Cases reported "Syncope"

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1/96. syncope two years after hysterectomy.

    A 61-year-old woman presented to the emergency department after experiencing palpitations, shortness of breath, and syncope while taking a shower. Her husband revived her with mouth-to-mouth resuscitation. She had had a similar episode three days earlier while making her bed and had lost consciousness for about 10 sec. She did not appear to have had a seizure. Five months earlier, while taking a walk, she had experienced dizziness, dyspnea, and chest pressure lasting about an hour. A workup at that time included cardiac catheterization, lung scanning, and esophagogastroduodenoscopy, but no abnormality was found. lower extremity edema was noted.
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2/96. Continuous haemodynamic monitoring in an unusual case of swallow induced syncope.

    A 69 year old man is described with a 12 year history of intermittent syncope associated with ingesting solid food, mainly after having fasted. He was taking enalapril, propranolol, bendrofluazide (bendroflumethiazide), omeprazole, finasteride, and aspirin. Detailed investigations, including gastrointestinal evaluation, measurement of various gut hormones, and autonomic testing, indicated no abnormality. A liquid meal, performed before fasting, failed to elicit an episode. However, a solid meal after an overnight fast provoked near-syncope. Continuous non-invasive haemodynamic monitoring (with a Portapres II) indicated a short lived rise in blood pressure and heart rate, followed by severe hypotension, a fall in stroke volume and cardiac output, and then bradycardia. This favoured an initial increase in sympathetic activity, followed by vasodepression due to sympathetic withdrawal or activation of humoral vasodilatatory mechanisms, with bradycardia secondary to impaired cardiac filling. Withdrawal of enalapril abolished the episodes. The unusual nature of this case, in which haemodynamic recordings continuously were made during and after swallow syncope, induced soon after food ingestion, is discussed.
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3/96. A case of sinus arrest and vagal overactivity during REM sleep.

    A young man presented with tachycardia and faintness after an episode of influenza. He underwent 24-h heart rate recordings, each of which documented episodes of sinus arrest lasting up to 7.2 seconds. All episodes occurred in the second half of the night and were always accompanied by severe bradycardia. Cardiac function tests failed to disclose anything abnormal. Two polysomnographic recordings demonstrated that the sinus arrests occurred during REM sleep. Power spectral analysis of heart rate variability showed that during the second half of the night there was an abnormal prevalence of vagal activity, particularly during REM sleep stages, presumably responsible for the bradycardia and fall in blood pressure. We speculate that the episodes of sinus arrest are linked to a central mechanism that triggers the autonomic imbalance during REM sleep.
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4/96. Interaction of genetic predisposition and environmental factors in the pathogenesis of idiopathic orthostatic intolerance.

    BACKGROUND: The hemodynamic and autonomic abnormalities in idiopathic orthostatic intolerance (IOI) have been studied extensively. However, the mechanisms underlying these abnormalities are not understood. If genetic predisposition were important in the pathogenesis of IOI, monozygotic twins of patients with IOI should have similar hemodynamic and autonomic abnormalities. methods: We studied two patients with IOI and their identical twins. Both siblings in the first twin pair had orthostatic symptoms, significant orthostatic tachycardia, increased plasma norepinephrine levels with standing, and a greater than normal decrease in systolic blood pressure with trimethaphan infusion. RESULTS: Both siblings had a normal response of plasma renin activity to upright posture. In the second twin pair, only one sibling had symptoms of orthostatic intolerance, an orthostatic tachycardia, and raised plasma catecholamines with standing. The affected sibling had inappropriately low plasma renin activity with standing and was 8-fold more sensitive to the pressor effect of phenylephrine than the unaffected sibling. CONCLUSIONS: We conclude that in some patients, IOI seems to be strongly influenced by genetic factors. In others, however, IOI may be mainly caused by nongenetic factors. These findings suggest that IOI is heterogenous, and that both genetic and environmental factors contribute individually or collectively to create the IOI phenotype.
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5/96. Successful treatment of severe orthostatic hypotension with cardiac tachypacing in dual chamber pacemakers.

    Orthostatic hypotension is an evolving and disabling disease usually observed in elderly patients with dramatic consequences on morbidity, mortality, and impairing the quality of life. We studied the effects of the pacing rate and AV interval on the blood pressure drop in the upright position in two patients with previously implanted pacemakers for sinus node dysfunction. Although the AV interval did not affect the blood pressure drop in the upright position, tachypacing at 100 paces/min improved it dramatically and prevented syncope. Cardiac tachypacing is a useful therapeutic option in severe refractory orthostatic hypotensive patients, especially those with chronotropic incompetence.
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6/96. orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency.

