed new onset severe left ventricle dysfunction. Pacemaker checks were normal and lead placement was confirmed. Though her troponin I was elevated, her coronary angiogram was normal. Contrast enhanced echocardiography suggested apical ballooning favoring Takotsubo cardiomyopathy. She was treated for heart failure and made a good recovery. Her follow-up echocardiography a month later showed significant improvement in left ventricle function.ConclusionsTakotsubo cardiomyopathy is mediated by a neuro-cardiogenic mechanism due to hypothalamic–pituitary–adrenal axis activation. It generally has a good prognosis. Complications though uncommon, can occur and include arrhythmias. Pacemaker insertion as a precipitant stressor is an infrequent cause of Takotsubo cardiomyopathy. As pacemaker insertions are more frequent in the elderly age group, this phenomenon should be recognized as a potential complication.

The Octopus Trap of Takotsubo and Stroke: Genetics, Biomarkers and Clinical Management.

Takotsubo cardiomyopathy (TC) is a reversible cardiomyopathy mimicking an acute coronary syndrome, usually observed in response to acute stress situations. The association between acute ischemic stroke and TC is already known, since it has been previously reported that ischemic stroke can be both a consequence and a potential cause of TC. However, the precise pathophysiological mechanism linking the two conditions is still poorly understood. The aim of our review is to expand insights regarding the genetic susceptibility and available specific biomarkers of TC and to investigate the clinical profile and outcomes of patients with TC and stroke. Since evidence and trials on TC and stroke are currently lacking, this paper aims to fill a substantial gap in the literature about the relationship between these pathologies.

Abstract #1185090: Levothyroxine Over-replacement Broke her heart, A rare cause of Takotsubo cardiomyopathy

Abstract #1185090: Levothyroxine Over-replacement Broke her heart, A rare cause of Takotsubo cardiomyopathy

Un cas inhabituel de cardiomyopathie de Takotsubo après implantation de pacemaker

Since its first description in Japan in 1990, Takotsubo (stress) cardiomyopathy has gained worldwide recognition. The disease is characterized by transient systolic and diastolic left ventricular dysfunction with a variety of wall-motion abnormalities. She predominantly affects elderly women and she is often preceded by an emotional or physical trigger. In the acute phase, the clinical presentation, electrocardiographic findings and biomarker profiles are often similar to those of an acute coronary syndrome. Although, the cause of Takotsubo cardiomyopathy remains unknown, the role of the brain–heart axis in the pathogenesis of the disease has been described. The potential role of catecholamine excess in the pathogenesis of Takotsubo cardiomyopathy has been long debated, and as such beta-blockers have been proposed as a therapeutic strategy. Currently, the treatment is not codified and it adapts according to clinical symptomatology. It seems difficult to summarize all the factors to provoque the cardiomyopathy, we describe a case of Takotsubo after a pacemaker (PM) implantation and to give a recent progress on this heart disease.

A rare case of chronic obstructive pulmonary disease induced Takotsubo cardiomyopathy in a male

Introduction: Takotsubo cardiomyopathy (TC) is a transient nonischemic cardiomyopathy causing wall motion abnormalities of a particular region of the heart, most commonly the apex. The classic presentation is of a postmenopausal female presenting with chest pain and congestive heart failure in response to an emotional stressor, but physical stressors may cause it as well. Uncommonly, men may present with this condition. We present a rare case of TC in a male, triggered by a COPD exacerbation. Case Report: A 62-year-old African American Male with a past medical history of COPD presented with shortness of breath, wheezing and chest tightness. The patient had increased his use of his albuterol inhaler to four times a day, which did not relieve his symptoms. His electrocardiogram showed right bundle branch block and nonspecific T wave changes and his troponins progressively increased to 2.47 ng/mL within 6 hours. Echocardiogram showed apical akinesis with a newly reduced ejection fraction of 30–35% Cardiac catheterization revealed nonobstructive coronary artery disease and apical ballooning consistent with Takotsubo cardiomyopathy. Since no other emotional or physical stressor such as sepsis could be identified, it was determined that the patient’s COPD was the trigger. The patient was treated medically for his COPD exacerbation until his symptoms resolved. Conclusion: This case illustrates the need for a wide differential diagnosis in patient presenting with signs of COPD exacerbation and elevated troponins. COPD causing Takotsubo cardiomyopathy is rare, but not surprising. Evidence is showing that TC is likely caused by increased catecholamine and adrenergic stimulation. COPD exacerbations upregulate the sympathetic nervous system, but the use of beta-2 agonists and anticholinergics as treatment may potentiate TC further based on their mechanisms of action. TC in males is a rare occurrence and it is important to consider that males present with TC differently. They present with more physical rather than emotional precipitators, like our patient and with higher incidence of cardiogenic shock and out-ofhospital cardiac arrest. While the cause of TC is slowly being elucidated, the reason for higher prevalence in females is still unclear.

