Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty patients with long-standing (mean 30 days) type I atrial flutter (AF) were treated with overdrive atrial pacing. To evaluate the effect of pretreatment with disopyramide (DISO), the study population was divided into 3 groups of 10 patients each: no therapy (Group A); intravenous DISO (maximum dose 250 mg in 1 hour) (Group B), oral DISO (400 mg/day for 4 days) (Group C). The mean cycle length of AF was 215 +/- 24 ms in Group A, 222 +/- 28 in B and 224 +/- 11 in C (NS). After DISO, AF cycle length increased to 287 +/- 24 in Group B (p less than 0.001) and to 264 +/- 29 in C (p less than 0.001). Overdrive pacing was performed from a maximum of 3 atrial sites up to the shortest paced cycle of 150 ms. Reversion to sinus rhythm (SR) occurred in 20% of patients in Group A, 70% in B and 50% in C. In all these cases SR was obtained with paced cycle length that was 70-90% of the baseline cycle length. Pacing was performed from a mean number of 2.1 sites per patient in Group A, 1.2 in B and 2.0 in C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration of atrial flutter to a faster form of AF occurred in 3, 3 and 4 patients, respectively. The administration of DISO prior to overdrive atrial pacing improves the rate of conversion to SR and allows an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. The administration of DISO is beneficial when overdrive atrial pacing is performed for the treatment of long standing AF in patients with organic heart disease.
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PMID:[Efficacy of disopyramide in the treatment of atrial flutter with overdrive pacing]. 274 66

Findings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient. Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation. Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia.
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PMID:Ventricular fibrillation in six adults without overt heart disease. 292 43

We describe our experience with 1000 electric cardioversions performed at the emergency ward in the Hospital of Cardiology y Neumology, National Medical Center I.M.S.S. The objectives are: 1. Report our experience. 2. Investigate if digitalis treatment should be discontinued before the procedure. 3. Determine if all patients should be on anticoagulant therapy for elective cardioversion. 4. Indicate the optimal anesthetic drug with minimal side effects. A therapeutic procedure was performed in 73% of our cases and an elective one in the remaining 27%. Patients were grouped as ischemic heart disease 26%, rheumatic heart disease 24%, chronic obstructive pulmonary disease 14%, systemic hypertensive heart disease 13%, without clinical heart disease 6%, preexcitation syndrome 6%, adult congenital heart disease 4%, with implanted pacemaker 2%, pregnancy 2% and diverse myocardial diseases 2%. As a cardiac arrhythmias atrial fibrillation was the main cause 45%. Atrial flutter represented 25%, atrial paroxysmal tachycardia was 21% and ventricular tachycardia 9%. A cardioversion was performed in 43% of patients under digitalis treatment at therapeutic levels, without complications. Atrial flutter reverted to sinus rhythm in 98% of the procedures, and atrial fibrillation in 97%. Elective cardioversion in patients with atrial fibrillation was achieved with energies of 200 joules in 82% of the procedures (P less than 0.001) and in atrial flutter with 100 joules in 89% of the cases (P less than 0.001). The most frequent complications were atrial and junctional premature beats in 41% of the cases. We consider this procedure a safe one, effective at the energy levels described, with no need for discontinuation of digitalis therapy, with no mandatory previous anticoagulant therapy, and with no contraindications on pregnancy or implanted pacemakers.
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PMID:[Electric cardioversion in the emergency service. Experience in 1000 cases]. 296 50

Fulguration of the site generator of arrhythmia was attempted in three 31, 33 and 55 year-old patients presenting ectopic atrial tachycardias resistant to various antiarrhythmic medications. Episodes of atrial fibrillation and flutter were also documented in two of them. Two patients had a surgically corrected congenital cardiopathy:interatrial communication or pulmonary stenosis. Mapping of the endocardial emergence point was carried out with electrodes placed 1 cm apart, demonstrating the high atrial origin of the tachycardia, near the right atrium. The auriculogram preceded the earliest possible ectopic P wave by 20 to 70 ms; its multiphasic and prolonged morphology, suggested a local intra-atrial conduction disorder in the three cases. Cathodic shocks were delivered at this site without complications with cumulative energies of 720 J, 480 J and 320 J, respectively. The fulguration was ineffective and revealed other arrhythmic sites in two patients. Only patient n1 has been asymptomatic since 24 months under a treatment with Sotalol 160 mg which had been previously ineffective.
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PMID:[Fulguration of foci of atrial tachycardia in the adult]. 304 46

