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)

Propafenone, an anti-arrhythmic medication recently introduced in class lc, was tested in a multicentric open study including 3,687 patients (mean age: 60 years), presenting a supra ventricular (n = 2,146, 59 p. cent), nodal (n = 351, 10 p. cent) or ventricular (n = 1,613, 44 p. cent) arrhythmia, in order to study its efficacy and tolerance. After exclusion of the patients on whom there was a contra-indications to the use of anti-arrhythmic drugs, Propafenone was administered orally, on a long-term basis, at the usual dose of 600-900 mg per 24 hours. The efficacy and tolerance were evaluated according to the usual clinical and paraclinical criteria (EKG, Holter) on the 15th day, then every month during the treatment period. The efficacy of the treatment was evaluated as very good in 54 p. cent of the cases, good in 25 p. cent of the cases, average in 8 p. cent of the patients and non-existent or non significant for 13 p. cent of the patients. Electrocardiographic alterations under Propafenone are already described: CF, PR, QRS. A cardiac undesirable side effect occurred 102 times, most often a sinus bradycardia type (n = 26), atrio-ventricular conduction disorders (n = 22) or intraventricular conduction disorders (n = 26), disorders of cardiac decompensation (n = 10) or arrhythmogenic effect (n = 18). Other side effects are gastro-intestinal in nature (taste alterations, nausea, vomiting, gastralgia) for 23 p. cent of the patients treated, neuro-sensorial in origin (dizziness, visual disorders, tremors) for 13 p. cent of the patients or of another nature for 5 p. cent of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Efficacy and tolerance of propafenone in the treatment of cardiac rhythm disorders. Evaluation of a multicenter open trial on 3,687 patients]. 329 28

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

A 65-year-old male with diabetes, hypertension, and mild renal failure developed dizziness and syncope one week after starting clonidine 0.45 mg/day. A continuous ECG recording revealed sinus bradycardia, nodal rhythm, and multiple episodes of sinus arrest lasting up to 4.5 seconds. Upon discontinuation of clonidine, serial continuous ECG recordings revealed gradual decrease in the number and duration of the sinus arrest episodes, until their complete disappearance shortly after the third day off clonidine. This report shows that clonidine may cause a concentration-dependent sinus node dysfunction in addition to the atrioventricular (AV) node abnormalities previously ascribed to it.
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PMID:Sinus arrest associated with clonidine therapy. 334 61

Penticainide is a new class I antiarrhythmic agent. Its electrophysiological effects and pharmacokinetic properties were studied in 28 patients undergoing endocavitary exploration for paroxysmal supraventricular tachycardia (10 cases), WPW syndrome involving an accessory pathway (5 cases), and unexplained dizziness (13 cases). Increasing doses of penticainide were infused in the first 18 patients (0.12 up to 3.5 mg kg-1). The next ten patients received 4 mg kg-1 over a 30 minute period. Penticainide shortened the sinus cycle length and increased the transnodal conduction time. The ventricular conduction time tended to increase. Atrial functional refractory period increased when atrioventricular nodal and ventricular refractory periods remained unchanged. In patients with previous supraventricular tachycardias all triggered arrhythmias were prevented with dosages higher than 2 mg kg-1 and related blood levels higher than 3 mg l-1. A dose-dependency of plasma and renal clearance was documented. Average Cmax values after 4 mg kg-1 was 7.37 +/- 1.28 mg l-1. No adverse events occurred during the trial and penticainide proved to be well tolerated.
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PMID:Electrophysiologic effects and pharmacokinetics of intravenous penticainide (CM 7857). 362 42

