Cases reported "Heart Block"

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1/16. Transvenous pacemaker insertion ipsilateral to chronic subclavian vein obstruction: an operative technique for children and adults.

    subclavian vein occlusion limits insertion of pacing electrodes in children and adults. The concern is greatest in children with a long-term need for pacing systems necessitating use of the contralateral vein and potential bilateral loss of access in the future. We describe an operative technique to provide ipsilateral access in chronic subclavian vein occlusion in five consecutive pediatric (n = 4, mean age 6.5 years) and adult (n = 1, age 70 with bilateral subclavian vein occlusion) patients in whom this condition was noted at the time of pacemaker or ICD implant. Occlusion was documented by venography. Pediatric cardiac diagnoses included complete heart block in all patients, tetralogy of fallot in three, and L-transposition of the great vessels in one. Percutaneous brachiocephalic (innominate) or deep subclavian venous access was achieved by a supraclavicular approach using an 18-gauge Deseret angiocath, a Terumo Glidewire, and dilation to permit one or two 9-11 Fr sheaths. Electrode(s) were positioned in the heart and tunneled (pre- or retroclavicularly) to a pre- or retropectoral pocket. Pacemaker and ICD implants were successful in all without any complication of pneumothorax, arterial or nerve injury, or need for transfusion. Inadvertent arterial access did not occur as compared with prior infraclavicular attempts. One preclavicularly tunneled electrode dislodged with extreme exertion and was revised. Ipsilateral transvenous access for pacemaker or ICD is possible via a deep supraclavicular percutaneous approach when the subclavian venous obstruction is discovered at the time of implant. In children, it avoids the use of the contralateral vein that may be needed for future pacing systems in adulthood. This venous approach provides access large enough to allow even dual chamber pacing in children and can be accomplished safely.
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2/16. Pacing-induced left ventricular dysfunction. Relationship with coronary perfusion.

    In a patient admitted with symptomatic complete heart block, a DDD pacemaker was implanted. Prior to implantation, echocardiography showed normal left ventricular function. Shortly after implantation, acute congestive heart failure developed with extensive regional hypo- and akinetic segments in the anteroseptal, anterolateral and apical region. Subsequent perfusion imaging with methoxyisobuticeisonitrite (MIBI) at rest demonstrated hypoperfusion in the same regions while coronary angiography showed normal epicardial coronary vessels. Thus, impaired regional coronary flow can be associated with cardiac stimulation, inducing marked deterioration of left ventricular function.
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3/16. Complete atrio-ventricular block as a major clinical presentation of the primary cardiac lymphoma: a case report.

    It is uncommon for malignant lymphomas to present primarily with cardiac invasion as the main clinical feature. What we are interested in is not only where the disease is, but also those symptoms that it may induce. Sudden onset of complete atrio-ventricular block is one of the most common clinical presentations. cardiac tamponade is another common disease entity which, if it locates over outlets of great vessels, may also exert symptoms of obstructive vessels. diagnosis can be made by needle aspiration under the guidance of transcutaneous or transesophageal echocardiography. Both CT scan and MRI play positive roles in the diagnosis of cardiac lymphomas, and the latter can even provide much more image information than the former. We report a 70-year-old male with primary cardiac lymphoma with initial clinical pictures of sudden onset of complete atrio-ventricular block. Chemotherapy was utilized with cyclophosphamide, vincristine and prednisolone (COP) initially for four courses and followed by adding doxorubicin (CHOP) for another three courses. The patient was still in remission status after treatment for 2 years.
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4/16. syncope in association with Prinzmetal variant angina.

    A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appeared free of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy.
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5/16. coronary artery disease obscuring giant cell myocarditis--a case report.

