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At least 1,657 records · Page 92Linked to original sources
PubMed1980

Comparison of newer antiarrhythmic agents.

In the past decade a number of new antiarrhythmic drugs ahve been introduced. They have been extensively used in the acute phase of myocardial infarction. Few, if any, long-term comparative trials of these newer agents have been reported. Most of these newer agents have been shown to be able to reduce the frequency of ventricular arrhythmias but not the mortality rate. Beta blockers and some antiplatelet adhesive drugs, however, have reduced the mortality rate following myocardial infarction. There is a need for long-term properly stratified trials of these effective agents.

Adrenergic beta-Antagonists↗
PubMed1986

Intolerance and ineffectiveness of mexiletine in patients with serious ventricular arrhythmias.

Fifty-one patients were treated with mexiletine over 10.4 +/- 16 months. The clinical arrhythmia in 25 (49%) was ventricular fibrillation (VF), 11 (22%) had sustained ventricular tachycardia (VT), and 15 (29%) had symptomatic nonsustained VT. Ischemic heart disease was present in 33 patients (66%), cardiomyopathy in nine (17%), and valvular or congenital heart disease in nine (17%). Only six (12%) remain on the drug. Arrhythmias recurred in 21 patients (41%): seven (14%) with VF, three (5%) with sustained VT, and 11 (22%) with symptomatic nonsustained VT. Intolerable side effects occurred in another 17 (33%). Seven patients (14%) died from nonarrhythmic-related deaths while taking mexiletine. Mexiletine was combined with a conventional type IA antiarrhythmic agent in 25 patients (49%). In 12 of these 25 patients (48%), ventricular arrhythmias recurred. These findings were not significantly different from those of the group treated with mexiletine alone, where arrhythmias recurred in 9 of 26 patients (35%) (p = NS). Thus mexiletine, alone or in combination with a type IA antiarrhythmic agent, has limited clinical utility in patients with life-threatening ventricular arrhythmias.

Cardiac Pacing, Artificial↗
PubMed1988

Long-term efficacy of mexiletine alone and in combination with class Ia antiarrhythmic drugs for refractory ventricular arrhythmias.

The efficacy of mexiletine used alone, and in combination with a class Ia antiarrhythmic drug, was assessed in 159 previously drug-refractory patients with ventricular tachycardia (VT) during serial electrophysiologic studies and during long-term (5-year) clinical follow-up. Electrically-inducible ventricular tachycardia was suppressed by mexiletine alone in 23% of patients tested, and a combined antiarrhythmic drug regimen was effective in 29% of the trials performed. Mexiletine was much more likely to be effective in patients presenting with nonsustained VT or ventricular fibrillation than in patients with sustained VT (p less than 0.005). After 1 and 4 years of treatment, 18% and 42% of the patients treated with mexiletine alone had died suddenly or suffered recurrent symptomatic VT, compared to 11% and 25% of patients treated with the combined antiarrhythmic drug regimens (p = NS). Mexiletine therapy was associated with frequent, though readily reversible, adverse reactions. However, mexiletine treatment had to be discontinued permanently in 8 of 92 patients (9%) because of intolerable side effects. We conclude that the added efficacy and possible improved arrhythmia-free survival associated with combining mexiletine with a class Ia agent should be further investigated.

Anti-Arrhythmia Agents↗
PubMed1995

Clinical presentation and long-term follow-up of athletes with exercise-induced vasodepressor syncope.

The purpose of this study is to report on a series of patients who were referred for evaluation of syncope that occurred during or immediately after exercise and in whom a diagnosis of vasodepressor syncope was established (9 women and 8 men; mean age of 28 +/- 17 years). The approach to management was individualized in each patient. All patients were monitored to determine the frequency and type of recurrent symptoms. The mean age at onset of symptoms was 23 +/- 16 years. In 10 patients syncope occurred only in association with exercise. Pharmacologic therapy was successful in normalizing the patients' response to upright tilt in each of the 10 patients in whom it was attempted. During a mean follow-up period of 35 +/- 9 months, none of the patients placed on pharmacologic therapy has had recurrent syncope. Seventeen (88%) of 19 patients have resumed participation in athletics. The results of this study demonstrate that vasodepressor syncope is a cause of syncope in athletes and that patients with exercise-related vasodepressor syncope can safely continue to participate in athletics.