Classically, the frequency of latent left-sided Kent bundles and ventricular tachycardia (VT) is increased in mitral valve prolapse (MVP). To verify this hypothesis, 23 patients with clinical and echocardiographic (M mode and 2D) signs of MVP underwent electrophysiological studies for dizziness or syncope (12 cases) or palpitations (11 cases). In addition to the standard electrophysiological studies, analysis of sinoatrial and atrioventricular conduction, they underwent programmed ventricular pacing (St V2): coupled and then paired St V2 in sinus rhythm and during ventricular pacing (100-150/min) under basal conditions (15 patients), after injection of 2 mg Atropine (6 patients), and 10 micrograms of Isoproterenol (4 patients). These manoeuvres showed that symptoms of dizziness were due to increased vagal tone in 6 cases (associated with paroxysmal nodal tachycardia--PNT--in 3 cases), to sinoatrial block in 2 cases (associated with atrial tachycardia in 1 case), to suprahisian conduction defects in 3 cases (associated with atrial tachycardia in 1 case) and to VT in 1 case. Palpitations were due to VT in 1 case, atrial tachycardia in 1 case and PNT in 9 cases. Our analysis showed a high incidence of PNT (10 cases) with normal inter critical ECG. These arrhythmias were due to intranodal reentry in 7 cases (70%), to a latent left-sided Kent bundle in 2 cases and to a paraseptal Kent bundle in 1 case. These PNT were characterised by induction during exercise (6 cases) and by their association with flutter-type reentry (5 cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mitral valve prolapse. Results of electrophysiological studies]. 392 28

Several mechanisms lead to attacks with unsuspected sudden and intermittent loss of consciousness. A major cause for such syncopes are arrhythmias. Only in rare cases it is possible to register an ECG during a typical attack despite many newer methods as long-term ECG (LT-ECG), exercise stress test and electrophysiologic investigations. LT-ECG does not record the ECG only during symptomatic periods (syncopes, dizziness, palpitations etc), but also registers asymptomatic AR, which can be precursors of SY. Carotid sinus massage is a valuable tool for the detection of a cardio-inhibitory Carotid-Sinus-Syndrome, which can be treated with PM-implantation. Exercise stress testing induces ventricular arrhythmias, which also indicates AR as underlying cause for SY. Using the invasive electrophysiologic investigation methods the importance measuring supraventricular parameters (SNRT, SA-, AH-interval) or parameters of the AV-nodal conduction (AH-, HV-interval) decreased in contrast to the ventricular stimulation techniques. With these invasive procedures ventricular tachycardias, ventricular flutter or fibrillation can be induced in selected patients, which indicates also a possible arrhythmogenic substrate for SY. In a suspected arrhythmogenic genesis of SY it has to be recommended to perform LT-ECG, carotid sinus massage, exercise stress testing and -- in selected patients -- electrophysiological investigations in addition to the routine-ECG to exclude or confirm arrhythmias as possible substrate for SY.
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PMID:[Diagnosis of syncopes in suspected arrhythmias]. 638 5

Verapamil hydrochloride, a prototype calcium antagonist, is now marketed in the United States for the acute treatment of supraventricular tachyarrhythmias and for chronic management of vasospastic and chronic stable angina. It inhibits the slow inward channel in in the heart and blocks calcium influx in smooth muscle. Its intrinsic negative inotropic action, which is apparent in isolated tissues, is offset in vivo by peripheral vasodilation. It has a mild, noncompetitive sympathetic antagonist effect; its most important electrophysiologic action is a depression of AV nodal conduction, accounting for its effect in supraventricular tachyarrhythmias. Its hemodynamic actions are characterized by a complex interplay of changes in preload, afterload, contractility, heart rate, and coronary blood flow. It does not depress cardiac function, except in severe heart failure. The drug has a mild dilator action on coronary arteries and reverses ergonovine-induced vasoconstriction. Controlled trials have established its role in Prinzmetal's variant angina, unstable angina, and chronic stable angina. It has also been found to be effective in obstructive cardiomyopathies. The potential role of verapamil in such conditions as hypertension, cardioprotection, and Raynaud's phenomenon needs further evaluation; at present these indications have not been approved by the Food and Drug Administration. The most common side effects include constipation, skin rash, and dizziness; AV block, heart failure, and sinus arrest may occasionally be encountered, especially when ventricular function is compromised or conduction system disease is present.
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PMID:Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics. 676 30