    BACKGROUND: orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, and syncope and associated with postural tachycardia and plasma norepinephrine concentrations that are disproportionately high in relation to sympathetic outflow. We tested the hypothesis that impaired functioning of the norepinephrine transporter contributes to the pathophysiologic mechanism of orthostatic intolerance. methods: In a patient with orthostatic intolerance and her relatives, we measured postural blood pressure, heart rate, plasma catecholamines, and systemic norepinephrine spillover and clearance, and we sequenced the norepinephrine-transporter gene and evaluated its function. RESULTS: The patient had a high mean plasma norepinephrine concentration while standing, as compared with the mean ( /-SD) concentration in normal subjects (923 vs. 439 /-129 pg per milliliter [5.46 vs. 2.59 /-0.76 nmol per liter]), reduced systemic norepinephrine clearance (1.56 vs. 2.42 /-0.71 liters per minute), impairment in the increase in the plasma norepinephrine concentration after the administration of tyramine (12 vs. 56 /-63 pg per milliliter [0.07 vs. 0.33 /-0.37 pmol per liter]), and a disproportionate increase in the concentration of plasma norepinephrine relative to that of dihydroxyphenylglycol. Analysis of the norepinephrine-transporter gene revealed that the proband was heterozygous for a mutation in exon 9 (encoding a change from guanine to cytosine at position 237) that resulted in more than a 98 percent loss of function as compared with that of the wild-type gene. Impairment of synaptic norepinephrine clearance may result in a syndrome characterized by excessive sympathetic activation in response to physiologic stimuli. The mutant allele in the proband's family segregated with the postural heart rate and abnormal plasma catecholamine homeostasis. CONCLUSIONS: Genetic or acquired deficits in norepinephrine inactivation may underlie hyperadrenergic states that lead to orthostatic intolerance.
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7/96. A case of arrhythmia-induced transient cerebral hyperaemia.

    Transient cerebral hyperaemia following an arrhythmia has not been previously demonstrated in humans. We report the effects of head-up tilt on a 78-year-old man with neurocardiogenic syncope. During tilt, an asymptomatic arrhythmia caused arterial blood pressure and transcranial Doppler-recorded cerebral blood flow velocity to fall markedly. Upon spontaneous resumption of sinus rhythm, cerebral blood flow velocity increased to values greater than those prior to the arrhythmia. This occurred prior to a full recovery of arterial blood pressure, indicating spontaneous transisent hyperaemia. Pressure-flow velocity graphs support current methods of measuring critical closing pressure and demonstrate a rise in critical closing and a fall in resistance-area product after the arrhythmia.
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8/96. Valsalva-induced syncope during apnea diving.

    A young man had two dangerous episodes of transient loss of consciousness during apnea diving in a swimming pool. Medical and neurologic examination results were normal. Standard autonomic test results (including heart rate variability, baroreflex sensitivity, tilt-table test, and Valsalva ratio) were unremarkable, with the exception of an increased blood pressure decrease during early phase II of the valsalva maneuver. syncope with arrhythmic myoclonic jerks could be evoked by a strong straining maneuver. Simultaneous physiologic recordings showed extreme blood pressure and cerebral blood flow velocity decreases and electroencephalographic slowing during syncope. The electrocardiogram showed a continuous sinus rhythm with a progressive tachycardia. The authors' findings were not compatible with baroreflex failure or vasovagal mechanisms (Bezold-Jarisch reflex activation) as the underlying causes. The authors concluded that mechanical factors (strong reduction of blood reflux to the heart) in combination with a reduced threshold of the brain for developing ischemia-related arrhythmic myoclonic jerks were responsible for Valsalva-induced syncope in the patient.
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9/96. subclavian steal syndrome: a rare but important cause of syncope.

    An elderly woman came to our emergency room for evaluation of a syncopal episode. While climbing a flight of stairs, she had turned her head to the left and abruptly passed out. Positive physical findings included blood pressure of 141/65 mm Hg (right arm) and 80/43 mm Hg (left arm), as well as nonpalpable left radial and brachial pulses that were detectable only by Doppler ultrasonography. Carotid duplex ultrasonography showed reverse flow in the left vertebral artery and an abnormal, stenotic distal left subclavian artery. magnetic resonance angiography confirmed complete occlusion of the left subclavian artery with classic subclavian steal. The patient had percutaneous transluminal angioplasty with stenting of the left subclavian artery and has remained asymptomatic through 2 years of follow-up with aggressive risk-factor modification.
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10/96. Atrioventricular dissociation exacerbating posturally-induced syncope.

    We report a case of an 85-year-old patient with posturally-induced syncope in whom symptoms were reproduced during tilt table testing in conjunction with development of an accelerated junctional rhythm with isorhythmic atrio-ventricular (AV) dissociation. That loss of AV synchrony was crucial to development of hypotension and syncope was demonstrated during electrophysiologic testing in which both an accelerated junctional rhythm and an inducible atypical AV nodal re-entrant tachycardia (AVNRT) were induced. The accelerated junctional rhythm was accompanied by moderate hypotension with the patient in the supine posture, whereas blood pressure was well maintained during atypical AVNRT despite a much faster ventricular rate. Thus, symptomatic hypotension due to AV dissociation, presumably the result of transient autonomic disturbance, may be another manifestation of neurally-mediated syncope.
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