    A case in which the diagnosis of idiopathic giant cell myocarditis was obscured by the presence of severe coronary artery disease is described. A 47-year-old man presented with recurrent inferior myocardial infarction and complete heart block. cardiac catheterization confirmed severe 2-vessel disease and left ventricular dysfunction. Incessant ventricular arrhythmia rapidly ensued, which did not respond to anti-arrhythmic therapy and overdrive pacing despite complete surgical revascularization. He eventually died. autopsy revealed giant cell myocarditis superimposed on coronary artery disease. Acute myocarditis masquerading as myocardial infarction has been well known, but virtually all reported cases had normal coronary arteries. This case illustrated the fact that even in the presence of obvious coronary artery disease the remote possibility of myocarditis should not be entirely disregarded. Although giant cell myocarditis is a rare and frequently fatal disorder, recent studies suggest that combined immunosuppressive therapy may improve the prognosis.
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6/16. vasculitis masquerading as aortic valve endocarditis.

    Small vessel vasculitis and endocarditis can both present with multisystem involvement and may present a diagnostic dilemma. Renal and cardiac involvement is common in small vessel vasculitis and rarely small vessel vasculitis may cause heart block. When a patient presents with diffuse symptoms, deteriorating renal function, and heart block, endocarditis and vasculitis should be included in the differential diagnosis. The case is discussed of a man with a history of aortic valve endocarditis who presented again with similar symptoms, deteriorating renal function, and heart block. There was no evidence of aortic valve endocarditis with abscess formation. A renal biopsy confirmed small vessel vasculitis and the patient responded promptly to immunosuppressive treatment. Correct diagnosis is essential in such cases, as immunosuppression in true endocarditis can be catastrophic. In this case, with the correct diagnosis, immunosuppression proved life saving and prevented erroneous aortic valve surgery.
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7/16. Sudden death in a case of cardiac amyloidosis immediately after pacemaker implantation for complete atrioventricular block.

    We report a patient with cardiac involvement associated with primary amyloidosis presenting marked left ventricular (LV) wall thickening, severely decreased systolic and diastolic function, and complete atrioventricular block (CAVB), who died suddenly of cardiac arrest caused by electro-mechanical uncoupling occurring immediately after permanent pacemaker implantation. Post mortem examination showed no procedural complications such as cardiac or venous perforation. The heart was densely infiltrated with amyloid fibrils, especially in the extracellular tissues surrounding the papillary vessels.
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8/16. chest pain in a young basketball player.

    A 32-year-old man was elbowed in the chest while fighting for a rebound in a recreational basketball game. He fell to the ground and his chest ached from the blow. Four days later he developed more severe chest pressure with dyspnea and came to the hospital. His chest wall was tender and his pulse slow, but the remainder of his physical examination was normal. Electrocardiogram showed sinus bradycardia, first-degree atrioventricular (AV) block, and occasional isorhythmic AV dissociation, but no ischemic ST-T changes. Cardiac troponin i rose to 1.74 ng/mL (normal <0.50). The patient therefore underwent coronary angiography, showing spiral dissection of the right coronary artery with extensive thrombus filling the distal portion of the vessel. Stenting was unsuccessful in restoring flow. This case highlights the potential dangers of blunt chest trauma in recreational sports and shows how angiography can distinguish myocardial contusion from coronary artery dissection.
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9/16. myxoma with a left-to-left shunt and fistula.

    We present the case of a 68-year-old man with a peculiar coincidence of cardiac pathologic findings: a huge left atrial myxoma, mitral insufficiency, a high degree atrioventricular block and three-vessel disease. The myxoma was vascularized from a dilated sinus arteriosus branch, giving rise to neovascularization at the base of the tumor. blood from the neovascularization gathered into a large cavern which fistulated into the left atrium, responsible for a left-to-left cardiac shunt.
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10/16. Lack of connection between the atria and the peripheral conduction system in a case of corrected transposition with congenital atrioventricular block.

    This is the first documented histologic study of the heart of a patient with corrected transposition of the great vessels and congenital atrioventricular (A-V) block with no connection between the atria and an anterior type of peripheral conduction system. Musculature in the superior (anterior) walls of both atria was absent, as was the anterior A-V node. The peripheral conduction system began with the bundle of his. In place of the absent atrial musculature, fibrosis and calcification were present. The relation of laboratory evidence of connective tissue dyscrasia in the mother to the congenital A-V block in the child is discussed.
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