The effects of encainide on ventricular arrhythmia and left ventricular function were studied in 21 patients with chronic, high-grade ventricular arrhythmia using a prospective, 3-month, placebo-controlled, single-blind trial design. Encainide caused a 96% decrease in the average hourly frequency of ventricular premature complexes (VPCs) and comparable reductions in salvos of nonsustained ventricular tachycardia (VT) and episodes of sustained VT. Intracardiac electrophysiologic testing showed prolonged intraatrial and intraventricular conduction times and increased atrial, atrioventricular nodal, and ventricular refractory periods with both i.v. and oral encainide without His-Purkinje block, despite marked prolongation of HV and QRS intervals. Induced repetitive ventricular beating after ventricular extrastimuli in 15 patients showed persistent repetitive ventricular beating with chronic oral encainide in seven patients, four of whom had sustained VT within 2 months of treatment on encainide. Encainide did not reduce exercise capacity or left ventricular ejection fraction at rest or during supine exercise. Minor adverse effects of encainide in 11 of 21 patients included dose-related visual disturbances, dizziness and sinus pauses (less than 3 seconds). Major adverse effects included the new appearance of sustained VT in three of 20 patients (15%). Oral encainide effectively reduces the frequency and grade of VPCs, prolongs intracardiac conduction times, and does not impair left ventricular performance. However, it is associated with frequent minor side effects and uncommon but potentially severe major side effects (sustained VT), both of which apparently have a direct relationship to the size of the dose.
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PMID:Treatment of frequent ventricular arrhythmia with encainide: assessment using serial ambulatory electrocardiograms, intracardiac electrophysiologic studies, treadmill exercise tests, and radionuclide cineangiographic studies. 680 10

The concept of sinus node disease is defined by a group of clinical and electrocardiographic features related to sinus node dysfunction whatever its mechanism; the organicity of the disease can be proven if total or subtotal histological alterations of the sinus node are demonstrated. The most typical symptoms are neurological (syncopes and dizziness). Sinoatrial block, sinus arrest, sinus bradycardia or bradyarrhythmia, and the bradycardia-tachycardia syndrome are the most usual electrocardiographic aspects. The diagnosis is often rendered difficult by the usually intermittent and frequently nonspecific character of the symptoms and of the ECG signs. Holter monitoring is often essential to resolve these difficulties. If the diagnosis remains dubious, the use of electrophysiological methods is necessary: direct recording of the sinus nodal intracardiac potential can now be added to the classical rapid and premature atrial stimulation, possibly complemented by pharmacological tests. Finally, therapeutic indications can be considered after a correct clinical, electrocardiographical and electrophysiological evaluation of the patient. Medical treatment alone is usually ineffective in controlling the attacks of arrhythmia and the neurological episodes. If the sinus nodal dysfunction is obvious and symptomatic, permanent pacing is the treatment of choice. Its short and medium term results are generally excellent, while the long term results, especially with regard to survival of the patients, could be improved by the most recent pacing techniques.
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PMID:[Sinus node disease - diagnosis and treatment]. 731 31

It is important for women to understand the risk of first onset and symptomatic exacerbation of paroxysmal supraventricular tachycardia (SVT) during pregnancy. Reports regarding the effects of pregnancy on first onset and symptomatic exacerbation of paroxysmal SVT have been controversial, and have not been conducted in a systematic fashion. Two hundred seven consecutive female patients diagnosed with symptomatic paroxysmal SVT were requested to respond to multiple questionnaires before electrophysiologic study and catheter ablation. A person-years data method was used to estimate risk of first onset of paroxysmal SVT during pregnancy. Exacerbation of paroxysmal SVT was assessed by a score scale including each of the following symptoms: palpitation, fatigue, rest dyspnea, effort dyspnea, dizziness, chest oppression, blurred vision, and syncope (total score change > 2 points). In the 107 patients with accessory pathway-mediated tachycardia, 7 patients had had a first onset of tachycardia during pregnancy (relative risk ratio 0.86, confidence interval 0.4 to 1.9, p = 0.35). In the 100 patients with atrioventricular nodal reentrant tachycardia, 1 patient had had the first onset of tachycardia during pregnancy (relative risk ratio 0.11, confidence interval 0.02 to 0.56, p = 0.004). Otherwise, 14 of the 63 patients (22%) with tachycardia in the pregnant and nonpregnant periods had exacerbation of symptoms during pregnancy. Thus, first onset of paroxysmal SVT during pregnancy was rare (3.9%), and pregnancy was associated with a low risk of first onset of paroxysmal SVT. However, symptoms of paroxysmal SVT were exacerbated during pregnancy in some patients.
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PMID:Effects of pregnancy on first onset and symptoms of paroxysmal supraventricular tachycardia. 757 23


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