Cases reported "Myocardial Stunning"

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1/16. myocardial stunning caused by sympathetic nerve injury after an operation on cervical vertebrae.

    In this case, electrocardiographic inverted T waves appeared after cervical laminaplasty and echocardiogram showed temporary wall motion abnormality. Myocardial metaiodobenzylguanidine (MIBG) uptake was obviously reduced in the same area where the wall motion abnormalities appeared in the echocardiogram, although no abnormalities were detected with myocardial thallium scintigraphy and coronary angiography. The myocardial stunning was caused by injury to the sympathetic nerves from a surgical procedure on the cervical vertebrae.
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2/16. myocardial stunning in hyperthyroidism.

    The cases of two patients with hyperthyroidism and acute left ventricular (LV) dysfunction with segmental wall motion abnormalities resulting in heart failure are reported. Both had electrocardiographic changes mimicking ischemic coronary artery disease. Treatment with antithyroid medications, beta blockers, and angiotensin-converting enzyme inhibitors rapidly restored LV function. The rapid reversibility suggests a role for myocardial stunning, an important entity to recognize in hyperthyroidism since this form of LV dysfunction can be reversed with appropriate treatment.
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3/16. myocardial stunning after streptokinase: what is the significance of the Q wave?

    A 58 year old woman presented with symptoms and electrocardiographic features consistent with acute infero-posterior myocardial infarction. The attempt at reperfusion with aspirin and thrombolytic treatment was deemed unsuccessful in view of Q wave development on ECG, a 48 hour period of hypotension and oliguria, and extensive wall motion abnormality on echocardiography. This was at variance with findings of a minimal cardiac enzyme rise. On the seventh day, list mode acquired, ECG gated, cineimages of perfusion and blood pool demonstrated strikingly normal perfusion despite continued contractile dysfunction. Six weeks later ECG, echocardiography, and radionuclide blood pool ventriculography had all normalised consistent with resolution of myocardial stunning. This practical method for the diagnosis of stunning, the significance of the ECG changes in particular the development of Q waves, and the time taken to resolution of this phenomenon are discussed.
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4/16. Stunned myocardium after hip arthroplasty.

    We report a case of ST-segment elevation occurring in all leads of the ECG during hip arthroplasty. It is thought that this resulted from a stunned myocardium because wall motion abnormalities were reversible, there was no evidence of fixed or vasospastic coronary occlusion and there was only a slight increase in serial cardiac enzymes. Treatment with nicorandil improved the patient's cardiac function. A [123I]MIBG test revealed a high myocardial washout rate, suggesting that the stunned myocardium was caused by exposure to excessive norepinephrine induced by anaesthesia or surgery.
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5/16. Coronary microvascular abnormality in the reversible systolic dysfunction observed after noncardiac disease.

    Acute reversible left ventricular wall motion abnormalities mimicking myocardial stunning have been reported with noncardiac disease and their coronary angiograms did not demonstrate organic stenosis or vasospasm in the epicardial coronary arteries. Thus, this mechanism has not yet been fully clarified. Two patients are reported as demonstrating acute reversible wall motion abnormalities after noncardiac disease. The electrocardiographic and echocardiographic findings mimicked myocardial stunning and confirmed the previous reports. The coronary angiograms did not show any corresponding coronary stenosis or vasospasm, but did show a reduced coronary flow reserve. Cardiac metaiodobenzylguanidine scintigraphy demonstrated regional defects involving the apex, a decreased heart/mediastinum ratio and an enhanced washout rate, which partially returned to normal after 3 months. Microvascular dysfunction and sympathetic nervous abnormalities might be responsible for the reversible contractile impairment.
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6/16. Anteroapical stunning and left ventricular outflow tract obstruction.

    Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.
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7/16. Extensive myocardial stunning showing transient regression of prolonged T wave inversion and prolonged sympathetic denervation.

    A 69-year-old woman was admitted to the hospital with palpitations. Although left ventriculography showed extensive akinesis except in the basal hyperkinetic segment, coronary angiography showed normal coronary arteries. 123I-metaiodobenzylguanidine (MIBG) accumulation was obviously reduced in the anteroseptal, apical and inferior areas. Inverted T waves developed on day 3 and disappeared on day 104 after transient regression. echocardiography showed normal left ventricular motion two weeks later. ergonovine provocation test showed no vasospasm and thallium-201 showed no perfusion defect on day 46. electrocardiography and MIBG returned to normal on day 216. These findings suggest prolonged sympathetic nerve injury in extensive myocardial stunning.
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8/16. Reversible left ventricular systolic dysfunction--reversibility of coronary microvascular abnormality.

    Reversible left ventricular wall motion abnormalities mimicking myocardial infarction have been reported in patients with a noncardiac illness. Their coronary angiograms do not demonstrate organic stenosis or epicardial coronary vasospasm. In this article, two cases of reversible left ventricular contraction abnormality are presented. electrocardiography showed deep inverted T waves in precordial leads, and the echocardiography revealed diffuse akinesis of the apical region in the acute phase. coronary angiography showed no significant stenosis or occlusion in either patient. thallium scintigraphy showed no defect, while the metaiodobenzylguanidine scintigraphy demonstrated significant defects in the apex. The relative coronary flow reserve ratio, measured with an intracoronary Doppler flow wire, was significantly reduced in both patients. Myocardial contrast echocardiography revealed a reversible perfusion defect in the apex in the acute phase in case 2. Transiently impaired coronary microcirculation was thought to be involved in the pathogenesis of the reversible left ventricular dysfunction observed in these patients.
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9/16. Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with hyperthyroidism.

    myocardial stunning with hyperthyroidism is rare. A 79-year old woman with hyperthyroidism was admitted to our hospital complaining of palpitations due to paroxysmal atrial fibrillation. An echocardiogram showed akinesis of the apical wall which was not observed 2 weeks before admission. cardiac catheterization performed in the acute phase showed normal coronary arteries and no evidence of provocative spasms. The wall motion abnormality disappeared entirely after 1 week in hospital. We report a case of transient left ventricular dysfunction, so called "takotsubo" cardiomyopathy, associated with hyperthyroidism.
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10/16. Intraventricular colloid cyst, hydrocephalus and neurogenic stunned myocardium.

    OBJECTIVE: To report the occurrence of neurogenic stunned myocardium in the context of a hydrocephalus due to a third ventricle colloid cyst. DESIGN: Case report. SETTING: Neurocritical care unit of a university hospital. PATIENT: The case of a 33-year-old woman with an intraventricular cerebral colloid cyst who developed hydrocephalus, cardiac arrest and survived is presented. Workup was consistent with neurogenic stunned myocardium in the context of acute hydrocephalus due to an intraventricular colloid cyst. RESULTS: The patient had decreased left ventricular ejection fraction, apex-sparing areas of hypokinesis and akinesis, wall motion abnormalities not matching a particular vascular territories, the peak troponin t level of 0.09 ng/ml and had normal coronary arteries at angiography. Seven days after the initial event the cardiac function recovered. Tumor resection was successfully performed. At 10 months after discharge, the only complaint was mild memory disturbance, she was completely functional with no evidence of seizures or of cardiac dysfunction. CONCLUSION: The sudden elevation of intracranial pressure, with the subsequent decreased cerebral perfusion pressure induces a vigorous cerebro-protective neuroendocrine system activation that can lead to the neurogenic stunned myocardium. Sudden death in patients with colloid cysts may be related to acute neurogenic cardiac dysfunction, and not necessarily cerebral herniation(s), as previously thought.
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