Cases reported "Cardiomyopathy, Dilated"

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1/75. Left bundle branch block in infants with dilated cardiomyopathy conveys a poor prognosis.

    We describe three infants <3 months of age seen consecutively with dilated cardiomyopathy who presented initially with left bundle branch block on the surface 12-lead electrocardiogram. Each infant subsequently had a poor outcome: two died and one required heart transplantation. These results suggest that the presence of left bundle branch block on the 12-lead electrocardiogram conveys a poor prognosis in infants with dilated cardiomyopathy.
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2/75. Acute dilated cardiomyopathy and central nervous system toxicity following propranolol intoxication.

    OBJECTIVE: We report a case of a 16-year-old boy who developed central nervous system (CNS) depression and acute dilated cardiomyopathy following ingestion of 3200 mg of propranolol in a suicide attempt. Early echocardiographic findings were the only sign of cardiac toxicity. DESIGN: A case report. SETTING: Pediatric intensive care unit of a teaching hospital. RESULTS: This child developed significant acute dilated cardiomyopathy and severe CNS depression 2 hours after ingesting 3200 mg of propranolol. The child was treated with gastric lavage, activated charcoal, and mechanical ventilation. Following the echocardiographic findings, treatment with isoprenaline hydrochloride and glucagon were given intravenously. Echocardiographic examination 12 hours following treatment showed normal left ventricular size and function. No change in pulse rate or blood pressure was reported on admission and during his hospitalization. DISCUSSION: In the early stages of propranolol and other lipophilic beta-blocker intoxication, severe CNS depression can develop in the absence of clinical signs of cardiac toxicity. Early echocardiographic evaluation is important and may prevent delay in diagnosis and treatment of cardiac toxicity.
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3/75. Right ventricular cardiomyopathy showing right bundle branch block and right precordial ST segment elevation.

    A 73-year-old man who had a family history of sudden death, experienced syncope. His electrocardiogram (ECG) presented right bundle branch block and right precordial ST segment elevation which are findings identical with those in brugada syndrome. The cardiac MRI showed right ventricular mild dilatation, and endomyocardial biopsy revealed fatty replacement of myocardial fibers. Though no ventricular tachyarrhythmias were induced during an electrophysiologic test, the effects on ECG of antiarrhythmic agents and autonomic modulations were similar to those in brugada syndrome. This case may suggest the relationship between brugada syndrome and right ventricular cardiomyopathy.
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4/75. Traumatic hemorrhage of occult pheochromocytoma: a case report and review of the literature.

    pheochromocytoma usually presents with gradual onset and mild to moderate symptoms, but may present acutely with severe symptoms. hemorrhage into pheochromocytoma is a rare cause of acute presentation that is often devastating to patients. We describe the case of a 34-year-old woman with hemorrhage into a previously undiscovered pheochromocytoma following a fall on a patch of ice. This is the first reported case of hemorrhagic pheochromocytoma associated with traumatic injury. Despite removal of the tumor within 18 hours of presentation, the patient suffered severe complications of massive catecholamine excess, including shock, cardiomyopathy, and adult respiratory distress syndrome. Animal studies have shown that early treatment with alpha blockers can prevent some, if not all of these complications. Proper management of hemorrhagic pheochromocytoma should include a high index of suspicion with early diagnosis and treatment with alpha blockers and surgical resection of the tumor when the patient is stable enough to tolerate the procedure.
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5/75. Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm.

    Endothelial dysfunction and effectiveness of treatment of calcium antagonists are suggestive of coronary artery spasm as an underlying disorder in dilated cardiomyopathy (DCM). The aim of this study is to determine whether or not the epicardial coronary artery spasm can induce severe cardiac dysfunction like DCM. Thirty-four consecutive patients with angiographically normal coronary arteries and diffuse left ventricular hypokinesis whose causes had been unknown underwent acetylcholine provocation test and left ventricular biopsy. Eight patients were excluded according to the clinical and laboratory data and biopsy findings suggesting myocarditis or other systemic diseases. According to the results of the acetylcholine provocation test, 17 patients were finally diagnosed as having DCM, and nine patients (35% of the study patients), who had acetylcholine-induced diffuse and multivessel coronary spasm, were diagnosed as having DCM-like vasospastic angina pectoris (VSA). Clinical and cardiac catheterization data including hemodynamics and biopsy findings were similar between the two groups except that left ventricular end-systolic volume was significantly greater in DCM than in DCM-like VSA. After the acetylcholine provocation test, DCM patients received both a beta blocker and an angiotensin-converting enzyme inhibitor, and DCM-like VSA patients received antianginal drugs. In echocardiographic findings at predischarge and those after 6-month drug treatment, both DCM-lke VSA and DCM showed significant reduction in end-diastolic and end-systolic diameters and significant increase in fractional shortening and ejection fraction, whereas changes in ejection fraction and fractional shortening were significantly greater in DCM-like VSA than those in DCM. Epicardial coronary artery spasm can induce diffuse and severe left ventricular dysfunction like DCM in VSA. Although antianginal drugs markedly improve left ventricular function of these patients, only the acetylcholine provocation test can identify DCM-like VSA.
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6/75. atrial flutter in the recipient atrium induced by premature beats arising from the donor atrium 10 years after orthotopic heart transplantation.