Our experience with the use of five new antiarrhythmic drugs for treating life-threatening arrhythmias in children will be briefly reviewed. Prevention of recurrent episodes of atrial flutter with digoxin and local anesthetic antiarrhythmic drugs often is only moderately successful, benefiting 65% of patients. Amiodarone is particularly useful for those patients who cannot be controlled on this regimen. We caution that the heart rate be monitored carefully when therapy with amiodarone is initiated in patients likely to have sick sinus syndrome. We have found mexiletine useful for controlling significant ventricular arrhythmias in patients with congenital heart disease. Likewise, 79% (11 of 14) of patients with ventricular tachycardia treated with amiodarone were well controlled. However, the range of disease categories (congenital heart disease, myocarditis, cardiomyopathy) in which amiodarone is effective is much broader than for mexiletine. Although other investigators have used amiodarone successfully for controlling supraventricular tachycardia in the Wolff-Parkinson-White syndrome or secondary to concealed accessory AV connections, we recommend surgical ablation. Propafenone has significantly improved our ability to control postoperative JET. Although JET is self-limited in duration and spontaneously remits, it frequently produces life-threatening hemodynamic compromise in the postoperative setting. Propafenone slows the ventricular rate into a range in which AV sequential pacing may be instituted. Generally, after 24 to 72 hours, the patient may be quickly weaned from propafenone. Chronic incessant supraventricular tachycardia (SVT) is frequently associated with a dilated cardiomyopathy. The two most common mechanisms of incessant SVT are PJRT and AET. We have found encainide and ethmozine extremely effective in suppressing tachycardia episodes in PJRT and AET, respectively. Medical therapy has been associated with few side effects.
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PMID:Newer antiarrhythmic drugs in children. 309 60

Flecainide and encainide (class IC) are presently under clinical evaluation in Italy. They prolong the duration of the QRS but not the period of ventricular repolarisation: the prolongation of QT is due solely to the prolongation of the Q-J. Flecainide and encainide are extremely powerful and are suitable for the treatment of reciprocating supraventricular paroxysmal tachycardia and of persistent reciprocating tachycardia, the prophylaxis of WPW atrial fibrillation including cases with a short anterograde refractory period of the anomalous pathway and the treatment of ventricular ectopic beats and ventricular tachycardia. Both drugs are probably effective for the treatment of atrial fibrillation. However, in the case of atrial flutter they are of little effect of sinus rhythm cardioversion; on the other hand they significantly prolong the duration of the A-A interval, with variable results on ventricular rate. Flecainide and encainide have 'parodoxical' arrhythmogenic effects, related to administration dosages, severity of the arrhythmia and seriousness of cardiopathy. Encainide shows peculiar pharmacokinetics due to hepatic oxidating metabolisation and to production of metabolites; among these the O-demethylencainide and the 3-methoxy-O-demethylencainide have an antiarrhythmic activity, which is probably more important than the encainide parent and is longer-lasting. There are 'extensive', 'poor' and 'non-metaboliser' subjects. This results in wide pharmacokinetic inter- and intraindividual variability which must be taken into account during clinical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flecainide and encainide. 310 89

The clinical efficacy, adverse effects and pharmacokinetics of flecainide were evaluated in 16 pediatric and young adult patients with supraventricular tachycardia (SVT). Patients had received an average of 2.8 drugs before flecainide was tried. The following mechanisms of supraventricular arrhythmias were determined in patients by intracardiac electrophysiologic studies: atrioventricular node reentry, 4; reentry through an accessory connection, 7; atrial automatic focus, 2; atrial flutter, 3. Twelve patients had normal cardiac anatomy and 4 had congenital heart disease. Each patient received 2.8 mg/kg/day of flecainide divided into 2 doses 12 hours apart. After 3 days, the dose was increased to 5.6 mg/kg/day if necessary. In 14 patients, serum flecainide concentrations measured 3 to 4 days after beginning therapy ranged from 0.1 to 0.8 micrograms/ml (mean 0.40). Flecainide successfully controlled SVT in 8 of 16 patients. SVT in 3 of 7 patients with accessory connections and in 3 of 4 patients with atrioventricular node reentry was successfully controlled. In 1 of 2 patients with atrial automatic tachycardia, SVT had been completely controlled over 16 months. Only 1 of 3 patients treated for atrial flutter responded. Follow-up for successfully treated patients ranged from 4 to 16 months (median 9). Seven patients continue to take flecainide. None of the patients had clinical congestive heart failure. No drug-related adverse effects were noted on the resting surface electrocardiogram. Flecainide rarely produced proarrhythmic effects in this series. The 2 that were observed were mild and caused no clinical problems. Noncardiovascular side effects also occurred infrequently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flecainide for supraventricular tachycardia in children. 313 35