Может ли кардиомиопатия такоцубо возникнуть вследствие инфаркта миокарда?

Takotsubo cardiomyopathy (TCM) is a well-known complication of many conditions associated with emotional or physical stress. Abnormal catecholamine release has been hypothesized to be the main cause of TCM. Myocardial infarction (MI) is associated with release of large amounts of catecholamines. We present here two cases in which patients simultaneously suffered from acute MI and TCM. In these elderly women without prior history of severe somatic diseases we have not revealed any external stressing factor responsible for the initiation of the disease. Therefore, we have considered primary coronary event (acute MI) to be a triggering factor of TCM manifestation.

Predictors of Short- and Long-Term Outcomes of Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy (TC) is a reversible cardiomyopathy with a benign short-term prognosis but is associated with recurrence rate of 10%. Clinical variables that predict long-term mortality and recurrence are unknown; 56 consecutive patients presenting to a single urban medical center who fulfilled the Mayo Clinic criteria for the diagnosis of TC were included. Patients were followed with 100% completeness; >60 clinical factors were analyzed, including presentation, treatment, electrocardiogram, and echocardiographic, angiographic, and demographic variables. Survival analysis was performed using the Kaplan-Meier function and Cox proportional hazards regression models. There were 15 deaths during follow-up: 5 in-hospital, 4 before 90days, and 6 after 90days. Mean survival was 4.47years (95% confidence interval 3.81 to 5.13). All short-term survivors had repeat ejection fraction evaluation demonstrating improvement; 45 of 56 patients were women and 96% were postmenopausal. The nonfatal recurrence rate was 1.8%. QTc interval at presentation was the factor most strongly predictive of overall outcome, after intubation. All patients with mortality had QTc intervals between 400 and 550 ms. In conclusion, this study demonstrates the prognostic significance of QTc prolongation at presentation in TC. Because the cause of TC involves intense catecholamine release and hyperadrenergic tone, the QTc may reflect the individual impact on myocardial repolarization and the balance between sympathetic innervation and parasympathetic compensation. In conclusion, in thisseries, TC was associated with an 8.9% in-hospital mortality, an additional 17.9% mortality after discharge, and a nonfatal recurrence rate of 1.8%. Moreover, the QTc on presentation with TC was predictive of outcome.

Takotsubo cardiomyopathy and transient thyrotoxicosis during combination therapy with interferon-alpha and ribavirin for chronic hepatitis C

