Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diphenylhydantoin (DPH) and Carbamazepine have been widely used as anticonvulsants and known to have antiarrhythmic properties. Previous reports have shown that arrhythmias such as sinus bradycardia and atrioventricular block can be induced by these agents. In this paper, sinoatrial block (SA block) induced by these agents which were used as anticonvulsants in 3 aged patients is reported. Thre patients, 2 women and 1 man, were over 60 years old. In 2 cases, administration of DPH for recurrent epileptic seizures was followed by SA block. After withdrawal of DPH, SA block disappeared, but resumption of DPH resulted in SA block again. In 1 of these 2 patients, overdrive suppression test revealed normal sinus node recovery time. In the third patient, in addition to DPH which was administered for epileptic seizures, Carbamazepine was given for shoulder pain, then SA block occurred. Withdrawal of these agents restored normal sinus rhythm and combined administration of these 2 agents again induced SA block. Autopsy revealed decreased conduction cells in the sinus node.
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PMID:Three cases of sinoatrial block induced by anticonvulsants. 73 79

A patient with an acute anterior wall myocardial infarction complicated by bilateral bundle branch block and paroxysmal AV block is presented. The following new, uncommon or unreported phenomena were documented: the simultaneous occurrence of phase-3 block in the right bundle branch and phase-4 block in the left bundle branch; the simultaneous occurrence of phase-4 block in both main bundle branches; phase-4 left posterior hemiblock associated with escape beats arising from the injured posterior division of the left bundle branch; supernormal conduction in the right bundle branck and 2:1 right bundle branch block related to supernormality. Most of these changes were, of course, not simultaneous, and their successive appearance was related to day-to-day and sometimes hour-to-hour variations in the degree and quality of the multifascicular injury caused by the infarct. In addition, the actions of several drugs upon automaticity and conduction were tested. The effects of amiodarone, lidocaine and isoproterenol were similar to those previously reported under comparable circumstances. At a moment when the patient had repeated episodes of paroxysmal AV block with severe Adams-Stokes seizures, the administration of a single i.v. dose of 0.25 mg of strophanthin suppressed totally the Adams-Stokes attacks through a significant enhancement of ventricular automaticity. If rapid implantation of an artifical pacemaker is not at hand, strophanthin may be life-saving in patients with acute paroxysmal AV block.
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PMID:Electrophysiologic and pharmacologic studies in a patient with acute myocardial infarction complicated by intraventricular and atrioventricular block. 119 12

A patient with 2 : 1-block and right-bundle-branch block is described, who developed a high-degree-AV block distal to the bundle of His during electrophysiological investigations. Rapid atrial pacing caused total AV block distal to the His bundle. Rapid pacing from the right ventricle also caused total AV block after sudden discontinuation of pacing. The duration of total AV block was 25 to 60 seconds and the preautomatic time 2300-4750 msec according to rate and duration of stimulation. These methods are considered as good tools to evaluate patients with severely diseased conduction system, who might develop total AV block or Adams-Stokes seizures.
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PMID:[Electric stimulation as a means for the diagnosis of atrioventricular conduction disorders]. 121 74

To determine the factors relating to prognosis, the records of 15 neonates with persistent prolongation of the QT interval on the electrocardiogram after the fourth day of life were reviewed. Patients were admitted for symptoms (syncope, cardiac failure, or seizures), abnormal auscultation with an irregular heart rate or bradycardia, or because of a family history of a long QT syndrome. All infants had a long QTc, ranging from 0.46 to more than 0.70 second. Eight patients who had a QTc over 0.60 second developed severe ventricular arrhythmias (torsades de pointes, ventricular tachycardia) or second-degree AV block. Twelve of 15 were treated with beta-blocking agents, combined with ventricular pacing in five cases. Four infants died in the first month of life; they all had a very long QT interval and had experienced ventricular arrhythmias and AV block. Six children are still being treated with beta-blocking agents for the long QT syndrome and are doing well. In five infants, electrocardiographic abnormalities were transient and the QT interval returned to normal within 1 year. Therefore (1) prolongation of the QT interval in neonates may be transient or may represent an early form of the long QT syndrome and (2) the length of the QT interval may provide data on prognosis: those with a QTc less than 0.50 second returned to normal; those with a QTc greater than 0.60 second were associated with severe arrhythmias and four of eight infants died.
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PMID:Prolonged QT interval in neonates: benign, transient, or prolonged risk of sudden death. 135 80

