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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with atrial flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of atrial flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing atrial flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for atrial fibrillation. The most effective way to terminate atrial flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable atrial flutter. The use of anticoagulation for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with atrial flutter although the risk appears less than that for atrial fibrillation. In the future, refinements and improvements in therapy for atrial flutter will likely be derived from a better understanding of its mechanism.
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PMID:Atrial flutter--update on the mechanism and treatment. 128 52

The effects of diltiazem hydrochloride (0.3 mg/kg i.v. over 2 min.) was studied by continuous electrocardiographic monitoring in 60 patients. Conversion to sinus rhythm was achieved in 55 patients (91%). Electrocardiographic findings were: undisturbed sinus rhythm in 20 patients; A-V junctional rhythm in 4 patients; complex ventricular arrhythmias (ventricular tachycardia or complex VPCs) in 19 patients. Patients with complex ventricular arrhythmias were matched against patients with normal sinus rhythm, with respect to the following parameters: age, sex, heart disease, tachycardia duration, tachycardia cycle length, sinus cycle length, pre- and post-infusion blood pressure. No differences between the two groups of patients were found. Ventricular arrhythmias occurring at the termination of supraventricular tachycardia are difficult to explain. Nevertheless, these arrhythmias are not associated with organic heart disease. They could be the expression of triggered activity.
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PMID:[Diltiazem in paroxysmal supraventricular tachycardia: electrocardiographic findings at termination]. 129 9

We have studied 36 patients (19 females and 17 males), controlled between 1973 and 1989, who suffered Wolff-Parkinson-White (WPW) pattern in their electrocardiogram. Epidemiological, clinical, diagnostic, therapeutic and evolutional data were reviewed. The mean age at the time of diagnosis was 4 years and 3 months, with 48% younger than six months of age. The average time for the follow-up period was 4 years and 2 months. There was not familiar occurrence. Six (16%) of the patients had associated heart disease. Seventeen (47%) had type A of WPW, 12 (33%) type B and 7 (20%) were not defined. An echocardiographic study was done in 20 patients (61%). Twenty-seven patients (75%) showed supraventricular tachycardia (SVT), which in 22 of these cases was the reason for seeking consultation. Children without SVT, 9 (25%), did not need any form of treatment. Twenty-four (889) of the patients with SVT required treatment to prevent recurrence. In the 27 studied episodes of SVT, Verapamil IV (55%) and vagal manoeuvres were the most efficient treatments. Seventeen (47%) of the patients presented a persistent WPW pattern and 11 (31%) experienced a normalization of their electrocardiogram with a mean time of 2 years-2 months.
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PMID:[Wolff-Parkinson-White disease in childhood: follow up of 36 cases]. 141 52

Fourteen patients (mean age, 48 +/- 19 years) with left ventricular dysfunction in the absence of underlying organic heart disease underwent catheter ablation (nine with direct-current energy and five with radiofrequency energy) to treat drug-refractory, symptomatic supraventricular reentrant tachycardia (mean duration of tachycardia, 22 +/- 17 years). Clinical tachycardias were accessory pathway-mediated tachyarrhythmia (12 patients) and atrioventricular nodal reentrant tachycardia (two patients). Changes of ventricular function after successful ablation, as assessed by radionuclide ventriculography and echocardiography, showed a decrease in left ventricular end-systolic dimension (39 +/- 6 mm to 34 +/- 6 mm; 32 +/- 6 mm; p < 0.05) and in left ventricular end-diastolic dimension (55 +/- 5 mm to 52 +/- 3 mm; 51 +/- 3 mm; p < 0.05) in the early (2 to 3 months) and late (6 to 8 months) follow-up periods, increase of nuclear ejection fraction (38% +/- 8% to 46% +/- 7%; p < 0.05) and fractional shortening (28% +/- 7% to 36% +/- 8%; p < 0.05) in the late follow-up period. Increase of fractional shortening was mainly due to decrease in the end-systolic dimension. These findings suggest that prolonged attacks of uncontrolled supraventricular tachycardia may result in left ventricular dysfunction, which is reversible after successful catheter ablation of the arrhythmias.
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PMID:Reversibility of left ventricular dysfunction after successful catheter ablation of supraventricular reentrant tachycardia. 146 7

A 62-year-old woman was admitted our hospital because of concussion of the brain. The level of consciousness improved within several days. Cardiac examination was performed because the patient had experienced feelings of fainting since one year previously, and heart murmur also was heard. The electrocardiogram showed WPW configuration. At the same time that she complained of feelings of fainting, the electrocardiogram showed supraventricular tachycardia. The echocardiogram showed displacement of the septal tricuspid leaflet and mild tricuspid valve, regurgitation. Cardiac catheterization was performed and, using the intracardiac electrocardiogram, we confirmed atrialized right ventricle. We diagnosed this patient as having Ebstein's anomaly with WPW syndrome. The clinical manifestations of this anomaly are quite variable, depending upon the spectrum of pathology and the presence of associated malformations. It is well documented that a considerable proportion of these patients are able to survive into adult life. However, the patient who survives into the sixth decade without a sign of heart failure is extremely rare. We speculate that this patient had not developed right ventricular failure until her 60's because she had a milder form of Ebstein's anomaly and did not have any other congenital heart disease.
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PMID:[A 62-year-old survivor with Ebstein's anomaly without right ventricular failure]. 148 Aug 34