    BACKGROUND: Several mechanisms for the genesis of supraventricular arrhythmias in patients after orthotopic heart transplantation have been reported. methods AND RESULTS: We describe a 58-year-old male patient in whom atrial flutter occurred 10 years after orthotopic heart transplantation. During an electrophysiological study, bidirectional conduction between the recipient and donor atria was found. atrial flutter in the recipient atrium was induced by programmed stimulation of the donor atrium using a single extrastimulus. The clinical symptoms were caused by atrial flutter arising from the recipient atrium with 1:1 to 3:1 conduction to the donor atrium. Mapping the anastomosis between the two atria indicated fragmented potentials at a discrete site of conduction. Delivery of radiofrequency energy at this site terminated conduction in both directions. Subsequent atrial pacing of the donor and recipient atria, respectively, demonstrated bidirectional conduction block. CONCLUSION: Symptomatic arrhythmias in patients after heart transplantation can indirectly originate from the donor atrium via bidirectional recipient-donor atrial conduction. This type of arrhythmia can be successfully treated with radiofrequency ablation.
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7/75. Inappropriate shock therapy in a heart failure defibrillator.

    A 63-year-old male with dilated cardiomyopathy underwent implantation of a "heart failure" defibrillator capable of biventricular pacing. He received an inappropriate shock 5 hours after the procedure. Stored electrograms revealed that during each sinus beat the ventricular channel recorded up to three separate events. These resulted from far-field atrial sensing by the coronary venous lead, appropriate right ventricular sensing, then delayed left ventricular sensing (the result of left bundle branch block). As a consequence of far-field left atrial sensing the two subsequent ventricular electrograms fell within the VF zone. Following an atrial premature beat, VF detection criteria were satisfied and shock therapy delivered. Although coronary venous lead repositioning eliminated far-field atrial sensing, double counting of the widely split right and left ventricular electrograms still occurred during sinus rhythm. Shortening the programmed AV delay resulted in constant biventricular pacing with a single electrogram.
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8/75. The Mount Sinai Hospital clinicalpathological conference: a 45-year-old man with Pompe's disease and dilated cardiomyopathy.

    This is an unusual case of a 45-year-old man, born in ecuador, with evidence of profound left ventricular dysfunction, dilated cardiomyopathy and marked myocardial hypertrophy. Preceding events were advanced atrioventricular block (necessitating pacemaker implantation) and atrial flutter. The diagnosis of Pompe's disease was established by endomyocardial biopsy and appropriate staining, which indicated abnormal glycogen storage.
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9/75. Myocardial perfusion and metabolic changes induced by biventricular pacing in dilated cardiomyopathy and left bundle branch block: description of a case evaluated by positron emission tomography.

    The effects of biventricular pacing on myocardial wall function are well known, but, at the moment, its real effects on myocardial metabolism are unclear. In patients affected by left bundle branch block, at positron emission tomography a septal defect of the uptake of 18F-fluorodeoxyglucose (FDG) was referred. There were no alterations in myocardial perfusion, suggesting possible metabolic damage. In this paper we report the case of a patient affected by dilated cardiomyopathy and left bundle branch block treated with a biventricular device. Biventricular pacing resolved both the wall motion alterations as well as the defect in FDG uptake present in the septal area. On the contrary, during biventricular pacing there were no modifications in myocardial perfusion as compared to basal evaluation.
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10/75. Case report: alternating exit sites in reentry circuit of ventricular tachycardia with nonischemic cardiomyopathy - relationship between ablation site and inner loop.

    We present a patient with nonischemic cardiomyopathy who had ventricular tachycardia (VT) with QRS morphology alternans. VTs of two QRS morphologies (VT1 and VT2) exhibiting a right bundle branch block pattern with inferior axis was induced by ventricular pacing. The morphology of the QRS complex during VT1 exhibited more distinctively inferior axis than those during VT2. Induced VTs had similar morphologies to clinically the documented VTs. Pacemapping at anterolateral site of the left ventricle during sinus rhythm produced the same QRS complex of VT1 in a surface 12-lead electrocardiogram. A mapping study was performed with an electrode catheter located at the same site of LV during sustained VT1. The analysis of the local electrograms and postpacing interval during concealed entrainment at the catheter mapping revealed this pacing site was at the inner loop of the reentry circuit. Radiofrequency catheter ablation was performed at this site. The morphology of VT1 changed to different QRS morphology (VT2) during the first delivery of radiofrequency energy and was terminated after 20 seconds of the application. Then VT with alternans of QRS morphology and cycle length of VT1 and VT2 was induced by ventricular pacing, and was abolished by the second application of radiofrequency energy at this same site, suggesting that this site was located in the exit site close to inner loop of the reentry circuit and the alternans of QRS morphology was linked to the change of exit site.
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