Cases reported "Syncope"

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11/45. exercise-induced bidirectional ventricular tachycardia with alternating right and left bundle branch block-type patterns--a case report.

    exercise-induced ventricular tachycardia in young adults may occur with various structural heart diseases or with structurally normal heart. The structural heart diseases reported to cause exercise-induced ventricular tachycardia in this patient population include arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy, dilated cardiomyopathy, myocarditis, congenital heart disease, and myocardial ischemia. The conditions well identified to cause exercise-induced ventricular tachycardia with structurally normal heart are congenital long-QT syndrome and familial polymorphic ventricular tachycardia. exercise-induced ventricular tachycardia may display polymorphic, monomorphic, or bidirectional morphologies. A case of exercise-induced catecholamine-sensitive bidirectional ventricular tachycardia with alternating right and left bundle branch block patterns is reported in a young boy in the absence of structural heart disease, the conditions causing bidirectional ventricular tachycardia, and family history of such an event or sudden cardiac death. The bidirectional tachycardia typically displays right bundle branch block in right precordial leads with alternating polarity of the QRS-complex in frontal plane leads but in this case the bidirectional morphology of tachycardia was caused by alternating right and left bundle branch block-type patterns. The conditions causing bidirectional ventricular tachycardia are digoxin toxicity, ischemic heart disease, hypokalemia, myocarditis, and familial polymorphic ventricular tachycardia syndrome but the exact cause in this patient remained obscure, and the possibility of an underlying electrical or ion channel disease of the heart could not be ruled out.
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ranking = 1
keywords = ventricular dysplasia, right ventricular dysplasia, arrhythmogenic right ventricular dysplasia, arrhythmogenic, arrhythmogenic right, cardiomyopathy, dysplasia
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12/45. A cardiac sodium channel mutation cosegregates with a rare connexin40 genotype in familial atrial standstill.

    Atrial standstill (AS) is a rare arrhythmia that occasionally appears to be genetically determined. This study investigates the genetic background of this arrhythmogenic disorder in a large family. Forty-four family members were clinically evaluated. One deceased and three living relatives were unambiguously affected by AS. All other relatives appeared unaffected. Candidate gene screening revealed a novel mutation in the cardiac sodium channel gene SCN5A (D1275N) in all three affected living relatives and in five unaffected relatives, and the deceased relative was an obligate carrier. In addition, two closely linked polymorphisms were detected within regulatory regions of the gene for the atrial-specific gap junction protein connexin40 (Cx40) at nucleotides -44 (G-->A) and 71 (A-->G). Eight relatives were homozygous for both polymorphisms, which occurred in only approximately 7% of control subjects, and three of these relatives were affected by AS. The three living AS patients exclusively coinherited both the rare Cx40 genotype and the SCN5A-D1275N mutation. SCN5A-D1275N channels showed a small depolarizing shift in activation compared with wild-type channels. Rare Cx40 genotype reporter gene analysis showed a reduction in reporter gene expression compared with the more common Cx40 genotype. In this study, familial AS was associated with the concurrence of a cardiac sodium channel mutation and rare polymorphisms in the atrial-specific Cx40 gene. We propose that, although the functional effect of each genetic change is relatively benign, the combined effect of genetic changes eventually progresses to total AS.
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ranking = 0.15721272199263
keywords = arrhythmogenic
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13/45. Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.

    A 67-year-old female with recurrent syncope and no obvious heart disease developed ventricular dysfunction, known as takotsubo cardiomyopathy, following a 90 s episode of polymorphic ventricular tachycardia originating from a ventricular extrasystole with a short coupling interval. cardiac catheterization performed 30 min after the arrhythmic event revealed angiographically normal coronary arteries, and left ventricular apical akinesis and basal hyperkinesis. An intracoronary injection of acetylcholine revealed no inducible coronary spasm, and an electrophysiological study revealed normal atrioventricular conduction and no inducible ventricular arrhythmia. Thirty hours after the arrhythmic event, electrocardiography revealed deeply inverted T waves in leads V3 to V6, I, and aVL, which continued for more than a week. Although no treatment was given to maintain hemodynamic stability, echocardiography revealed normal left ventricular contraction 14 days after the onset of the ventricular dysfunction. The reversible ventricular dysfunction might have been induced by altered catecholamine dynamics due to the persistent syncope during the occurrence of tachycardia.
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ranking = 0.0076750877589391
keywords = cardiomyopathy
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14/45. Recurrent syncope in a patient after myocardial infarction.

    A patient with ischemic cardiomyopathy presented with burning pain of his body surface with consecutive orthostatic intolerance and recurrent syncopes. A diagnosis of acute autonomic dysfunction was made and the patient was treated with midodrine, resulting in restoration of orthostatic tolerance after 6 weeks of therapy.
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ranking = 0.0015350175517878
keywords = cardiomyopathy
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15/45. Abnormal His-Purkinje system conduction leading to complete atrioventricular block in patients with hypertrophic cardiomyopathy: a report of 3 cases.