Seven out of 829 pediatric cardiac patients (0.84%) were found to have sinus node dysfunction (SND) over the past seven years. Of the seven patients, three had structurally normal hearts. One of these three patients had long QT syndrome. In four patients, structural heart disease was noted. In three of these four patients the sinus node dysfunction was attributed to cardiac surgery. The age of onset of SND ranged from four months to eight years. Presenting symptoms and signs included syncope, near-syncope, seizure and congestive heart failure. Two patients were asymptomatic. Five patients had episodic sinus pause. Sinus or junctional bradycardia was noted in four patients. Three had tachy-bradycardia. High grade atrioventricular block was noted in one patient. Treadmill exercise test revealed a nonsustained ventricular tachycardia in two patients. All seven patients were found to have prolonged maximal corrected sinus node recovery time. Prolonged intra-atrial conduction time was found in three, prolonged AV nodal conduction time in one, and prolonged His-Purkinje conduction time in one patient during the electrophysiologic study. All seven patients showed abnormal results in intrinsic heart rate study. Anti-arrhythmic drugs were prescribed. During the follow-up study, no patient died, but two patients received a pacemaker implantation. Because of the extent of their conduction system diseases, it is recommended that patients with SND should be thoroughly investigated.
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PMID:Sinus node dysfunction in children. 151 8

A 35-year-old man was hospitalized after a sudden onset of transient syncopal attack without accompanying complaints of headache or nausea. He was slightly disorientated but neurologically normal. He had a blood pressure of 150/90mmHg and a pulse rate of 40/min. An ECG showed marked sinus brady-cardia with ventricular escaped rhythm followed by advanced atrioventricular (AV) block. Some components of conducted ventricular beats showed aberration. There was no significant ST or T wave abnormality in normally captured QRS components except for prominent T in leads II, III and aVF. At first, we thought that he might require temporary pacing because of Adams-Stokes attack. However, after administration of atropine sulfate, the ECG returned to normal sinus rhythm with heart rate of 88/min. Then he began to complain of headache followed by a convulsive seizure. A CT scan and angiogram revealed a ruptured aneurysm at the top of the basilar artery, which was successfully clipped. A wide spectrum of ECG changes can be demonstrated in practically all patients with subarachnoid hemorrhage (SAH). Prolonged QT interval, ST-T changes, U wave, sinus tachycardia, or ventricular premature complex are the common abnormalities probably caused by increased circulating catecholamine. As bradyarrhythmia in patients with SAH is an uncommon finding, its mechanism has not yet been defined. Transient sinus bradycardia with advanced AV block in this patient might have been caused not by elevated intracranial pressure (Cushing phenomenon) but by drastic discharge of the parasympathetic nerve. This case serves to illustrate the vigilance required in determining whether abnormalities of cardiac rhythm are instrumental in causing neurological symptoms and signs or a disorder of cerebral function.
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PMID:[A case of subarachnoid hemorrhage with sick sinus and advanced AV block]. 151 79

A 14-month-old child ingested approximately 800 mg (70 mg/kg) of nifedipine. When first examined, the child was unresponsive, markedly hypotensive, and hyperglycemic. According to electrocardiographic results, there was a third-degree atrioventricular block that rapidly progressed to cardiac arrest. Following successful cardiopulmonary resuscitation, mechanical ventilation and resuscitation with intravenous normal saline, calcium chloride and dopamine were required to restore perfusion, reverse metabolic acidosis, and stabilize vital signs. Complications related to nifedipine intoxication included the development of pulmonary edema and possible infarction in the posterior parietal and occipital lobes associated with cortical blindness and the development of seizures with an abnormal electroencephalogram. The patient recovered without clinically apparent residua. Massive nifedipine overdose in infants represents a potentially life-threatening event that requires prompt medical attention. Reported cases of nifedipine intoxication were reviewed and therapeutic interventions were discussed.
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PMID:Nifedipine poisoning in a child. 235 87

