Cases reported "Bundle-Branch Block"

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11/64. 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, arrhythmogenic right ventricular dysplasia, arrhythmogenic right, cardiomyopathy, dysplasia
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12/64. Entrainment of ventricular tachycardia with a permanent biventricular pacemaker.

    Biventricular pacing has been introduced as a treatment for congestive heart failure. These devices presently pace and sense from two disparate ventricular sites. Antitachycardia pacing (ATP) is used for termination of sustained monomorphic ventricular tachycardia (VT) and has been incorporated with simultaneous dual site ventricular pacing for treatment of VT. We report a case of entrainment of sustained monomorphic VT in a 62-year-old female with an ischemic cardiomyopathy and VT, who received a biventricular pacemaker-implantable cardioverter defibrillator, Contak CD (Guidant, St. Paul, MN). Biventricular pacing sites were at the right ventricular apex and the middle of the anterior cardiac vein on the left ventricle. The entrained VT has a left bundle branch block and left axis deviation morphology with a cycle length of 350 msec. ATP at 270 msec produced concealed entrainment of an induced VT. Only one pacing site demonstrated capture. The inability to capture both pacing sites simultaneously was the result of ventricular refractoriness at one of the sites during ATP of the VT. The entrance and exit points of the loop for VT appeared to rest between the two pacing sites in the intraventricular septum. This case illustrates one of the sensing limitations of today's biventricular pacing defibrillator systems.
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ranking = 0.00058189969216386
keywords = cardiomyopathy
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13/64. Hypertrophic non-obstructive cardiomyopathy caused by disorder of the myofiber texture.

    A case of hypertrophic non-obstructive cardiomyopathy caused by a disorder of the myofiber texture was observed in a 10 year old boy. The heart weighed 390 g and showed concentric hypertrophy of the left and right ventricles as well as of the ventricular septum. Additional findings consisted in an abnormal septum membranaceum and a accessory tricuspid valve leaflet. Severe cardiac hypertrophy was associated with prominent interstitial and subendocardial fibrosis, and pronounced intimal fibrosis of the intramural arteries. Electron microscopy revealed various degrees and stages of hypertrophy of the myocardial cells combined with severe degenerative changes. Additional changes of the sinus node and conduction system were responsible for a tachycardia-bradycardia syndrome, complete left bundle branch block and final total AV-block.
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ranking = 0.0029094984608193
keywords = cardiomyopathy
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14/64. Biventricular pacing with coronary bypass and Dor's ventriculoplasty.

    We applied biventricular pacing to a patient with severe ischemic dilated cardiomyopathy (left ventricular [LV] ejection fraction 19%, LV end-diastolic volume 360 mL, and complete left bundle branch block). An epicardial LV lead was surgically implanted concomitant with on-pump beating coronary artery bypass grafting and Dor's endoventricular circular patch plasty. Biventricular pacing immediately achieved the resynchronization of the LV contraction, and improved cardiac function as well as reducing mitral regurgitation. Biventricular pacing combined with cardiac surgery for patients with cardiomyopathy and complete left bundle branch block may produce beneficial effects on LV function.
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ranking = 0.0011637993843277
keywords = cardiomyopathy
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15/64. A newly characterized SCN5A mutation underlying brugada syndrome unmasked by hyperthermia.

    Febrile illness has been rarely reported to modulate ST segment elevation in right precordial leads on ECG or even precipitate ventricular fibrillation in patients with brugada syndrome. We report the case of a patient whose Brugada ECG pattern was unmasked by hyperthermia secondary to acute cholangitis. Serial ECGs showed progressive attenuation of ST segment elevation as body temperature gradually returned to normal. Structural heart disease was ruled out. Intravenous flecainide injection reproduced a less remarkable ST segment elevation. Genetic screening demonstrated a single amino acid substitution (H681P) in the SCN5A gene, thus confirming the diagnosis of brugada syndrome. in vitro expression of this newly characterized genetic defect revealed novel biophysical abnormalities consisting of a shift in both steady-state activation and inactivation, resulting in a 60% reduction of sodium window current. Thus, SCN5A-H681P mutation induces a significant loss of transmembrane current and is clinically associated with a pathologic phenotype that is elicited by hyperthermia. overall the observed clinical features are in agreement with previous observations and strongly suggest that fever may be an environmental modifier among brugada syndrome patients with a detrimental (and possibly arrhythmogenic) effect on cardiac repolarization.
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ranking = 0.12493094109152
keywords = arrhythmogenic
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16/64. An underrecognized subepicardial reentrant ventricular tachycardia attributable to left ventricular aneurysm in patients with normal coronary arteriograms.

