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

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
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PMID:Frequent neurologic toxicity associated with amiodarone therapy. 653 58

Syncope occurs in up to 20% of patients with supraventricular tachycardias and is suggestive of rapid and dangerous arrhythmias. Incidence, pathomechanism and consequences of syncope in supraventricular tachycardia are reviewed in this presentation. Frequent symptoms in supraventricular tachycardias are palpitations, dizziness or dyspnea. Syncope is more uncommon, however, if a sensation of rapid heart beat precedes a syncope, a causal relationship between arrhythmia and syncope has to be considered. When the surface ECG shows no abnormalities, Holter monitoring or exercise testing usually fail to record a suspected tachycardia, therefore, electrophysiologic study should be performed to verify the underlying arrhythmia. In patients with unexplained syncope supraventricular arrhythmias can be established in up to 15% of patients. However, interpretation of electrophysiologic results has to be performed carefully because functional abnormalities like dual AV nodal pathways can be found in up to 10% of asymptomatic patients. The prognostic value of syncope as a marker for rapid tachycardia or sudden cardiac death is still in discussion. Syncope in patients with Wolff-Parkinson-White syndrome may help to identify patients at risk for ventricular fibrillation due to rapid conduction over an atrioventricular accessory pathway during atrial fibrillation. Syncope in young patients (< 25 years) with Wolff-Parkinson-White syndrome was found to be associated with a short anterograde refractory period (< 220 ms) of the pathway. However, most of the studies were performed retrospectively in selected patients referred to the centers because of severe symptoms, therefore the predictive value of syncope in unselected patients with supraventricular tachycardia remains uncertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Syncope in supraventricular tachycardia. Incidence, pathomechanism and consequences]. 833 Aug 52

During a follow-up of 24 +/- 20 months after treatment with an implantable cardioverter-defibrillator (ICD), 101 of 241 patients (42%) received > or = 1 spontaneous ICD shocks with documentation of the rhythm leading to shock by Holter or telemetry monitoring or stored electrograms by the device. Sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was documented in 67 of the 101 patients (66%) with electrocardiographically documented shocks, nonsustained VT in 4 patients (4%), supraventricular tachyarrhythmias in 41 patients (41%), and normal sinus or pacemaker rhythm in 10 patients (10%). No, mild (palpitations and/or mild dizziness) and severe symptoms (presyncope/syncope) preceded spontaneous ICD shocks in 20 (30%), 33 (49%) and 27 (42%) of the 67 patients, respectively, with electrocardiographically documented VT or VF, and in 23 (56%), 16 (39%) and 1 (2%) of the 41 patients, respectively, with electrocardiographically documented supraventricular tachyarrhythmias. Three of the 4 patients with nonsustained VT had mild symptoms, and 1 patient with nonsustained VT had presyncope. None of the 10 patients with spurious discharges during normal sinus or pacemaker rhythm had symptoms preceding the ICD shocks. It is concluded that (1) most patients with either electrocardiographically documented VT/VF or a non-VT/VF rhythm preceding spontaneous ICD shocks have no or mild symptoms preceding the shock, and (2) severe symptoms preceding ICD shocks suggest sustained VT or VF as the underlying rhythm, although severe symptoms rarely occur in patients with supraventricular tachyarrhythmias or nonsustained VT.
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PMID:Symptoms and electrocardiographically documented rhythm preceding spontaneous shocks in patients with implantable cardioverter-defibrillator. 851 86

A 62-year-old male patient with coronary artery disease and drug refractory sustained ventricular tachycardia received an implantable cardioverter defibrillator (PRX III, model 1720, CPI) with a transvenous lead system (Endotak, model 0115, CPI) in combination with a subcutaneous array electrode (SQ array, model 049, CPI). The intraoperative defibrillation threshold was 15 J and was confirmed 1 week later at the hospital discharge test. Three months after discharge from hospital the patient reported 5 shocks during moderate physical exertion followed by a tachycardia associated with dizziness which terminated spontaneously. The print out of the stored electrogram showed a supraventricular tachycardia (probably sinus tachycardia) with a heart rate of 154/min which activated the device. Antitachycardia pacing did not terminate the supraventricular tachycardia, and hence shock therapy was delivered. The first shock (34 J) converted the supraventricular tachycardia to a ventricular tachycardia with a heart rate of 178/min, which was not terminated by four consecutive 34 J DC shocks. There was no hint of a device or lead failure. Determination of the defibrillation threshold reconfirmed the 15 J value for termination of ventricular fibrillation. However, neither a 1 J shock nor a 34 J shock terminated a monomorphic sustained ventricular tachycardia (cycle length 340 ms) induced by noninvasive programmed electrical stimulation. The ventricular tachycardia was, however, reproducibly terminate by antitachycardia pacing. It is concluded that an inappropriate high-energy DC shock might induce a sustained ventricular tachycardia. However, a sufficient defibrillation threshold for the termination of ventricular fibrillation does not necessarily mean that a sustained ventricular tachycardia will be terminated by a high-energy DC shock.
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PMID:[Shock-induced, but not terminated ventricular tachycardia in a patient with implantable defibrillator]. 871 42