A permanent pacemaker was inserted in eight patients with the long QT syndrome. All had recurrent syncope or seizures, six had documented torsade de pointes and four had aborted sudden death. Among the eight patients, permanent pacing was instituted in three who were unsuccessfully treated with both a beta-adrenergic blocking agent and left cardiothoracic sympathectomy, and in two who proved refractory or intolerant to beta-blockers. Another three patients had pacemaker implantation and long-term beta-blocker therapy because of spontaneous atrioventricular (AV) block in one, aborted sudden death in one and patient preference in one. After pacing (70 to 85 beats/min), there was no significant change in the mean corrected QT interval, but the mean QT interval decreased significantly (534.4 +/- 51.4 to 425.6 +/- 18.9 ms, p less than 0.0001). Over a mean follow-up period of 35.1 +/- 18.9 months, all patients are alive and currently free of syncope. One patient without a history of stress-induced syncope had two syncopal episodes (believed to be due to hyperventilation) while under severe emotional stress, but has been symptom free for the past 5 years. One patient with an atrial demand (AAI) pacemaker developed dizziness due to documented episodes of AV block, but remains asymptomatic after conversion to atrial rate-responsive dual chamber (DDD) pacing. Either atrial or ventricular pacing combined with beta-blocker therapy appears to be effective treatment for a subset of patients with the long QT syndrome, by either preventing episodes of torsade de pointes or alleviating symptoms due to bradycardia from beta-blocker therapy.
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PMID:Permanent cardiac pacing in patients with the long QT syndrome. 362 66

Deaths from tricyclic antidepressant (TCA) overdose are usually due to arrhythmias and/or hypotension. Tricyclic antidepressant toxicity is due mainly to the quinidine-like actions of these drugs on cardiac tissues. Slowing of phase 0 depolarisation of the action potential results in slowing of conduction through the His-Purkinje system and myocardium. Slowed impulse conduction is responsible for QRS prolongation and atrioventricular block, and contributes to ventricular arrhythmias and hypotension. Therapies that improve conduction, e.g. hypertonic sodium bicarbonate, are useful in treating these toxic effects. Other mechanisms contributing to arrhythmias include abnormal repolarisation, impaired automaticity, cholinergic blockade and inhibition of neuronal catecholamine uptake. Toxicity may be worsened by acidaemia, hypotension or hyperthermia. Sinus tachycardia is due to the anticholinergic effects of the tricyclic antidepressants as well as blockade of neuronal catecholamine reuptake. Sinus tachycardia is generally well-tolerated and requires no therapy. Sinus tachycardia with QRS prolongation may be difficult to distinguish from ventricular tachycardia. Electrocardiograms obtained using oesophageal or atrial electrodes may be useful in determining the relationship of atrial and ventricular activity. Although QRS prolongation alone is not compromising, it is a marker for patients at highest risk of developing seizures, arrhythmias or hypotension. Ventricular tachycardia (monomorphic) is a consequence of impaired myocardial depolarisation and impulse conduction. Hypertonic sodium bicarbonate may partially correct impaired conduction and be of benefit in treating ventricular tachycardia. Since hypertonic sodium bicarbonate appears to act by increasing the extracellular sodium concentration as well as by increasing extracellular pH, hyperventilation may be less effective. Hypertonic sodium bicarbonate is of particular benefit in patients who are acidotic, since acidosis aggravates cardiac toxicity. However, administration of hypertonic sodium bicarbonate is beneficial even when blood pH is normal. Lignocaine (lidocaine) may be useful in treating ventricular tachycardia but should be administered cautiously to avoid precipitating seizures. Ventricular bradyarrhythmias are due to impaired automaticity or depressed atrioventricular conduction and can be treated by placement of a temporary pacemaker, or with a chronotropic agent, e.g. isoprenaline (isoproterenol), with or without concomitant vasoconstrictors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tricyclic antidepressant poisoning. Management of arrhythmias. 378 39

Many patients admitted for observation to the intensive care unit after a drug overdose do not ultimately require intensive care interventions. We retrospectively analyzed data on 209 overdose cases to determine whether clinical assessment in the emergency room could identify patients at risk for complications. Patients were classified as low risk when none of the following high-risk criteria were present in the emergency room: need for intubation; seizures; unresponsiveness to verbal stimuli; arterial carbon dioxide pressure (tension) greater than or equal to 45 mm Hg; any rhythm except sinus; second- or third-degree atrioventricular block; QRS greater than or equal to 0.12 s; or systolic pressure less than 80 mm Hg. Of 151 low-risk patients, none developed a high-risk condition after admission, and none required an intensive care intervention. The use of these predictive criteria in our patient population would have eliminated over half the intensive care days without compromising quality of care.
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PMID:Predicting the clinical course in intentional drug overdose. Implications for use of the intensive care unit. 380 May 15


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