This study examined the role of electrophysiologic study in the evaluation of patients with unexplained syncope. The incidence of abnormalities (conduction disease, supraventricular tachycardia, ventricular tachycardia) was compared in patient groups with and without heart disease, and the effect of treatment of these abnormalities on recurrence of syncope was examined. Electrophysiologic study was performed in 111 consecutive patients with syncope, with antiarrhythmic medications being discontinued 1 week prior to study. There was no mortality associated with the procedure and only 9 patients (8%) had complications (groin haematoma, atrial fibrillation or brady-arrhythmias persisting after the procedure). Abnormalities were detected in 31 of 73 patients with heart disease (42%) but in only 6 of 38 patients with no heart disease (16%, P less than 0.01). During follow-up, syncope recurred in 2 of 37 patients (5%) treated because of abnormal findings, compared with a recurrence rate of 24% (18 of 74 patients) in the untreated group (P less than 0.05). Probability of remaining free from syncope at 2 years was 0.94 in the treated group and 0.72 in the untreated group (P less than 0.05). Mortality during follow-up was confined to the heart disease group with 5 of 30 treated patients in this group dying (17%) compared with 3 of 43 untreated patients (7%, P = not significant). Syncope patients with heart disease were thus more likely to have a diagnostically useful study than patients with normal hearts. Treatment directed at correction of abnormalities detected at electrophysiologic study reduced recurrence of syncope but did not significantly affect mortality. Syncope did not appear to be a prelude for sudden death in patients with normal hearts. Electrophysiologic study had no mortality and low morbidity.
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PMID:Electrophysiologic studies in patients with unexplained syncope. 157 41

One thousand three hundred patient's stress tests were analyzed to value arrhythmia outline and its relationship with anamnesis and clinical data. The patients were divided into two groups: group A, with no arrhythmias at rest, and group B with arrhythmias at rest. All classic nosographic arrhythmias were considered. In some teenager patients with arrhythmias at rest and no organic cardiopathy, anomalies disappeared during stress, showing the benignity of the phenomenon. Supraventricular stress induced arrhythmias has 1.2% of incidence in normal subjects, but 81% in heart disease patients. Supraventricular tachycardia was induced in 6 patients. Ventricular stress induced arrhythmias are found in 4.9%. Two cases of sudden death occurred in our groups.
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PMID:[Ergometric test in the diagnostic and prognostic evaluation of arrhythmia]. 172 16

Determining safe and effective antiarrhythmic therapy in paediatric patients requires definition of the mechanism of the arrhythmia, determination of associated risk factors for treatment (such as the presence of congenital cardiac defects, myocarditis or cardiomyopathy), and monitoring for potential drug side effects related to the treatment. A number of modalities for non-invasive evaluation of arrhythmias is available, including ECG, 24-hour ambulatory Holter monitoring, and transtelephonic ECG transmission. Arrhythmias requiring medical treatment in children with normal cardiac anatomy and function include supraventricular tachycardia (SVT), ventricular tachycardia (VT) and primary atrial tachycardias. SVT is treated acutely with vagal manoeuvres or drugs which slow AV conduction [adenosine (adenine riboside), edrophonium, phenylephrine or verapamil]. When medical conversion is not achieved, transoesophageal overdrive pacing or direct current (DC) cardioversion may be required. Long term drug therapy for SVT includes first-line treatment with digoxin, verapamil or propranolol. Ventricular tachycardia is managed acutely with DC cardioversion and intravenous lidocaine (lignocaine). Chronic drug regimens include mexiletine, propranolol or amiodarone. In children with structural congenital heart disease or myocardial dysfunction, hazards of drug therapy for arrhythmias include depression of cardiac function, proarrhythmia (drug-induced worsening of arrhythmias), and conduction abnormalities. Care must be taken to choose medication regimens which are likely to be effective with minimum risk of potentiating abnormal haemodynamics or conduction.
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PMID:Cardiac arrhythmias in childhood. Diagnostic considerations and treatment. 172 43

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.
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PMID:Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug. 173 70

The authors used programmed ventricular stimulation in 38 patients who had during Holter monitoring severe ventricular arrhythmias (greater than or equal to Lown 4a). The group comprised patients with IHD (22x), hypertrophic (11x) and dilatating cardiomyopathy (2x). Three patients had no organic heart disease. Nine patients were treated at the time of examination with antiarrhythmic drugs. In a total of 16 patients it proved possible to provoke ventricular tachycardia (VT)--four times permanent ventricular tachycardia, 12x transient ventricular tachycardia (NSVT). In the group of treated patients SVT was provoked twice and NSVT also twice, always in patients who took amiodarone. Using programmed ventricular stimulation the following antiarrhythmic drugs were tested: mexiletine, cordarone, ajmaline. The capacity of all tested antiarrhythmics in the prevention of VT was comparable. A total of two patients died during the investigation, in both cases a sudden death. One suffered from hypertrophic cardiomyopathy, one from IHD. In both on Holter monitoring NSVT episodes were revealed. Programmed stimulation provoked in both SVT, both were treated at the time of death with tested antiarrhythmics. The authors conclude that programmed ventricular stimulation is a suitable method for rationalization of antiarrhythmic treatment, the clinical results, however, do not correspond to laboratory results. They recommend therefore to use also Holter monitoring of patients at risk.
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PMID:[Determination of anti-arrhythmia therapy of ventricular arrhythmias based on programmed ventricular stimulation]. 179 55


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