BackgroundThyroid dysfunction is a common complication of chronic hepatitis C (CHC) and its therapy. Takotsubo cardiomyopathy (TCM) is a multifactorial, stress related cardiomyopathy, rarely reported in association with thyrotoxicosis. Simultaneous occurrence of TCM and thyrotoxicosis due to hepatitis C and its treatment has never been reported.Case presentationA 47-year-old woman was admitted for acute chest pain, dyspnea, palpitations and diaphoresis. She had been diagnosed with CHC and had undergone 7 months of IFNα and Ribavirin therapy. At admission electrocardiogram (ECG) showed ST segment elevation, negative T waves and troponin was elevated suggesting ST segment elevation myocardial infarction (STEMI). Echocardiography demonstrated left ventricular apical akinesia and ballooning, with a left ventricular ejection fraction (LVEF) of 35%. Contrast angiography showed normal epicardial coronaries, yet a ventriculogram revealed left ventricular apical ballooning, consistent with TCM. Cardiac MRI showed left ventricle apical ballooning and no late enhancement suggesting the absence of any edema, scar or fibrosis in the left myocardium. She was diagnosed with non-autoimmune destructive thyroiditis: TSH=0.001 mU/L, free T4=2.41 ng/dl, total T3=199 ng/dl and negative thyroid antibodies. The thyroid ultrasonography showed a diffuse small goiter, no nodules and normal vascularization of the parenchyma. Following supportive treatment she experienced a complete recovery after a few weeks and she successfully completed her antiviral treatment, with no thyroid or cardiovascular dysfunction ever since. In patients treated with IFNα for CHC, the prevalence of thyroid dysfunction varies between 2.5–45.3% of cases. TCM is a stress related cardiomyopathy characterized by elevated cardiac enzymes, normal coronary angiography and an acute, transient, left ventricular apical dysfunction that mimics myocardial infarction. Most of the patients survive the initial acute event, typically recover normal ventricular function within one to four weeks and have a favorable outcome, as was the case with our patient. Thyrotoxicosis induced stress cardiomyopathy is rare and has been mostly reported in association with Graves’ disease, thyroid storm, thyrotoxicosis factitia or following radioiodine therapy for toxic multinodular goiter.ConclusionRoutine thyroid screening should be done in patients receiving IFN-alpha and Ribavirin for CHC and thyrotoxicosis should be considered as a possible and treatable underlying cause of TCM.

Repeated use of albuterol inhaler as a potential cause of Takotsubo cardiomyopathy.

Patient: Female, 78Final Diagnosis: Takotsubo cardiomyopathySymptoms: Chest discomfort, chest pain, dyspnea, short of breathMedication: —Clinical Procedure: —Specialty: CardiologyObjective:Unusual or unexpected effect of treatmentBackground:Takotsubo cardiomyopathy is an increasingly recognized cardiac condition that usually results from an acute stressor. Some medications are becoming recognized as possible stressors. Albuterol is widely used in general medicine. We report an unusual link between Takotsubo cardiomyopathy and albuterol.Case Report:A 78-year-old woman presented to our emergency department for chest pain of 2-day duration. The patient had been taking albuterol inhaler therapy for worsening shortness of breath followed by chest pain. Her albuterol use was excessive. There were no other acute stressors. The electrocardiogram showed ST-elevations in the anterior and inferior leads. Emergent coronary angiography showed noncritical coronary artery disease and left ventriculography showed apical ballooning.Conclusions:When patients taking albuterol present with acute chest pain in the absence of other etiologies, beta-agonist-induced Takotsubo cardiomyopathy should be considered.

Epicardial coronary artery spasm as cause of capecitabine-induced tako tsubo cardiomyopathy

