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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise myocardial-thallium scintigraphy plays a fundamental role in the diagnosis of coronary artery disease. Once exercise is not always feasible, pharmacological stress became a possible alternative. The authors review the mechanism of action, administrations protocols, indications and side effects of the drugs used for this purpose: dipyridamole, adenosine and dobutamine. Dipyridamole causes coronary hyperemia by increasing the interstitial levels of endogenous adenosine. Perfusion defects result from the mismatch of coronary reserve in different coronary territories. The drug administration is classically performed with a 0.142 mg/kg/min dosage e.v. for 4 minutes, total of 0.56 mg/kg. It is possible to use a greater dose of 0.84 mg/kg e.v. for 10 minutes, increasing sensitivity without loss of specificity for diagnosis of coronary artery disease. Oral dipyridamole protocols with 300 and 400 mg were used with similar results for sensitivity and specificity. The oral protocol has the disadvantage of delayed onset and longer action. Including several dipyridamole studies, 87% was obtained for sensitivity and 84% for specificity, in the diagnosis of CAD. Dipyridamole scintigraphy has been applied to myocardial infarction risk stratification, cardiac risk evaluation of patients proposed to noncardiac surgery and therapeutic efficacy evaluation of reperfusion techniques (angioplasty and surgery). The secondary effects of dipyridamole are frequent, however mild and well tolerated. They occur in half the patients, the most frequent, facial flushing (2%), dizziness (5%), nausea (4%), vomiting (1%), headaches (11%) and chest pain (26%). Some important complications were reported although rare: myocardial infarction, ventricular fibrillation and bronchospasm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of pharmacologic stimulation with myocardial perfusion scintigraphy in the evaluation of patients with ischemic cardiopathy]. 129 Jun 55

We examined, a 64 year old man with hypertrophic nonobstructive cardiomyopathy (HNCM) accompanied with dizziness. Twenty-four hour ECG monitoring showed sinus bradycardia and sinoatrial block. Electrophysiologic study demonstrated inducible sustained ventricular tachycardia (VT) by continuous rapid high right atrum pacing during which systolic blood pressure fell to 40 mmHg. Induced VT degenerated into ventricular fibrillation in ten seconds. We implanted a DDD pacemaker for sick sinus syndrome (SSS) and administrated 90mg/day of diltiazem for VT. Treadmill exercise test was carried out while the patient was taking diltiazem and no arrhythmia was induced. This case of HNCM is rare in that he presented both sick sinus syndrome and sustained VT.
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PMID:[A case of nonobstructive hypertrophic cardiomyopathy associated with ventricular tachycardia and sick sinus syndrome]. 143 57

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

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of the Class I antiarrhythmic agent moricizine hydrochloride are reviewed. Moricizine is chemically similar to the phenothiazines but does not appear to block dopaminergic receptors. Its major electrophysiologic actions are a concentration-dependent decrease in maximum rate of phase 0 depolarization; increased rates of phase 2 and 3 repolarization, decreased action potential duration, and decreased effective refractory period. Moricizine causes a dose-related prolongation of the PR interval and of AV nodal, infranodal, and intraventricular conduction times but has little effect on ventricular repolarization. The antiarrhythmic and electrophysiologic effects are not correlated with plasma concentrations of the drug or its metabolites. Moricizine reduces the occurrence of ventricular premature contractions (VPCs), couplets, and nonsustained ventricular tachycardia. It appears to suppress symptomatic nonsustained ventricular tachycardia, sustained ventricular tachycardia, and ventricular fibrillation or flutter. Moricizine appears to be as effective as quinidine and more effective than disopyramide, propranolol, and imipramine but less effective than flecainide and encainide at reducing VPCs. Moricizine continues to be evaluated in the Cardiac Arrhythmia Suppression Trial, which was designed to assess the long-term benefit of arrhythmia suppression in patients with left ventricular dysfunction after myocardial infarction. Moricizine seems to be better tolerated than quinidine, disopyramide, and imipramine and to have less proarrhythmic potential than flecainide or encainide. Noncardiac adverse effects include dizziness, nausea, and headache. Cimetidine appears to decrease moricizine clearance, and decreased theophylline clearance has been reported in subjects given moricizine. The usual adult dosage of moricizine hydrochloride is 600-900 mg/day given in three divided doses; an every-12-hour regimen may be used in some patients. Because of the risk of proarrhythmic effects, indications are limited to treatment of documented life-threatening arrhythmias. Moricizine will compete with other agents as first-line therapy for life-threatening arrhythmias.
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PMID:Moricizine: a new class I antiarrhythmic. 227 51

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

During the 1986 World's Exposition held in Vancouver, British Columbia, the types and frequencies of emergency medical problems were assessed. The average number of patients seeking care was 3.93 +/- 0.95 per 1,000 visitors (daily range, 1.94 to 6.8). Patient loads were linearly related to gate attendance, but the correlation was imperfect (P less than .001, r = .63). Only 4.4% of patients evaluated on site by nurses and paramedics were referred for additional testing and treatment: of these patients, 30% had suspected serious musculoskeletal injury, 16% had abdominal pain, and 25% had complaints of chest pain, dizziness, or loss of consciousness. Lay employees (security personnel) were trained to use automatic external defibrillators. There were six cardiac arrests (0.3 per million visitors). Two patients collapsed with ventricular fibrillation, were defibrillated by lay personnel, quickly regained consciousness, and survived. The other arrests were associated with asystole or electromechanical dissociation; no shocks were inappropriately given, and all four died. We conclude that four of every 1,000 persons at this assembly sought emergency medical care, that 95% of the problems seen were minor with few requiring physician skills, and that the automatic external defibrillator was suited for this setting and could be used by lay responders to provide early definitive treatment.
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PMID:Emergency medical care requirements for large public assemblies and a new strategy for managing cardiac arrest in this setting. 291 79

Four patients with mitral valve prolapse and ventricular tachycardia or fibrillation were described. Case 1 was a 46-year-old man with syncope due to ventricular fibrillation. Case 2 was a 36-year-old woman with palpitation and dizziness due to ventricular tachycardia. Case 3 was a 47-year-old man with palpitation and dizziness due to ventricular tachycardia. Case 4 was a 38-year-old man with syncope due to torsade de pointes. Left ventriculograms showed mitral valve prolapse in all cases. Coronary arteriograms were also normal, supporting a noncoronary etiology of the arrhythmia. Patients with unexplained ventricular arrhythmias should be screened for mitral valve prolapse.
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PMID:[Four cases of mitral valve prolapse associated with ventricular tachycardia]. 325 7

Marked prolongation of the electrocardiographic QT interval often is associated with a distinctive form of ventricular tachycardia characterized by the gradual oscillation around the baseline of the peaks of successive QRS complexes. This was named torsades de pointes, or "twisting of the points." This form of ventricular tachycardia tends to be rapid and self-terminating and often occurs in clusters, leading afflicted patients to present with recurrent dizziness and syncope. Ventricular fibrillation and sudden death are common.
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PMID:Ventricular tachyarrhythmias in the long QT syndromes. 614 38


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