Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 67-year-old man with Wolff-Parkinson-White syndrome type A presented with second degree atrioventricular block in anomalous pathway and complete infra-Hisian block in the His-Purkinje pathway. He had increasingly frequent attacks of dizziness not related to exercise. A permanent ventricular demand pacemaker was successfully implanted following intracardiac electrophysiological studies.
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PMID:Wolff-Parkinson-White syndrome (type A) complicated by heart block in both normal and accessory pathways. 71 75

Although analysis of the surface electrocardiograms is usually sufficient in the diagnosis and management of patients with cardiac arrhythmias, electrophysiologic studies can improve diagnostic, therapeutic, and prognostic decisions. Indications for electrophysiologic studies appear to include the following: (1) asymptomatic patients with chronic second degree AV block, both type I and type II with or without bundle branch block; (2) asymptomatic patients with complete AV block; (3) symptomatic patients with bundle branch block and 1:1 AV conduction; (4) patients with bundle branch block complicating acute myocardial infarction; (5) patients with electrocardiograms suggesting pseudo AV block; (6) symptomatic patients with sinus bradycardia, in whom the causal relationship is not clear enough to justify pacing therapy; (7) patients with frequent, troublesome paroxysmal supraventricular tachycardia; (8) patients with Wolff-Parkinson-White syndrome and frequent paroxysmal supraventricular tachycardia; (9) patients with recurrent paroxysmal ventricular tachycardia; (10) patients with syncope or severe dizziness in whom the causal mechanism is not defined.
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PMID:Clinical judgement is not sufficient for the management of conduction defects (indications for diagnostic electrophysiologic studies). 84 90

In two patients with WPW syndrome Type A suffering from syncopes and dizziness intermittent high degree A-V block was observed. The analysis of the surface Ecg revealed in the first case a complete A-V block within the normal conduction system at the level of the A-V node. In the second case there was a constant left bundle branch block with intermittent block in the right fascicle (intermittent trifascicular block). In both cases the preexcitation syndromes could be best explained by accessory tracts bypassing the normal nodal system left side. One-to-one conduction through the bypass occurred only at a distinct range of cycle lengths, at lower frequencies the accessory tracts were refractory and a IInd or IIIrd degree A-V block occurred. However, outside this frequency zone some P waves were conducted through the accessory tracts without changes in cycle lengths. The findings support the thesis of at least two functionally different atrioventricular pathways in patients with preexcitation syndrome.
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PMID:[Severe atrioventricular block in 2 cases with pre-excitation syndrome]. 96 Sep 77

20 patients with WPW syndrome and recurrent tachyarrhythmias were studied clinically and electrophysiologically. The localization and electrophysiological properties of accessory pathways and other heart structures were estimated before the surgical treatment. 13 patients (pts) suffered syncope in the course of atrial flutter or atrial fibrillation with heart rate greater than 300/min, often proceeding into ventricular fibrillation or atrioventricular tachycardia greater than 260/min, which sometimes proceeds into atrial/ventricular fibrillation. 6 pts experienced dizziness or fainted during tachyarrhythmias or rhythm changes. In 15 pts antiarrhythmic drugs in monotherapy or various combinations did not prevent recurrence of tachyarrhythmias. In 4 of 5 other pts only amiodarone was effective but the drug was discontinued due to serious adverse effects. The lack of good effect of antiarrhythmic drug therapy can be based on mutually unfavorable electrophysiologic properties of the accessory pathways and other heart structures. Pts who experienced syncope had a particularly short effective refractory period (ERP) of the accessory pathways in ante- and retro-grade direction and short ERP of the ventricle muscle. Additionally, there were multiple accessory pathways, heart muscle impairement and frequent ventricular premature beats--factors triggering the tachyarrhythmias.
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PMID:[Clinical and electrophysiological indications for surgical treatment in patients with Wolff-Parkinson-White syndrome]. 160 82

We present our experience on the efficacy of propafenone in ten symptomatic patients with Wolff-Parkinson-White syndrome. The symptoms were dizziness in seven patients and syncope in three patients. While experiencing the symptoms, three of them presented an episode of atrial fibrillation, the shortest preexcited RR intervals being 140, 190, and 200 ms. In the other seven patients, the ECG was not recorded during the symptoms, but an episode of atrial fibrillation was subsequently induced by transesophageal pacing. The shortest preexcited RR intervals during induced atrial fibrillation were 180, 200, 270, 240, 230, 250, and 200 ms. Seven patients had both atrial fibrillation and supraventricular tachycardia. Propafenone (1-2 mg/kg) administered IV in only the patients with sustained atrial fibrillation (spontaneous in two and induced in one patient) prolonged the shortest preexcited RR intervals from 190, 200, and 180 ms to 340, 335, and 340 ms. In the other seven patients, propafenone was not given IV because atrial fibrillation rapidly deteriorated into ventricular fibrillation (one patient) or spontaneously reverted within 1-2 minutes to sinus rhythm (six patients). After oral propafenone, serial trans-esophageal pacing studies reinduced atrial fibrillation in 4 of 6 patients (the shortest preexcited RR intervals increased from 190, 180, 200, and 270 ms to 420, 320, 340, and 380 ms); only in one patient was it possible after propafenone to induce an atrial flutter without preexcitation. After propafenone therapy in 4 of 7 patients, supraventricular tachycardia was not inducible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Propafenone in Wolff-Parkinson-White syndrome at risk. 207 78