We treated 22 children, aged 3 days to 16 years 6 months (median 11 years 1 month), with flecainide for a variety of arrhythmias where a Class I agent was indicated. In 16, conventional antiarrhythmic treatment had failed. Structural heart disease was present in nine. The arrhythmia was paroxysmal re-entry atrioventricular tachycardia in nine; paroxysmal atrial tachycardia, flutter or fibrillation in five; paroxysmal ventricular tachycardia in five and frequent ventricular extrasystoles (with couplets) in three. Sinus rhythm was achieved in all four children who received flecainide during tachycardia (three received intravenous flecainide, one oral). During follow-up of 3-24 months (median 12 months), arrhythmia control was obtained in 13 children (59%). Combination therapy was used in seven of these; with digoxin in four and a beta blocker in three. Flecainide doses used in this study ranged from 1-11 mg kg-1 day-1 (median 4 mg kg-1 day-1), 25-297 mg m-2 day-1 (median 113 mg m-2 day-1). The median, pre-dose flecainide concentration in those responding to therapy was 225 micrograms l-1 and in those failing to respond was 417 micrograms l-1. An arrhythmogenic effect occurred in one child.
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PMID:Experience with flecainide for the treatment of cardiac arrhythmias in children. 314 91

We studied 16 patients with electrocardiographic evidence of advanced interatrial block and retrograde activation of the left atrium (P greater than or equal to 0.12 s, and diphasic (+/-) P waves in leads II, III, and VF). Eight patients had valvular heart disease, four had dilated cardiomyopathy and four had other forms of heart disease. Patients with valvular heart disease and cardiomyopathy were compared with a control group of 22 patients with similar clinical and echocardiographic characteristics, but without this type of interatrial block. Patients with advanced interatrial block and retrograde activation of the left atrium had a much higher incidence of paroxysmal supraventricular tachyarrhythmias (93.7%) during follow-up than did the control group, (27.7%) (P less than 0.001). Eleven of 16 patients (68.7%) with advanced interatrial block and retrograde activation of left atrium had atrial flutter (atypical in seven cases, typical in two cases, and with two or more morphologies in two cases). Six patients from the control group (27.7%) had sustained atrial tachyarrhythmias (five atrial fibrillation and one typical atrial flutter). The atrial tachyarrhythmias were due more to advanced interatrial block and retrograde activation of left atrium and frequent atrial extrasystoles than to left atrial enlargement, because the control group with a left atrium of the same size, but without advanced interatrial block and retrograde activation of left atrium and with less incidence of atrial extrasystoles, had a much lower incidence of paroxysmal tachycardia.
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PMID:Interatrial conduction block and retrograde activation of the left atrium and paroxysmal supraventricular tachyarrhythmia. 320 76

Long-lasting (mean 30 days) type I atrial flutter was treated with overdrive pacing in 30 patients (mean age 69 years) with organic heart disease. To evaluate the effect of pretreatment with disopyramide, the study population was divided in 3 groups of 10 patients each: group A, no disopyramide therapy; group B, intravenous disopyramide (maximum dose 250 mg in 1 hour); and group C, oral disopyramide (400 mg daily for 4 days). There were no differences in baseline cycle length of atrial flutter among the 3 groups before drugs were given. The stimulation protocol included overdrive atrial pacing up to the shortest paced cycle of 150 ms performed at a maximum of 3 atrial sites. Reversion to sinus rhythm occurred in 2 patients in group A, 7 in group B (p less than 0.01) and 5 in group C. Pacing was performed from a mean number of 2.1 sites/patient in group A, 1.2 in group B and 2.0 in group C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration to a faster form of atrial flutter occurred in 3, 3 and 4 patients, respectively, and reversion to sinus rhythm occurred in all patients who had intravenous disopyramide and in 1 who took the drug orally. The administration of disopyramide before overdrive pacing improved the rate of conversion to sinus rhythm and allowed an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. Disopyramide is beneficial when overdrive atrial pacing is performed for the treatment of long-standing atrial flutter in patients with organic heart disease.
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PMID:Facilitating influence of disopyramide on atrial flutter termination by overdrive pacing. 328 18


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