Cases reported "Myocardial Stunning"

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1/5. 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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2/5. Tako-Tsubo cardiomyopathy: new insights into the possible underlying pathophysiology.

    Tako-Tsubo cardiomyopathy is characterised by an atypical distribution of left ventricular (LV) dysynergy with apical ballooning and compensatory basal hyperkinesis. coronary angiography is normal. Several substrates have been put forward to explain the underlying pathophysiology such as raised catecholamine levels (due to physical or emotional stress), multivessel epicardial coronary spasm or diffuse microvascular spasm. However, the pathophysiology has not yet been fully clarified. We present a series of cases whose findings could explain the mechanism underlying this syndrome. Four consecutives patients, all female, were admitted with the clinical features typical of Tako-Tsubo syndrome. In all, severe widespread transient LV mid-apical a/dyskinesia was associated with a mid-cavity dynamic obstruction which resolved prior to the resolution of the LV wall motion abnormalities. In all cases the dynamic LV obstruction was related to localised mid-ventricular septal thickening. After improvement in wall motion, a low-dose strain/strain rate dobutamine stress-echocardiography (DSE) was performed to determine the underlying ischaemic substrate. This provoked an LV mid-cavity gradient at peak dose in all. Regional deformation changes during DSE showed the affected myocardium to have the typical response diagnostic of regional stunning. CONCLUSION: We postulate that an important unrecognised factor in the development of Tako-Tsubo cardiomyopathy is the presence of abnormal myocardial functional architecture (such as localised mid-ventricular septal thickening), which in the presence of dehydration and/or raised catecholamine levels due to physical or emotional stress, leads the development of a severe transient LV mid-cavity obstruction. This effectively sub-divides the LV into two functionally different chambers with a marked increase in wall stress in the high pressure distal apical chamber. This, in combination with the abnormal high circulating catecholamine levels, induces widespread sub-endocardial ischaemia which is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels the interventricular gradient resolves and distal function recovers. Low dose SR/S DSE confirms that the distal ischaemic substrate is myocardial stunning.
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3/5. Levosimendan: a promising treatment for myocardial stunning?

    We report a case of a 55-year-old male undergoing major orofacial cancer surgery. A stent to the left anterior descending artery had been implanted for ischaemic heart disease 3 years previously. Twenty-four hours after uneventful anaesthesia and surgery, the patient developed myocardial infarction and cardiogenic shock. Immediate percutaneous transluminal coronary angioplasty, intra aortic balloon counterpulsation, and catecholamine therapy failed to stabilise haemodynamics. In light of successful reperfusion therapy and an only moderate elevation of troponin i, myocardial stunning rather than myonecrosis was considered to be the major contributor to life-threatening left ventricular failure. Therefore, the calcium-sensitising drug levosimendan, which exerts positive inotropic activity without increasing myocardial oxygen demand, was administered as a rescue medication. Within 24 h, levosimendan resulted in decreased filling pressures, reduced left ventricular end-diastolic volume, and augmented systemic pressures. Seven days following surgery, the patient was discharged from the intensive care unit in good clinical condition.
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4/5. norepinephrine, enoximone, and nitric oxide for treatment of myocardial stunning and pulmonary hypertension in a newborn with diaphragmatic hernia.

    A newborn with right diaphragmatic hernia suffered myocardial stunning and suprasystemic pulmonary hypertension secondary to postpartal asphyxia. In addition to conventional therapy, norepinephrine, enoximone, and inhalational nitric oxide were successfully used. norepinephrine improved myocardial perfusion pressure; the addition of enoximone, a phosphodiesterase-inhibitor, to beta-adrenergic agents increased cardiac performance. with decreasing concentrations of inhalational nitric oxide, severe pulmonary hypertension resolved after a few days, suggesting that transient endothelial dysfunction was partially responsible for pulmonary vasoconstriction in the newborn with congenital diaphragmatic hernia.
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5/5. Hibernating myocardium caused by isolated, radiation induced left main stem coronary artery stenosis.

    A 45 year old man presented with a five week history of worsening exertional dyspnoea and orthopnoea. He had also noted mild, bilateral ankle swelling. The patient had been diagnosed with stage III Hodgkin's lymphoma in 1968 at the age of 21. During the same year he underwent total nodal irradiation followed by chemotherapy in 1971. He had remained entirely asymptomatic over the course of the next 24 years with no evidence of relapse. Cardiac catheterisation undertaken soon after admission revealed a tight left main stem stenosis with a left dominant system. Left ventriculogram showed severe, global hypokinesia, and raised left ventricular end diastolic pressure (22 mm Hg). Urgent coronary artery bypass graft surgery was carried out. He made an uncomplicated recovery and his condition improved sufficiently to allow discharge eight days following the procedure. His heart failure slowly resolved and repeat transthoracic echocardiogram performed six months after surgery showed an unequivocal improvement in left ventricular function. Left ventricular ejection fraction continued to improve and increased from 23% at two months to 42% at two years. He currently remains entirely asymptomatic off all medication.
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