Antidromic circus movement tachycardia was documented in 36 of 345 consecutive patients with Wolff-Parkinson-White syndrome undergoing detailed electrophysiologic evaluation. Twenty-six patients were men and 10 were women (mean age +/- standard deviation 26 +/- 12 years [range 12 to 45]). Multiple accessory pathways were identified in 12 of these 36 patients (33%). Ten of the patients (67%) with clinically documented antidromic tachycardia had multiple accessory pathways. Dizziness and syncope occurred in 61 and 50% of patients with antidromic circus movement tachycardia. Six patients had clinical documentation of atrial fibrillation, and 4 patients (11%) were resuscitated from ventricular fibrillation. In the 36 patients, 56 distinct antidromic tachycardias were recorded and several different pathways were observed. Orthodromic tachycardia was the most frequently associated arrhythmia (72%). Dual atrioventricular nodal pathways were present in 12 patients (33%); however, atrioventricular nodal tachycardia could be initiated in only 2 of them. Interruption of the accessory pathway was successfully performed in all 20 patients undergoing surgery.
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PMID:Clinical and electrophysiologic characteristics of patients with antidromic circus movement tachycardia in the Wolff-Parkinson-White syndrome. 222 Jun 35

Paroxysmal atrial fibrillation (PAF) in patients with manifest WPW syndrome can be a life-threatening arrhythmia by deterioration into ventricular fibrillation. In patients with asymptomatic WPW pattern, the first PAF may lead to ventricular fibrillation or sudden death. Therefore, the purpose of this study was to predict a fatal PAF in patients with asymptomatic WPW pattern. The patient population was divided into two groups: (1) 145 patients with manifest WPW syndrome, excluding intermittent ones (32 with an episode of PAF, 49 with AV reciprocating tachycardia alone, and 64 without any episode of paroxysmal tachyarrhythmia), and (2) mixed group of patients with and without WPW syndrome (36 with an episode of PAF and 66 without PAF). The results were as follows: (1) (a) out of 32 patients with WPW syndrome and PAF, 8 patients were observed to have both the shortest preexcited R-R interval of less than 200 msec during PAF and the shortest antegrade effective refractory period of the accessory pathway (ERP-AP) of less than 250 msec, 7 of whom had dizziness or syncope during PAF and 2 died suddenly during the follow-up period; (b) 21 (32.8%) out of 64 patients with asymptomatic WPW pattern showed the shortest antegrade ERP-AP less than 250 msec; (2) patients with PAF had a higher tendency to develop repetitive atrial firing (RAF), as well as fragmented atrial activity (FAA), which were induced using programmed atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prediction of a fatal atrial fibrillation in patients with asymptomatic Wolff-Parkinson-White pattern. 227 12

The antiarrhythmic effect of oral propafenone was evaluated in 10 patients with Wolff-Parkinson-White syndrome presenting with non-ventricular arrhythmias (paroxysmal supraventricular tachycardia n = 7, atrial fibrillation or flutter n = 3). The mean age was 38 +/- 13 years, the dose varied from 300 to 900 mg three times a day (mean 450 +/- 188) and the mean follow-up period was 7 +/- 3.5 months. All patients' drug responses were assessed on 12-lead electrocardiograms and 24-hour ambulatory Holter monitoring. Electrophysiologic studies were performed in cases of sustained tachycardia while echocardiography identified 2 cases with mitral valve prolapse. Four of 10 (40%) patients became asymptomatic on a starting propafenone dose of 300 mg, while 6 (60%) had recurrences necessitating an increase in dose for the complete control of the symptoms. We observed a slight slowing of the heart rate and an increase of the mean Q-T interval (P less than 0.001). Three patients reported minor side effects including nausea, dizziness and constipation that were tolerable and dosage dependent. It is concluded that propafenone is an effective and well tolerated drug for the treatment of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome.
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PMID:Propafenone in the prevention of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome. 233 10

Encainide is classified as a type Ic antiarrhythmic agent. Absorption is essentially complete, but bioavailability is variable because of first-pass metabolism. Two metabolic phenotypes, extensive and poor metabolizers, have been identified. O-demethyl encainide and 3-methoxy-O-demethyl encainide are active metabolites of encainide and contribute significantly to its antiarrhythmic effect. In clinical trials, encainide has been shown to be highly effective in suppressing premature ventricular contractions and ventricular tachyarrhythmias. The drug is useful in treating ventricular arrhythmias refractory to other agents. Encainide is also moderately effective in supraventricular arrhythmias involving an accessory pathway. It is highly effective in cases of Wolff-Parkinson-White syndrome, where the accessory pathway has a short refractory period. Common adverse effects of encainide are dizziness, visual disturbances, nausea, and headache. Encainide appears to be a safe and effective antiarrhythmic agent with few adverse effects and negligible hemodynamic effects. Encainide may be a useful agent for ventricular and supraventricular arrhythmias, particularly those refractory to other agents.
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PMID:Encainide: a new antiarrhythmic agent. 308 Mar 1

Encainide is an antiarrhythmic drug with class IC activity which has been used in the treatment of life-threatening ventricular arrhythmias, symptomatic ventricular arrhythmias and supraventricular arrhythmias. The antiarrhythmic activity is due to the parent drug and its two principal active metabolites, and in the extensive metabolising phenotype (90% of patients), metabolites are present in plasma at higher concentrations than encainide itself. Encainide produces little haemodynamic change in patients with left ventricular dysfunction and thus has considerable therapeutic potential in view of its efficacy in patients with ventricular tachycardia, premature ventricular complexes and the Wolff-Parkinson-White syndrome. However, this potential is reduced by a tendency for encainide to aggravate arrhythmia in a proportion of patients. At present there is no reliable method of identifying patients at risk for this potentially serious side effect. The most common non-cardiac side effects are dizziness and blurred vision which seldom necessitate withdrawal of treatment. Thus, encainide has proved effective in controlling ventricular tachyarrhythmias including those which have not been controlled by other antiarrhythmic drugs.
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PMID:Encainide. A review of its pharmacological properties and therapeutic efficacy. 312 Dec 75


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