Adolescent↗
PubMed1980

Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of fallot.

The electrophysiologic characteristics of sustained ventricular tachycardia occurring after total repair of tetralogy of Fallot are reported. Four patients, 8 to 31 years of age, who had spontaneous episodes of sustained ventricular tachycardia underwent electrophysiologic study to determine the mechanism and site of origin of the tachycardia. In each patient, the tachycardia could be reproducibly initiated and terminated by programmed electrical stimulation. In two patients, initiation and maintenance of the tachycardia depended on the development and perpetuation of continuous electrical activity in the right ventricular outflow tract. These observations suggested a reentrant mechanism. In each patient, catheter endocardial mapping demonstrated the site of origin to be the right ventricular outflow tract. In two patients intraoperative mapping showed the reentrant circuit originating at the site of healed right ventriculotomy site. We conclude that sustained ventricular tachycardia after repair of tetralogy of Fallot in our patients was caused by reentry at the site of the previous operation in the right ventricular outflow tract.

Adolescent↗
PubMed1984

New directions in antiarrhythmic drug therapy.

Cardiac arrhythmia causing sudden cardiac death is a serious worldwide public health problem. Antiarrhythmic agents have been available for therapy, but the conventional agents cause a high degree of intolerable side effects. The recent development of many new experimental antiarrhythmic agents has increased our capacity to effectively treat cardiac arrhythmias. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise testing and 24-hour ambulatory Holter monitoring, it can reasonably be decided which patient needs therapy and if therapy is going to be effective. Both aspects of the sudden death equation, ectopy frequency (triggering mechanism) and the ability to propagate sustained ventricular tachycardia (substrate), may be examined. Careful follow-up is needed to determine continued drug efficacy and the presence of side effects that may compromise patient compliance with therapy. If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate. A comprehensive approach to arrhythmia management may begin to reduce the high incidence of sudden death due to fatal arrhythmias.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of congestive heart failure on the pharmacokinetics and pharmacodynamics of antiarrhythmic agents.

Changes in the pharmacokinetics of antiarrhythmic agents should be expected in patients with congestive heart failure (CHF). The direction of the changes, however, is not always predictable. The volume of distribution is often decreased by as much as 40%, and loading doses should, therefore, be appropriately reduced. Drug clearance may also be diminished due to decreased blood flow to the liver and kidneys, as well as decreased hepatic drug-metabolizing activity. Infusion rates should similarly be lowered to avoid toxicity. However, decreases in both volume of distribution and clearance may result in little, if any, change in elimination half-life, despite higher plasma concentrations. On the other hand, the elimination half-life of antiarrhythmic agents that have a large volume of distribution and are highly cleared by the liver may be twice as long in patients with CHF compared with normal subjects. Thus, the total daily dose of drug should also be lower in these patients. In addition, the time necessary to reach steady state is longer, so that premature dose escalation may lead to excessive drug accumulation. In terms of their pharmacodynamic effects, all antiarrhythmic agents have the potential to manifest a degree of negative inotropy, which must be anticipated as a possible side effect in patients with CHF. Some of the newer agents, such as tocainide and encainide, appear to cause only minimal myocardial depression. Other potential complications of all antiarrhythmic therapy include proarrhythmia and possible drug interactions with digitalis and diuretics.

Amiodarone↗
PubMed1993

Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion.

