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1/4. Apical ballooning of the left ventricle: first series in white patients.

    BACKGROUND: A cardiac syndrome of "apical ballooning" was recently described, consisting of an acute onset of transient extensive akinesia of the apical and mid portions of the left ventricle, without significant stenosis on the coronary angiogram, accompanied by chest symptoms, ECG changes, and a limited release of cardiac markers disproportionate to the extent of akinesia. Until now, this syndrome has been reported only in Japanese patients. OBJECTIVE: To describe 13 white patients who presented with this syndrome over the previous four years. RESULTS: All but one of the patients were women with a mean age of 62 years. Eight of them presented with chest pain, of whom six had cardiogenic shock. In nine patients a triggering factor was identified: emotional stress in three, trauma in one, pneumonia in one, asthma crisis in one, exercise in two, and cerebrovascular accident in one. In all patients left ventriculography showed very extensive apical akinesia ("apical ballooning") in the absence of a significant coronary artery stenosis, not corresponding with the perfusion territory of a single epicardial coronary artery. Mean maximal creatine kinase MB and troponin rise were 27.4 microg/l (range 5.2-115.7 microg/l, median 16.6 microg/l) and 18.7 microg/l (range 2.0-97.6 microg/l, median 14.5 microg/l), respectively. Six patients were treated with intra-aortic balloon counterpulsation. One patient died of multiple organ failure. On necropsy, no myocardial infarction was found. In the 12 survivors, left ventricular systolic function recovered completely within three weeks. CONCLUSIONS: This is the first series of "apical ballooning" to be reported in white patients. Despite dramatic initial presentation, left ventricle function recovered completely within three weeks in the survivors.
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2/4. Percutaneous cardiopulmonary support aids resuscitation from sustained ventricular tachycardia.

    A 67-year-old man was transferred to hospital because of acute circulatory failure resulting from sustained left ventricular tachycardia (LVT) and dysfunction. Transthoracic echocardiography revealed severely impaired left ventricular contraction and dyskinesis of the apical wall. Neither anti-arrhythmic agents nor direct current cardioversion was effective; the patient was resuscitated by immediate use of percutaneous cardiopulmonary support and intraaortic balloon counterpulsation. Ventricular contraction returned to normal following restoration of normal sinus rhythm with amiodarone and cibenzoline. The pathogenesis of LVT accompanied by transient ventricular dyskinesis is discussed with regard to the efficient use of a mechanical circulatory support system in resuscitation.
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3/4. Biventricular assist device as a bridge to cardiac transplantation in the treatment of peripartum cardiomyopathy.

    Peripartum cardiomyopathy is an unexpected complication of the puerperium with a high mortality rate. Appropriate therapy requires accurate identification of this disease, which is frequently difficult in a patient who has been previously healthy. Medical therapy using alteration of intravascular volume (to optimize ventricular preload), the addition of inotropic agents (to correct ventricular function), and intra-aortic balloon counterpulsation (to improve afterload reduction) is the first line of therapy. Surgical therapy, involving cardiac transplantation, is the ultimate treatment. This therapeutic modality, however, is limited by a lack of available organs for transplant. The development of devices to be used as a "bridge" is gaining acceptance and use as a pretransplantation procedure. This use may be considered particularly fundamental in otherwise healthy young women with peripartum cardiomyopathy. These patients frequently can have almost complete recovery and rehabilitation. We report the case of a young woman with peripartum cardiomyopathy who had a favorable outcome. We performed medical and surgical therapy, insertion of a temporary "bridge" device, and ultimately cardiac transplantation.
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keywords = counterpulsation
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4/4. Cardiogenic shock: therapy and prevention.

    Cardiogenic shock is defined as profound circulatory failure resulting in insufficient tissue perfusion to meet resting metabolic demands. It occurs in approximately 7.5% of patients with acute myocardial infarction. Treatment strategies include inotropic agents, use of intra-aortic balloon counterpulsation, and revascularization. Current evidence supports the use of primary angioplasty. Surgery should be considered in patients with triple-vessel disease. If early catheterization is not available, thrombolytic therapy should be given to eligible patients and transfer to an interventional facility should be considered. Effective therapy for shock must also include a prevention strategy. This requires identification of patients at high risk for shock development and selection of patients who are candidates for aggressive intervention.
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keywords = counterpulsation
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