Cases reported "Syncope"

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1/15. 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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2/15. Anomalous coronary artery arising from the opposite sinus: descriptive features and pathophysiologic mechanisms, as documented by intravascular ultrasonography.

    BACKGROUND: Anomalous coronary artery originating from the opposite sinus of valsalva (ACAOS) can cause syncope, myocardial infarction, and sudden death in the absence of critical, fixed stenosis. In the following cases, intravascular ultrasonography (IVUS) was used to document the functional anatomy in ACAOS. This application has not been previously reported in the literature. methods AND RESULTS: In four patients with symptomatic ACAOS and IVUS, the anomalous vessels had a tangential proximal course, and a proximal intramural tract of variable length had fixed lateral compression that worsened during systole. By pressure wire, no significant gradient was present at baseline or after adenosine administration. ergonovine provocation elicited no spasticity of proximal ectopic segments. dobutamine, atropine, and rapid saline infusion provoked no symptoms or angiographic changes but did provoke subtle IVUS changes. To correlate these changes with the prognosis, further longitudinal evaluation, involving larger series, will be required. CONCLUSION: IVUS and pressure-wire methods may be valuable for subclassifying ACAOS and other coronary anomalies in terms of their pathophysiologic repercussions and for substantiating individual indications for treatment. To establish definitive recommendations and protocols, a larger study will be required.
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3/15. A case of vasovagal syncope with convulsions--the effects of midodrine hydrochloride.

    A 42-year-old female had suffered from repeated syncope. She had vasovagal syncope with convulsions from vasodilatation and cardiac standstill which lasted for 9.8 sec. The 60 degrees head-up tilt test, nitroglycerin injection and isoproterenol infusion provoked vasovagal reaction. Although a beta blocker was not effective in preventing tilt-induced hypotension and bradycardia, midodrine hydrochloride (alpha-1 stimulant) or atropine prevented it. In this patient, insufficient constriction of capacitance vessels might have played an important role in activation of an inhibitory reflex from cardiopulmonary mechanoreceptors which caused hypotension and bradycardia.
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4/15. vertigo secondary to isolated pica insufficiency: successful treatment with balloon angioplasty.

    BACKGROUND: The posterior inferior cerebellar arteries (pica) arise from the intracranial segments of the vertebral artery (VA). We report a case where a nondominant isolated vertebral artery, which terminated in pica, was stenotic. This resulted in brainstem-lower cerebellar ischemia, corrected with balloon angioplasty. CASE DESCRIPTION: A 62-year-old male presented primarily with transient vertigo, syncope, and dizziness and was diagnosed with transient ischemic attack. Angiography of the left vertebral artery (VA) demonstrated a small-caliber vessel terminating in pica with a 90% stenosis at the C6 level. angioplasty of the left VA was performed with excellent resolution of the stenosis. CONCLUSIONS: This case illustrates cerebellar insufficiency in a unique case where the pica was isolated, supplied by a small- caliber VA. Correction of the stenosis improved the patient's symptomatology and prevented an inferior brainstem-cerebellar infarction.
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5/15. Moyamoya syndrome after prophylactic cranial irradiation for acute lymphocytic leukemia.

    A 9-year-old boy presented with an episode of syncope, and MR imaging revealed bilateral internal carotid artery stenosis with moyamoya vessel formation. He had had prophylactic cranial irradiation at a total dose of 24 Gy for the treatment of acute lymphocytic leukemia at the age of 4. Following this, he was in a complete state of remission for 6 years. During an observation period of a year after the onset of syncope, MR imaging showed development of multiple ischemic lesions in both hemispheres. He developed a transient ischemic attack of mild motor weakness in his arm and an indirect anastomosis was performed on the severely affected side at the age of 10. Radiation-induced vasculopathies are known to be associated with primary diseases of intracranial tumors, but the frequency is unclear. Ours is the third case in whom prophylactic cranial irradiation for a hematological disorder might have induced cerebral vasculopathies.
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6/15. Hypersensitive carotid sinus syndrome due to neurofibromatosis-1 and manifested by repeated episodes of syncope.

    A 28-year-old patient with neurofibromatosis-1 presented with syncope. The exam demonstrated a mass adjacent and inferior to the right occiput that extended to the posterior lateral right-sided neck. Initial invasive and noninvasive testing was negative. Imaging of her head and neck demonstrated a large neurofibroma enveloping her right carotid sinus without vessel occlusion or evidence of malignancy. An event recorder documented asystole. A pacemaker was implanted to avoid the surgical morbidity of removing the neck mass. The patient has since been free of syncope. We believe neurofibromatosis-1 should be included in the differential of syncope.
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7/15. Permanent transvenous pacing after a Mustard procedure.

    We report the case of a 20-year-old man born with transposition of the great vessels who underwent emergency balloon septostomy and subsequently a Mustard procedure. When aged 20 years, he had several syncopal attacks due to sinoatrial disease for which he was simply and successfully paced transvenously in VVI mode.
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8/15. Reversible cerebral segmental vasoconstriction.

    vasoconstriction is not recognized as a cause of cerebrovascular disease except in the vasospasm seen following subarachnoid hemorrhage and possibly in migraine. However, we found four patients to have transient, fully reversible vasoconstriction and dilatation prominently involving arteries around the circle of Willis. All four patients were evaluated for severe headaches and fluctuating or recurring motor or sensory deficits. No cause for the clinical syndromes and angiographic abnormalities was found. Similar patients are reported in the literature under various nosologies. This newly recognized clinical-angiographic syndrome should be differentiated from other known causes of vessel constriction and dilatation; the precipitants of reversible vasoconstriction may then be better defined.
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9/15. Diffuse triple-vessel coronary artery spasm complicated by idioventricular rhythm and syncope.

    A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.
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10/15. Diffuse disseminated atheroembolism. Three cases with neuro-ophthalmic manifestation.

    Neuro-ophthalmic manifestations led to the diagnosis of diffuse disseminated atheroembolism (DDA) in three men whose systemic symptoms had remained unexplained for years. The cholesterol emboli that cause DDA originate from friable plaques in the aorta and great vessels. Ophthalmologists should be alert to the diagnosis of DDA in patients with elevated ESRs, stroke, transient amaurosis, or cholesterol emboli in the fundi. early diagnosis is important because arteriography, endarterectomy, and anticoagulation seem to increase the risk of serious, even fatal, embolization in these patients.
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