Cardiotoxicity of fluoropyrimidines like the orally administered capecitabine and the intravenous 5-fluorouracil (5-FU) is a well-known clinical challenge [1, 2]. The cardiotoxic effects of both agents seem to occur through the same mechanisms [3]. However, capecitabine-induced cardiotoxicity is less common because it obtains its pharmacological active form through a three-step enzymatic conversion, while the last step is catalyzed by the enzyme thymidine phosphorylase, which is more active in neoplastic tissues [4, 5]. But this enzyme is also actively expressed in arteriosclerotic plaques, which is thought to be one potential mechanism leading to coronary side effects, especially in patients with a history of coronary artery disease [3]. Until today, numerous reports have shown cardiac side effects of fluoropyrimidines. However, there is no explicit evidence of capecitabine as a direct trigger for tako tsubo cardiomyopathy (TTC). Amongst other causes, coronary artery spasm is discussed as a potential cause of TTC [6]. Epicardial vasospasm is a widely accepted hypothetical pathomechanism of 5-FU-associated cardiac side effects [7, 8]. Therefore, fluoropyrimidines could be plausible triggers for TTC and the following case will strengthen this possible connection. An 81-year-old female with metastatic breast cancer was admitted to our emergency unit with acute chest pain and severe dyspnoea. The symptoms began at about 4 p.m., shortly after a 1-h workout as part of a diabetes group training. On the same day, in the morning at about 9 a.m., the patient had received the first dose of capecitabine (1,500 mg). The patient did not report any extraordinary emotional stress, but had a history of obstructive coronary artery disease. Five years ago she had undergone percutaneous coronary intervention in the left anterior descending coronary artery (LAD). The patient further suffered from insulin-dependent diabetes mellitus type 2, hypercholesterolemia, hypertension and peripheral vascular disease. On admission the symptoms were relieved by sublingual nitroglycerin, but recurred after a few minutes. The electrocardiogram (ECG) showed sinus rhythm with ST-segment elevations, which had not been detected in a routine ECG 3 weeks ago (Fig. 1a). High sensitive cardiac troponin T concentration was 282 pg/ml (n \ 14 pg/ml). The patient was treated with acetylsalicylic acid (500 mg intravenous), clopidogrel (600 mg orally) and heparin (5,000 units intravenous) because of the suspicion of acute ST-elevation myocardial infarction. No abnormalities were discovered by physical examination. Blood pressure was 140/63 mm/Hg. Cardiac catheterization was performed immediately. Ventriculography showed apical dyskinesia Electronic supplementary material The online version of this article (doi:10.1007/s00392-013-0636-4) contains supplementary material, which is available to authorized users.

A rare cause of takotsubo cardiomyopathy in the ICU

A rare cause of takotsubo cardiomyopathy in the ICU

Takotsubo Cardiomyopathy Associated with Thyrotoxicosis: A Case Report and Review of the Literature

Takotsubo or stress-induced cardiomyopathy is a form of reversible cardiomyopathy commonly associated with emotional or physical stress. Thyrotoxicosis has been identified as a rare cause of Takotsubo cardiomyopathy, with only 12 cases reported in the literature. Here, we report a case of thyroid storm presenting with Takotsubo cardiomyopathy in the setting of Graves' disease. A 71-year-old woman presented with abdominal pain, vomiting, confusion, and history of weight loss. She was initially diagnosed and treated for diabetic ketoacidosis at another hospital and was transferred to our hospital one day after initial presentation because of concern for acute coronary syndrome. A diagnosis of Takotsubo cardiomyopathy was made on the basis of cardiac catheterization. At that time, she was diagnosed and treated for thyroid storm. Follow-up 7 weeks later revealed improvement of her cardiac function and near-normalization of thyroid hormone levels. In this patient, who presented with symptoms of heart failure, acute coronary syndrome was initially considered, but the diagnosis of Takotsubo cardiomyopathy associated with thyroid storm was ultimately made based on cardiac catheterization and laboratory investigation. Thyrotoxicosis is associated with adverse disturbances in the cardiovascular system. Takotsubo cardiomyopathy could be a presenting manifestation of thyroid storm, perhaps related to excess catecholamine levels or sensitivity.

Acute Mitral Regurgitation in Suspected Acute Coronary Syndrome: What Is the Cause?

Patients presenting with acute chest pain and suspected acute coronary syndrome (ACS) who have nonobstructive coronary disease on angiography, but new regional wall motion abnormalities are often diagnosed with takotsubo cardiomyopathy (TTC). The cause of TTC is often physical or emotional stress, and this clinical syndrome occurs more often in women than men. When hemodynamically significant mitral regurgitation (MR) accompanies TTC, the mechanism must be carefully elucidated, as systolic anterior motion (SAM) of the mitral valve can cause significant MR and left ventricular outflow tract (LVOT) obstruction. These patients can be conservatively managed, with SAM-associated MR and LVOT obstruction resolving with medical therapy as TTC-associated left ventricular (LV) dysfunction resolves, as opposed to true ACS where further intervention for MR is often necessary. This case report describes 2 cases of TTC presenting with severe MR, who were initially thought to have ACS-associated MR caused by ischemia, but on further echocardiographic interrogation were found to have SAM-associated MR which resolved along with resolution of LV wall motion abnormalities on medical therapy by follow-up echocardiography.