It is often suggested but never proven that atrial function is not affected during atrial flutter, nor after its conversion to normal sinus rhythm. To evaluate this hypothesis, a prospective study was performed in 22 patients (age range 20 to 88 years) with atrial flutter. Diastolic transmitral flow was analyzed with echo-Doppler before and after conversion. After randomization, conversion was attempted with overdrive pacing or up to two 50 J shocks. If the initial method was unsuccessful, a 200 J shock was administered. All patients were converted to sinus rhythm with this protocol. Shortly after conversion (at 1 and 6 hours), atrial contribution to ventricular filling was absent in 4 of 22 patients. In the remaining 18 patients, atrial contribution to ventricular filling was small. Atrial contribution to transmitral flow improved from 20 to 27% within 24 hours (p < 0.01) and increased further to 38% at 6 weeks (p < 0.005). Peak velocity of late diastolic filling increased from 0.28 m/s after 1 hour to 0.39 m/s after 24 hours (p < 0.0001) and improved even further during later follow-up. In 1 patient, an effective atrial systole was not observed until the 14th day. Cardiac output did not change significantly during the study period. No differences were observed between the conversion modalities. In conclusion, atrial dysfunction is present immediately after conversion of atrial flutter to normal sinus rhythm. This dysfunction occurs also after overdrive pacing and can last > 1 week. The findings suggest that stasis in the atria can remain temporarily present after successful conversion of atrial flutter to sinus rhythm.

Adult↗
PubMed1982

Ventricular ectopy: etiology, evaluation, and therapy.

Ventricular ectopy occurs commonly. Its significance is related to the degree of complexity and the associated cardiac substrate. Coronary artery disease is the most frequent underlying cause, followed by cardiomyopathy and valvular disease. Symptomatic ventricular arrhythmias require treatment, whereas benign simple ventricular ectopy does not; however, the treatment of asymptomatic high-grade ventricular ectopy remains controversial. Therapy first must be directed toward the cardiac disease. Evaluation of the patient includes Holter monitoring, echocardiography, radionuclide studies, exercise testing, cardiac catheterization, and electrophysiologic testing. Programmed stimulation is useful in the diagnosis and prognosis of ventricular tachycardia, as well as in the evaluation of drug regimen efficacy. After treatment of ischemia and/or failure, specific antiarrhythmic agents, conventional and investigational, alone or in combination, are systematically selected. Should medical therapy alone be insufficient, consideration is given to surgical procedures such as subendocardial resection or ventriculotomy, often in combination with bypass grafting, aneurysmectomy, or valvular replacement. Electronic devices, including pacemakers or automatic internal defibrillators, may also be useful in certain selected cases. Suggested guidelines are proposed for a standardized approach, although therapy for each patient must still be individualized.

Adrenergic beta-Antagonists↗
PubMed1995

Effect of membrane surface potential on the uptake and the inhibition of cationic compounds in rat intestinal brush-border membrane vesicles and liposomes.

The effect of membrane surface potential on the uptake of tryptamine, an organic cation, by rat intestinal brush-border membrane vesicles was investigated. In the presence of an inside-negative K(+)-diffusion potential, the manner of initial uptake of tryptamine appeared to be pH-dependent and the uptake in the acidic medium was lower than that in the neutral medium. Changes in surface potential of brush-border membrane vesicles were monitored using 8-anilino-1-naphthalenesulfonic acid (ANS) and the results suggested that the membrane surface potential (negative charge on the membrane surface) decreased in the acidic medium. A good correlation was observed between the K(+)-diffusion potential-dependent uptake of tryptamine and membrane surface potential monitored by ANS at various pH levels. The uptake of tryptamine by liposomes (large unilamellar vesicles), which contained various amounts of dipalmitoylphosphatidylserine (DPPS), was also examined. The uptake of tryptamine decreased with a decrease of DPPS content in the liposomes, and was correlated with the membrane surface potential monitored by ANS. Moreover, the effect of organic cations on the uptake of tryptamine by intestinal brush-border membrane vesicles was examined. The uptake of tryptamine was inhibited by tetracaine and imipramine. The inhibitory effect of these cations was well correlated with changes in the membrane surface potential in the presence of tetracaine or imipramine. These results suggest that the K(+)-diffusion potential-dependent uptake of tryptamine by intestinal brush-border membrane vesicles is affected by membrane surface potential, and the inhibition of tryptamine uptake originates in changes in the membrane surface potential caused by the organic cations.

Animals↗