Cases reported "Bradycardia"

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1/14. Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure.

    We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.
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2/14. Hypertrophic cardiomyopathy complicated by severe bradycardias: a pedigree report.

    We describe four patients with nonobstructive hypertrophic cardiomyopathy (HCM) from an extended Chinese family. The patients had remarkably similar physical and echocardiographic findings including a harsh localized systolic murmur and apical left ventricular hypertrophy. All four had severe sinus bradycardia and atrial-ventricular conduction block (AVB) manifest by recurrent syncope. Two died suddenly due to bradycardia. Holter monitoring showed no tachycardias. Late potentials were not present. We conclude that this unusual form of HCM may be caused by a new and as yet unknown gene mutation.
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3/14. Postictal asystole during ECT.

    BACKGROUND: Asystole is an uncommon but potentially fatal complication of electroconvulsive therapy (ECT). Several risks for poststimulus asystole have been described, but risks for asystole at other times have not. METHOD: Two instances of ECT postictal asystole in healthy adult males are reported. Features in common are identified. RESULTS: features shared differ from risk factors for poststimulus asystole. In common were adult but not geriatric age, male sex, good physical and cardiac health, mesomorphic habitus, anticholinergic pretreatment, vigorous ECT seizure, and low resting heart rate. Both patients showed postictal bradyarrhythmia at the previous ECT. CONCLUSIONS: Postictal asystole has apparent similarities to postexertional asystole in athletes. The combination of higher pretreatment doses of an atropinic agent, a sympatholytic agent, and close monitoring of postictal cardiac rhythm should be considered with patients similar to ours, especially after occurrence of postictal bradyarrhythmia.
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4/14. Favorable outcome in a pregnancy with complete fetal heart block and severe bradycardia.

    BACKGROUND:Pregnancies complicated by congenital heart block usually have a poor prognosis when there is severe fetal bradycardia.CASE:We present a pregnancy with fetal heart rate of 40 beats per minute. She previously delivered a child with third-degree heart block by cesarean at 28 weeks. This pregnancy was complicated by a high ribonucleoprotein antibody anti-Ro/SSA titer and fetal bradycardia. The patient was treated with steroids and beta-mimetics. The fetus continued to grow normally with reassuring biophysical profiles. After fetal lung maturity documentation at 34 weeks, she delivered by repeat cesarean a healthy 2349-g infant who required a permanent pacemaker.CONCLUSION:Reassuring antepartum testing and normal growth in pregnant women with anti-Ro/SSA antibodies and congenital heart block may allow expectant management until fetal maturity.
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keywords = physical
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5/14. Pacemaker channel dysfunction in a patient with sinus node disease.

    The cardiac pacemaker current I(f) is a major determinant of diastolic depolarization in sinus nodal cells and has a key role in heartbeat generation. Therefore, we hypothesized that some forms of "idiopathic" sinus node dysfunction (SND) are related to inherited dysfunctions of cardiac pacemaker ion channels. In a candidate gene approach, a heterozygous 1-bp deletion (1631delC) in exon 5 of the human HCN4 gene was detected in a patient with idiopathic SND. The mutant HCN4 protein (HCN4-573X) had a truncated C-terminus and lacked the cyclic nucleotide-binding domain. COS-7 cells transiently transfected with HCN4-573X cDNA indicated normal intracellular trafficking and membrane integration of HCN4-573X subunits. Patch-clamp experiments showed that HCN4-573X channels mediated I(f)-like currents that were insensitive to increased cellular cAMP levels. Coexpression experiments showed a dominant-negative effect of HCN4-573X subunits on wild-type subunits. These data indicate that the cardiac I(f) channels are functionally expressed but with altered biophysical properties. Taken together, the clinical, genetic, and in vitro data provide a likely explanation for the patient's sinus bradycardia and the chronotropic incompetence.
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6/14. stroke rehabilitation therapy in a patient with a cardiac pacemaker for chronic atrial fibrillation.

    A 65-year-old man was implanted with an artificial pacemaker for chronic bradycardic atrial fibrillation associated with hypertensive heart disease. Five years after the pacemaker implantation, he suffered from a cerebral embolism. Approximately 4.5 months after the ictus, he was transferred to the rehabilitation ward. He had flaccid left hemiplegia and severe disuse syndrome. He could not sit and could tilt his head up for only two minutes because of severe orthostatic hypotension. By modulating the rate-responsive mode of the pacemaker every 2-4 weeks, we were able to rehabilitate the patient. Thus, the patient could sit in a wheelchair for more than three hours. This case emphasizes the importance of examining the mode and function of a previously implanted artificial pacemaker. In accord with varying rehabilitation programs and gradual improvement in a patient's physical activities, periodic modulation of a programmable pacemaker can lead to a better functional outcome during rehabilitation therapy.
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7/14. Resting tachycardia, a warning sign in anorexia nervosa: case report.