Takotsubo cardiomyopathy in a patient with pulmonary embolism

Takotsubo cardiomyopathy is an acute cardiac syndrome characterized by transient regional wall motion abnormalities of the left ventricular apex or midventricle. Patients often present with chest pain or dyspnoea, ST-segment elevation, and minor elevations of cardiac enzyme levels. Takotsubo cardiomyopathy has been associated with severe emotional or physical stress such as severe burns, spinal cord injury, subarachnoid haemorrhage, and multiple traumas. We report a case of takotsubo cardiomyopathy in a 79-year-old woman with pulmonary embolism. Although pulmonary embolism has been listed as a potential cause of takotsubo cardiomyopathy, this is the first case reported with this association.

An Angiographic and Intravascular Ultrasound Study of the Left Anterior Descending Coronary Artery in Takotsubo Cardiomyopathy

The precise cause of takotsubo cardiomyopathy (TC) remains controversial. Plaque rupture with transient thrombotic occlusion of a transapical left anterior descending coronary artery (LAD) has been advanced as a potential mechanism. To explore this hypothesis, the investigators analyzed data from 11 patients prospectively enrolled in the Rhode Island Takotsubo Cardiomyopathy Registry who underwent coronary angiography and intravascular ultrasound evaluation of the LAD during their initial presentation. Despite the presence of nonobstructive coronary artery disease, no culprit lesion was identified in any patient. Similarly, the course of the LAD failed to account for the characteristic left ventricular apical ballooning seen in TC. In conclusion, an atherosclerotic coronary lesion in the LAD causing an aborted myocardial infarction may not be the primary underlying cause of TC, and nonobstructive coronary artery disease and TC may coexist without a direct causal association.

Multidisciplinary assessment of tako tsubo cardiomyopathy: a prospective case study

BackgroundThe cause of tako tsubo cardiomyopathy remains unclear. We used a multidisciplinary approach to investigate if a common pathophysiological denominator could be outlined.MethodsWithin 3 days following symptom presentation and again after 3 months we investigated all patients coming to our institution and diagnosed with tako-tsubo cardiomyopathy. Patients underwent extensive biochemical screening. Left ventricular function was evaluated by echocardiography and contrast-enhanced cardiac magnetic resonance imaging. Cardiac autonomic function was studied by heart rate variability and signal-averaged electrocardiogram and posttraumatic stress and depression were investigated by questionnaires (the Posttraumatic Stress Syndrome 10-Questions Inventory, PTSS-10 and the Montgomery-Åsberg depression rating scale, self rated version, MADRS-S).ResultsDuring 2 years, 13 consecutive patients were included. Markers of myocardial damage and heart failure were slightly to moderately elevated and ejection fraction (echocardiography and MRi) was moderately reduced at hospitalization and improved to normal values in all patients. Signal averaged ECG demonstrated a statistically significant shorter duration of the filtered QRS complex in the acute phase as compared to follow-up. In heart rate variability analysis, SDNN and SDANN were shorter acutely compared to follow-up. Two patients fulfilled criteria for posttraumatic stress syndrome while 7 patients were in the borderline zone. There was a statistically significant inverse correlation between PTSS-10 score and QRS duration in the signal-averaged ECG (r = -0.66, P = 0.01).ConclusionsPatients with tako tsubo cardiomyopathy have altered cardiac autonomic function and a high incidence rate of borderline or definite posttraumatic stress syndrome acutely. This is in line with findings in patients with myocardial infarction and does not allow conclusions on cause and effect.