    This case report describes three hypertrophic cardiomyopathy patients with abnormal His-Purkinje conduction and complete atrioventricular block with attacks of syncope and cardiopulmonary arrest. Although arrhythmias are common in hypertrophic cardiomyopathy, complete atrioventricular block is very rare. Prolonged QRS duration and abnormal His-Purkinje system conduction may result in complete atrioventricular block.
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ranking = 0.0092101053107269
keywords = cardiomyopathy
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16/45. Catecholaminergic polymorphic ventricular tachycardia: successful emergency treatment with intravenous propranolol.

    Catecholaminergic polymorphic ventricular tachycardia (VT) is a rare arrhythmogenic disorder, which may cause sudden death and whose relationships with mutations in cardiac ryanodine receptor gene have been recently established.The present article reports a catecholaminergic polymorphic VT case of a 9-year-old girl, without any previous history of syncope, who has been found unconscious while playing and referred comatose to pediatric intensive care unit.The electrocardiogram pattern showed runs of bidirectional and polymorphic VT degenerating into ventricular fibrillation, without QT interval abnormalities. Various attempts of cardioversion, lidocaine, and magnesium sulfate intravenous infusions were only partially effective.Owing to catecholaminergic polymorphic VT highly suggesting electrocardiogram pattern, intravenous propranolol was administered, achieving immediate VT interruption. Long-term nadolol therapy effectively prevented further arrhythmias, with no relapses up to 10 months later; a good neurologic recovery was also obtained.Genetic evaluation revealed in this patient-but not in relatives-a mutation in ryanodine receptor gene on chromosome 1.
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ranking = 0.15721272199263
keywords = arrhythmogenic
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17/45. Near-syncope after exercise.

    syncope and near-syncope are great diagnostic challenges in medicine. On the one hand, the symptom may result from a benign condition and pose little or no threat to health other than that related to falling. On the other hand, syncope or near-syncope can be the manifestation of a serious underlying condition that poses an imminent threat to life. patients with a cardiac cause of syncope are at far greater risk of dying in the first year after an episode of syncope or near-syncope than individuals with a noncardiac cause. A cardiac cause of syncope should be considered in every patient with syncope or near-syncope, but it is particularly common in older patients or in patients with known structural heart disease, arrhythmia, or certain electrocardiographic abnormalities. Although many diagnostic tests may be helpful in the evaluation of syncope and near-syncope, the history, physical examination, and electrocardiogram pinpoint the cause in many circumstances. syncope after exercise may be due to left ventricular outflow tract obstruction from aortic stenosis or hypertrophic obstructive cardiomyopathy but can also suggest the diagnosis of postexercise hypotension in which an abnormality in autonomic regulation of vascular tone or heart rate results in vasodilation or bradycardia after moderate-intensity aerobic activity. The patient discussed in this case highlights the importance of the clinical history in the evaluation of this condition, since the diagnosis was revealed as the patient's story was described and eventually acted out.
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ranking = 0.0015350175517878
keywords = cardiomyopathy
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18/45. Torsade de pointes in a case of pheochromocytoma--an unusual presentation of an uncommon disease.

    We report the case of a middle aged lady with dilated cardiomyopathy, presenting with recurrent syncope due to torsade de pointes. Further evaluation revealed that she had a pheochromocytoma which caused the arrhythmia.
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ranking = 0.0015350175517878
keywords = cardiomyopathy
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19/45. Cardiac involvement in Emery-Dreifuss muscular dystrophy.

    Emery-Dreifuss muscular dystrophy (EDMD) is a common form of muscular dystrophy frequently involving cardiac muscle, thus leading to dilated cardiomyopathy. Clinical outcome and prognosis is frequently determined by the involvement of the cardiac conduction system causing symptomatic bradyarrhythmias, as well as tachyarrhythmias and, if untreated, frequent sudden cardiac death. Typical features of the cardiac involvement of EDMD are presented, caused by a novel missense mutation in the splice receptor sequence of intron 6 of the LMNA gene on chromosome 1, encoding for the lamin A/C gene, consistent with the autosomal dominant form of EDMD.
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ranking = 0.0015350175517878
keywords = cardiomyopathy
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20/45. Multiple exercise induced syncopal episodes in a young woman due to arrhythmogenic right ventricular dysplasia.

    A case of a young woman with multiple exercise induced syncopal episodes due to arrhythmogenic right ventricular dysplasia is described. The report emphasizes the importance of exercise induced syncope and the management is described.
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ranking = 4.9846498244821
keywords = ventricular dysplasia, right ventricular dysplasia, arrhythmogenic right ventricular dysplasia, arrhythmogenic, arrhythmogenic right, dysplasia
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