    BACKGROUND: In patients with apparently normal hearts, ventricular tachycardia (VT) may only involve the subepicardial myocardium. methods AND RESULTS: Four patients with exercise-induced fast VT with right bundle branch block morphology were investigated. ECG showed a small q wave in leads II, III, and aVF during sinus rhythm (SR) in all 4 patients. Left ventricular angiography showed small inferolateral aneurysms in all patients. Coronary arteriograms were normal in all 4 patients. Six unstable VTs (cycle length, 200 to 305 ms) and 1 stable VT (cycle length 370 ms) were reproducibly induced in the 4 patients. During SR, endocardial mapping was normal in all 4 patients, and epicardial mapping showed fragmented and late potentials in the left inferolateral wall anatomically consistent with the left ventricle aneurysm. During tachycardia, epicardial mapping showed a macroreentrant VT with focal endocardial activation in the patient with stable VT, whereas in 2 patients with unstable VT, a diastolic potential was only recorded and coincided with the late potential in the same area. Epicardial ablation was performed in 3 patients and successfully abolished those VTs. No VT recurred in 2 patients during follow-up of 2 and 9 months. Clinical VT recurred 6 months after the ablation and was successfully ablated in a repeated epicardial ablation in 1 patient. In the remaining patient without epicardial ablation, an implantable cardiac defibrillator was implanted. There were multiple shocks during a follow-up of 31 months. CONCLUSIONS: In patients with normal coronary arteriograms and left ventricle aneurysm, exercise-induced VT with right bundle branch block morphology may have a subepicardial arrhythmogenic substrate, which may be amenable to epicardial ablation.
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ranking = 0.12493094109152
keywords = arrhythmogenic
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17/64. Left bundle branch block and right axis deviation due to severe coronary heart disease.

    The simultaneous occurrence of left bundle branch block and right axis deviation is very rare and occurs mainly in patients with cardiomyopathy. This paper describes a 61-year-old man with end stage ischaemic heart disease who presented with this unique electrocardiographic abnormality.
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ranking = 0.00058189969216386
keywords = cardiomyopathy
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18/64. The hemodynamic benefit of biventricular pacing therapy on mitral regurgitation as demonstrated in a patient with ischemic cardiomyopathy and intermittent left bundle branch block.

    We report a 75-year-old man with ischemic cardiomyopathy who had mitral regurgitation which was increased markedly by intermittent left bundle branch block (LBBB). He complained of angina-like chest pain that was preceded by episodes of LBBB. During LBBB, a marked elevation of the V wave in the pulmonary capillary wedge pressure was shown, and an increase in mitral and tricuspid regurgitation was observed with color Doppler echocardiography. Biventricular pacing (BVP) therapy was selected so as to protect the patient from episodes of LBBB. After BVP, the patient did not experience chest pain or dyspnea. This case sheds valuable light on the ongoing investigation of the hemodynamic benefit of BVP.
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ranking = 0.0029094984608193
keywords = cardiomyopathy
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19/64. exercise-induced left bundle branch block in a young female athlete.

    An 11-year-old female, in apparent good health, was referred to our Institute because of exercise-induced left bundle branch block detected during a Master's step test performed to obtain the clearance for competitive sport. The tests that we performed to investigate the possible causes were all negative. We suspect, however, that the left bundle branch block is the initial sign of cardiomyopathy. If our suspicions are correct, close follow-up is important to chart the possible progression of the disease.
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ranking = 0.00058189969216386
keywords = cardiomyopathy
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20/64. A case of pediatric cardiomyopathy with severely restrictive physiology.

    A rare case of a 6-year-old male with idiopathic familial cardiomyopathy manifesting severely restrictive physiology is reported. The patient showed congestive heart failure with dilatation of both atria with a normal ventricular cavity. A square-root configuration was revealed in the ventricular pressure tracings. His elder brother had died of hypertrophic cardiomyopathy at the age of 3 years. Endomyocardial biopsy disclosed marked disorganization of muscle bundles with hypertrophy of the myocytes and interstitial fibrosis. The patient died suddenly during hospitalization. autopsy revealed diffuse hypertrophy of both the ventricular walls and the ventricular septum with extensive myocardial disorganization and interstitial fibrosis. These advanced myopathic changes in the myocardium may have been related to the restrictive physiology in this case.
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ranking = 0.0034913981529832
keywords = cardiomyopathy
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