Takotsubo Cardiomyopathy Is Not Due to Plaque Rupture: An Intravascular Ultrasound Study

Plaque rupture with subsequent transient thrombotic coronary occlusion by a fast-dissolving clot is one of the proposed pathogenic mechanisms in Takotsubo cardiomyopathy (TC). The aim of this study was to seek evidence for the hypothesis of transient coronary thrombosis as the underlying mechanism of TC by means of intravascular ultrasound (IVUS). In our database of 63 consecutive patients with TC we identified 10 patients (16%) who had undergone IVUS during their initial left heart catheterisation. A median length of 67 mm of the left anterior descending artery was analyzed (interquartile range [IQR]: 63.3-70.1 mm). Median lumen diameter, median vessel diameter, median plaque and media volume were 2.9 mm (IQR: 2.7-3.1 mm), 4.2 mm (IQR: 3.8-4.4 mm), and 90.9 mm(3) (IQR: 70.4-101.4 mm(3)), respectively. Plaque rupture, positive remodeling, and presumed intracoronary thrombus were absent in all patients. In conclusion, plaque rupture does not account for the regional wall motion abnormalities observed in TC. The previously reported observation of plaque rupture in TC seems to constitute an incidental finding. We suggest that the theory of aborted myocardial infarction as the underlying cause of TC should be abandoned once and for all.

Successful Retrial of ECT Two Months After ECT-Induced Takotsubo Cardiomyopathy

heart failure; however, recovery of cardiac function is often complete within the first week following the insult. Cardiac enzymes may be mildly elevated, but on cardiac catheterization there is usually no evidence of coronary artery disease, or only "mild luminal irregularities" may be noted (7). Contraction band necrosis may be seen on biopsy in the more serious cases. The cause of takotsubo cardiomyopathy is unknown, but several mechanisms have been suggested, including ischemia from coronary artery spasm, microvascular spasm, and direct myocyte injury (5).

P-23 Comparison of Myocardial Damage in Takotsubo Cardiomyopathy and Sympathetic Nerve Distribution Pattern of Myocardium in Human Heart

Background: The cause of takotsubo cardiomyopathy is still unknown. Several mechanisms have been proposed, including neurologically mediated myocardial stunning. Objective:We assessed the relationship between myocardial damage and sympathetic nerve distribution pattern in myocardium in takotsubo cardiomyopathy. Methods: Endomyocardial biopsied specimens in 2 takotsubo cardiomyathy patients with transient left ventricular ouflow tract obstuction were studied. These specimens were evaluated the pattern and area of myocarcdial damage by microscope and electron microscope. We compared these results and nerve distribution pattern in normal human heart that had already been studied by immunohistochemical staining using anti-tyrosine-hydroxylase (TH) antibody for the detection of sympathetic nerve. Results: Hypercontraction of myocardium and cardiac myocyte loss was detected as myocardial damage in the biopsied myocardium of takotsubo cardiomyopathy. These myocardial damages were seen in the small areas and these area patterns were similar to the peripheral TH-positive nerve distribution patterns in the myocardium. Conclusion: These results suggest that myocardial damage may be related to peripheral sympathetic nerve in takotsubo cardiomyopathy.

Catecholamines and Estrogen Are Involved in the Pathogenesis of Emotional Stress‐induced Acute Heart Attack

Emotional stress triggers takotsubo cardiomyopathy in postmenopausal women. Clinical analysis of autonomic nervous function has revealed a transient increase of sympathetic nervous activity and decrease of vagal nervous activity. Immobilization (IMO) stress of rats can reproduce the electrocardiographic and left ventriculographic changes that occur in takotsubo cardiomyopathy, both of which are prevented by combined blockade of alpha- and beta-adrenoceptors. Estrogen supplementation partially attenuated these cardiac changes. It also attenuated the IMO-induced increase of c-Fos immunoreactivity, or c-fos mRNA expression in the lateral septum, medial amygdaloid nucleus, paraventricular hypothalamic nucleus, dorsomedial hypothalamic nucleus, laterodorsal tegmental nucleus, and locus ceruleus; these regions contain central sympathetic neurons and neurons with immunoreactive estrogen receptors. It also downregulated c-fos mRNA expression in the adrenal gland and the heart, suggesting an increase of estrogen attenuated the stress-induced hypothalamo-sympathoadrenal outflow from the central nervous system to the target organs. Estrogen treatment also upregulated the levels of cardioprotective substances, such as atrial natriuretic peptide and heat shock protein 70, in the heart. These data suggest that reduction of estrogen levels following menopause might be involved in the primary cause of takotsubo cardiomyopathy both by indirect action on the nervous system and by direct action on the heart.