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

The metabolic fate of most antihistamines is not clearly established. The drugs usually appear to be extensively metabolized,mainly in the liver. Some second generation antihistamines are metabolized principally by the cytochrome P-450 microsomal enzyme system, mainly by the isoenzyme 3A4 (CYP3A4), although other isoenzyme,including CYP1A2 and CYP2D6, also may be involved. However,other second generation antihistamines appear to be only minimally metabolized in the liver. Serious cardiac effects (prolongation of the QT interval, arrhythmias, torsades de pointes, ventricular fibrillation, arrest, hypotension, palpitations, syncope, dizziness, and/or death) have been reported rarely in patients receiving terfenadine or astemizole. Cardiotoxic effects ussually were associated with higher than recommended dosages and/or increased plasma concentrations of the drugs and their active metabolites. No clinically important adverse effects or changes in the QT intervals were reported after concomitant administration of ketoconazole with fexofenadine. Patients receiving an azole, antifungal, a macrolide, quinine or grapefruit juice also appear to be at substantial risk of such toxicity, probably secondary to interference with metabolism of the antihistamine. Second-generation H1 receptor antagonist have been studied extensively in the treatment of asthma. Many of these drugs have been reported to inhibit eosinophil and basophil chemotaxis and therefore might have an effect on the inflammatory reactions that characterise this disease. Safe use of antihistamines during pregnancy has not been established; therefore, the drugs should not be used in women who are or may become pregnant unless the potential benefits justify the possible risks to the fetus. Antihistamines should not be administered to premature or full-term neonates. Young children may be more susceptible than adults to the toxic effects of antihistamines.
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PMID:[Projection of new antihistamines]. 1086 85

Sudden death is a tragic complication of hypertrophic cardiomyopathy. We report the case of a young patient with hypertrophic cardiomyopathy in whom an episode of atrial fibrillation triggered ventricular fibrillation and cardiac arrest. A 21-year-old man with nonobstructive hypertrophic cardiomyopathy underwent cardioverter-defibrillator implantation for primary prevention of sudden death, after risk stratification with noninvasive strategies. After 6 weeks, during a moderate effort, the patient had a syncopal episode, preceded by palpitations and dizziness, and terminated by the cardioverter-defibrillator. Device interrogation revealed an episode of atrial fibrillation with high ventricular response, spontaneously followed by ventricular tachycardia/fibrillation. Atrial fibrillation is a potential trigger of life-threatening arrhythmias and sudden death in patients with hypertrophic cardiomyopathy. Clinical investigation of risk markers for sudden death should be encouraged to identify high-risk patients who may benefit from a prophylactic therapy with an implantable cardioverter-defibrillator.
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PMID:Noninvasive risk stratification prevents sudden death due to paroxysmal atrial fibrillation in hypertrophic cardiomyopathy. 1693 87

This review describes the common effects of psychotropic drugs on the cardiovascular system and offers guidance for practical management. Selected reports from the literature describing common side effects associated with psychotropic drugs are reviewed, and suggestions for further reading are given throughout the text. Orthostatic hypotension is the most common adverse autonomic side effect of antipsychotic drugs. Among the atypical antipsychotics the risk of orthostatic hypotension is highest with clozapine and among the conventional drugs the risk is highest with low potency agents. Rarely, orthostatic hypotension may result in neurocardiogenic syncope. QTc prolongation can occur with all antipsychotics but an increased risk is seen with pimozide, thioridazine, sertindole and zotepine. QTc prolongation is a marker of arrhythmic risk. Torsade de pointe, a specific arrhythmia, may lead to syncope, dizziness or ventricular fibrillation and sudden death. Heart muscle disease presents most commonly in the elderly as chronic heart failure, but myocarditis and cardiomyopathy, although relatively rare, are devastating, but potentially reversible complications of psychotropic drug therapy have been particularly linked to clozapine treatment. Patients with severe mental illness (SMI) are a 'high risk' population with regard to cardiovascular morbidity and mortality. It is probable that many patients accumulate an excess of 'traditional' risk factors for the development of cardiovascular disease, but other mechanisms including psychotropic drugs may also be influential in increasing risk in this vulnerable group. These risks need to be seen in the context of the undoubted therapeutic efficacy of the psychotropic armamentarium and the relief that these drugs bring to those suffering from mental disorder.
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PMID:Cardiac side effects of psychiatric drugs. 1809 18

Prolongation of the ventricular repolarisation manifests itself as a prolongation of the QT intervall on the surface ECG and represents a major risk for a special form of ventricular tachycardia called "torsades de pointes". Torsades de pointes are often self limited and are associated with palpitations, dizziness or syncope. Degeneration into ventricular fibrillation and sudden cardiac death can occur. In addition to the various forms of the congenital long QT syndrome many drugs, such as antiarrhythmic drugs class IA and III, antibiotics, antihistamines, antidepressants, and methadone are known to prolong the QT interval. Most of these drugs block a specific potassium channel substantially involved in the ventricular repolarisation. In addition, drug interaction or disturbances of drug metabolism may play a major role in the acquired form of the long QT syndrome. The individual risk and the potential of a pharmacologic substance to prolong the QT interval are not predictable. Certain risk factors identify patients at higher risk for drug-induced prolongation of the QT interval. Correctable factors include electrolyte disorders (e.g. hypokalemia) and concomitant administration of different QT prolonging drugs. External defibrillation is the therapy of choice in the hemodynamic unstable patient presenting torsades de pointes. In hemodynamic more stable patients application of intravenous magnesium can terminate torsades de pointes (membrane stabilizing properties). Temporary external or transvenous pacing at high heart rate might terminate incessant torsades de pointes by decreasing QT interval. Repeated ECG controls during therapy with QT prolonging drugs are mandatory, especially when drug doses are changed, additional drugs are prescribed, or in case of vomiting and diarrhea. QT prolongation in individual medical therapy is not always predictable. Therefore, updated lists of drugs with the potential of QT prolongation are available on the Internet (e.g. www.qtdrugs.org ).
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PMID:[Drug induced QT prolongation]. 1836 52


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