138 research outputs found

    Recurrent takotsubo cardiomyopathy in the setting of transient neurological symptoms: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>First described in Japan, takotsubo cardiomyopathy is increasingly becoming recognized worldwide as a cause of sudden and reversible diminished left ventricular function characterized by left apical ballooning and hyperkinesis of the basal segments, often with symptoms mimicking a myocardial infarction. Associated with physical or emotional stress, its exact pathogenesis has not been established, though evidence supports a neurohumoral etiology. Additionally, recurrence of this condition is rare. In this report, we present a rare case of recurrent takotsubo cardiomyopathy in a post-menopausal woman who presented with transient neurological complaints on both occasions.</p> <p>Case presentation</p> <p>We present a rare case of a 76-year-old Caucasian woman with no history of congestive heart failure who presented to our emergency department twice with transient neurological complaints. On the first occasion, she was found to have transient aphasia which resolved within 24 hours, yet during that period she also developed symptoms of congestive heart failure and was noted to have a new, significantly depressed ejection fraction with apical akinesis and possible apical thrombus. One month after her presentation a repeat echocardiogram revealed complete resolution of all wall motion abnormalities and a return to baseline status. Seven months later she presented with ataxia, was diagnosed with vertebrobasilar insufficiency, and again developed symptoms and echocardiography findings similar to those of her first presentation. Once again, at her one-month follow-up examination, all wall motion abnormalities had completely resolved and her ejection fraction had returned to normal.</p> <p>Conclusion</p> <p>Though the exact etiology of takotsubo cardiomyopathy is unclear, a neurohumoral mechanism has been proposed. Recurrence of this disorder is rare, though it has been reported in patients with structural brain abnormalities. This report is the first to describe recurrent takotsubo cardiomyopathy in a patient with transient neurological symptoms. In our patient, as expected in patients with this condition, complete resolution of all left ventricular abnormalities occurred within a short period of time. It is important for clinicians to be aware of this increasingly recognized syndrome, including its association with recurrence, especially in the clinical setting of neurologic dysfunction.</p

    Emotional stress as a trigger of myasthenic crisis and concomitant takotsubo cardiomyopathy: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Myasthenia gravis is a neuromuscular junction post-synaptic autoimmune disorder. Myasthenic crisis is characterized by respiratory failure requiring mechanical ventilation. Takotsubo cardiomyopathy is a rare clinical syndrome defined as a profound but reversible left ventricular dysfunction in the absence of coronary artery disease.</p> <p>Case presentation</p> <p>We report a unique case of a 60-year-old Hispanic woman with myasthenia gravis who developed takotsubo cardiomyopathy and concomitant myasthenic crisis that appear to have been triggered by a stressful life event. On admission, she presented with severe mid-sternal chest pain and shortness of breath shortly after a personally significant stressful life event. A pertinent neurological examination showed bilateral facial weakness and right ptosis. The left ventriculogram showed apical ballooning with hyperdynamic proximal segments with sparing of the apex. Her troponin I level was elevated, while cardiac catheterization revealed no significant coronary artery disease. The findings were consistent with takotsubo cardiomyopathy. Shortly after cardiac catheterization, she developed bilateral ophthalmoparesis and significant bulbar and respiratory muscle weakness. Forced vital capacity values were persistently less than 1 L. The patient developed respiratory failure and required endotracheal intubation. After plasmapheresis and corticosteroid treatment, her clinical course improved with successful extubation. A normal left ventricle chamber size and a normal ejection fraction were noted by an echocardiogram repeated 10 months later.</p> <p>Conclusion</p> <p>This is the first reported case of the simultaneous triggering of both takotsubo cardiomyopathy and myasthenic crisis by the physiologic consequences of a state of severe emotional stress. We hypothesize that the mechanism underlying the rare association of takotsubo cardiomyopathy with myasthenic crisis involves excessive endogenous glucocorticoid release, a high-catecholamine state, or a combination of both. We advocate careful cardiac monitoring of myasthenia gravis patients during acute emotional or physical stress, as there is potential risk of developing takotsubo cardiomyopathy.</p

    Tako-tsubo cardiomyopathy after administration of ergometrine following elective caesarean delivery: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Tako-tsubo cardiomyopathy (stress-induced cardiomyopathy or transient left ventricular ballooning) is characterized by clinical suspicion of an acute myocardial infarction with transient apical or midventricular dyskinesia of the left ventricle without significant coronary stenosis on angiography. The etiology of this disease remains obscure. One of the possible causes is myocardial ischemia induced by coronary vasospasm due to sympathetic activation. It has been hypothesized that the application of ergometrine could induce tako-tsubo cardiomyopathy.</p> <p>Case presentation</p> <p>We report the case of a 28-year-old Turkish woman who developed tako-tsubo cardiomyopathy after administration of ergometrine for release of placenta and prevention of bleeding during the post-partum phase in the course of an elective caesarean delivery. Tako-tsubo cardiomyopathy was diagnosed by echocardiography and urgent cardiac magnetic resonance imaging. A coronary angiography was not performed because of the absence of myocardial necrosis or ischemia and signs of myocarditis on cardiac magnetic resonance imaging.</p> <p>Conclusion</p> <p>This life-threatening disease should be excluded in the differential diagnosis by comparing the symptoms with those of typical heart failure, particularly after use of ergometrine.</p

    Dobutamine stress echocardiography for assessing the role of dynamic intraventricular obstruction in left ventricular ballooning syndrome

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    <p>Abstract</p> <p>Background</p> <p>Dynamic intraventricular obstruction has been observed in patients with left ventricular ballooning syndrome (LVBS) and has been hypothesized as a possible mechanism of the syndrome. The aim of this study was to assess the prevalence and significance of dynamic intraventricular obstruction in patients with LVBS.</p> <p>Methods and Results</p> <p>Dobutamine stress echocardiography was carried out in 22 patients with LVBS (82% apical), all women, aged 68 ± 9 years. At baseline 1 patient had a > 30 mmHg LV gradient; during stress a LV gradient > 30 mm Hg developed in 6/21 patients (28%) and was caused by systolic anterior motion of the mitral valve in the 3 patients with severe gradient (mean 116 ± 29 mmHg), who developed mitral regurgitation and impaired apical wall motion and by obstruction at mid-ventricular level in the other 3 with a moderate gradient (mean 46 ± 16 mmHg). Compared with patients without obstruction those with obstruction had a greater mean septal thickness (11.6 ± .6 vs 9.8. ± 3, p < .01), a higher prevalence of septal hypertrophy (71% vs 7%, p < .005) and a higher peak wall motion score index (1.62 ± .4 vs 1.08 ± .4, p < .01).</p> <p>Conclusion</p> <p>Spontaneous or dobutamine-induced dynamic LV obstruction is documented in 32% of patients with LVBS, is correlated with the presence of septal hypertrophy and may play a role in the development of LVBS in this subset of patients. In those without septal hypertrophy a dynamic obstruction is rarely induced with dobutamine and is unlikely to be a major pathogenetic factor of the syndrome.</p
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