    BACKGROUND: Among psychiatric disorders, anorexia nervosa has the highest mortality rate. During an exacerbation of this illness, patients frequently present with nonspecific symptoms. Upon hospitalization, anorexia nervosa patients are often markedly bradycardic, which may be an adaptive response to progressive weight loss and negative energy balance. When anorexia nervosa patients manifest tachycardia, even heart rates in the 80-90 bpm range, a supervening acute illness should be suspected. CASE PRESENTATION: A 52-year old woman with longstanding anorexia nervosa was hospitalized due to progressive leg pain, weakness, and fatigue accompanied by marked weight loss. On physical examination she was cachectic but in no apparent distress. She had fine lanugo-type hair over her face and arms with an erythematous rash noted on her palms and left lower extremity. Her blood pressure was 96/50 mm Hg and resting heart rate was 106 bpm though she appeared euvolemic. Laboratory tests revealed anemia, mild leukocytosis, and hypoalbuminemia. She was initially treated with enteral feedings for an exacerbation of anorexia nervosa, but increasing leukocytosis without fever and worsening left leg pain prompted the diagnosis of an indolent left lower extremity cellulitis. With antibiotic therapy her heart rate decreased to 45 bpm despite minimal restoration of body weight. CONCLUSIONS: bradycardia is a characteristic feature of anorexia nervosa particularly with significant weight loss. When anorexia nervosa patients present with nonspecific symptoms, resting tachycardia should prompt a search for potentially life-threatening conditions.
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ranking = 7.8647311256361
keywords = physical examination, physical
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8/14. Atrioventricular conduction disturbances in a young patient with Fabry's disease without other signs of cardiac involvement.

    A 30 year-old male patient with a history of Fabry's disease, was referred to hospital with symptoms of dizziness, hypotension and weakness. Fabry's disease had been diagnosed 2 years before, based on angiokeratoma and hypohidrosis on physical examination and complete lack of alpha-galactosidase A on laboratory examination. The ECG on admission demonstrated sinus bradycardia, with a poor response to atropine administration. Echocardiograms on admission and 2 years before were normal, as well as Holter ambulatory ECG recording. Subsequent electrophysiological study demonstrated mild AV conduction disturbances at a site proximal to His, and the patient was simply advised to be regularly followed up. It can therefore be concluded that even young patients with Fabry's disease and normal echocardiograms might develop cardiac symptoms due to AV conduction abnormalities.
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keywords = physical examination, physical
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9/14. Congenital atrial standstill associated with coinheritance of a novel SCN5A mutation and connexin 40 polymorphisms.

    BACKGROUND: Congenital atrial standstill has been linked to SCN5A. Incomplete penetrance observed in atrial standstill has been attributed in part to the digenic inheritance of polymorphisms in the atrial-specific gap junction connexin 40 (Cx40) in conjunction with an SCN5A mutation. OBJECTIVES: The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation identified in a family with atrial standstill. methods: family members of an apparently sporadic case of atrial standstill underwent genetic screening of SCN5A and atrial-specific genes including Cx40. Biophysical properties of the wild-type (WT) and mutant SCN5A channels in a heterologous expression system were studied using the whole-cell patch clamp technique. RESULTS: The novel SCN5A mutation L212P was identified in the proband (age 11 years) and his father. The father was in normal sinus rhythm. The proband had no P waves on surface ECG, and his right atrium could not be captured by pacing. The recombinant L212P Na channel showed a large hyperpolarizing shift in both the voltage dependence of activation (WT: -48.1 /- 0.9 mV; L212P: -63.5 /- 1.5 mV; P < .001) and inactivation (WT: -86.6 /- 0.9 mV; L212P: -95.6 /- 0.8 mV; P < .001) and delayed recovery from inactivation. Further screenings for genetic variations that might mitigate L212P dysfunction revealed that the proband, but not his father, carries Cx40 polymorphisms inherited from his asymptomatic mother. CONCLUSION: These results suggest that genetic defects in SCN5A most likely underlie atrial standstill. Coinheritance of Cx40 polymorphisms is a possible genetic factor that modifies the clinical manifestation of this inherited arrhythmia.
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10/14. bradycardia during methadone therapy in an infant.

    OBJECTIVES: To report the occurrence of bradycardia associated with the use of methadone administered to prevent withdrawal in an infant with physical tolerance following long-term opioid therapy in the pediatric intensive care unit setting. DESIGN: Retrospective case report. patients AND RESULTS: methadone (0.1 mg/kg) was administered to a 6-month-old infant following prolonged use of intravenous fentanyl for sedation during respiratory failure requiring mechanical ventilation. Approximately 30-60 mins after the first dosing of methadone, the infant's heart rate decreased from his baseline of 130-140 beats/min to 80-90 beats/min for 30 seconds. After the third dose of methadone, the heart rate decreased to a sinus bradycardia of 60-70 beats/min for 4 mins. The episodes resolved with tactile stimulation. Over the next 18 hrs, there were repeated episodes of bradycardia. None of these episodes were associated with hypotension, apnea, change in oxygen saturation, decreased peripheral perfusion, or other signs of hemodynamic instability. The methadone was withdrawn and the intravenous fentanyl infusion was restarted. Eight to 10 hrs after administration of the last dose of methadone, the episodes of bradycardia resolved and the patient remained in a normal sinus rhythm with a heart rate of 120-140 beats/min. CONCLUSION: methadone's three-dimensional structure shares similarities with calcium channel antagonists. Although it has been reported in the adult literature, there are no previous reports of bradycardia occurring with methadone therapy in infants. Although there were no deleterious physiologic effects related to the bradycardia in our patient, methadone should be used cautiously in patients who may not tolerate alterations in heart rate.
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