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At least 1,315 records · Page 73Linked to original sources
PubMed1999

Chronotropic, inotropic, dromotropic and coronary vasodilator effects of bisaramil, a new class I antiarrhythmic drug, assessed using canine isolated, blood-perfused heart preparations.

The cardiovascular effects of a new class I antiarrhythmic drug, bisaramil, were examined using canine isolated, blood-perfused heart preparations. Bisaramil exerted negative chronotropic, inotropic and dromotropic effects as well as coronary vasodilator action, which are qualitatively the same as those of classical class I drugs. The selectivity of bisaramil for the intraventricular conduction vs the other cardiac variables was compared with that of disopyramide and flecainide. Bisaramil was the most selective for intraventricular conduction, while it was the least selective for ventricular muscle contraction. We conclude that bisaramil may become a useful antiarrhythmic drug with less cardiac adverse effects.

Animals↗
PubMed1977

Resistant ventricular tachycardias and recurrent cardiac arrests. 96 episodes.

A 66-year-old man suffered an acute myocardial infarction complicated by multiple episodes of ventricular tachycardia and 96 episodes of ventricular fibrillation requiring cardioversion over a period of 55 days. Following ventricular aneurysmectomy, the ventricular tachycardia persisted. This converted to regular sinus rhythm with a regimen of disopyramide phosphate, quinidine, and propranolol.

Aged↗
PubMed1989

Failure of corticosteroid therapy to prevent induction of ventricular tachycardia in sarcoidosis.

Programmed ventricular stimulation was performed in a patient with sarcoidosis who exhibited an episode of sustained ventricular tachycardia. Sustained rapid ventricular tachyarrhythmias requiring cardioversion for termination were induced by double right ventricular apical extrastimuli during control, and treatment with disopyramide, quinidine, and fluocortolone. In contrast, only four repetitive ventricular complexes were induced during combined therapy with quinidine, mexiletine and amiodarone. While receiving the latter regimen, the patient has been asymptomatic during 28 months of follow-up.

Adult↗
PubMed1988

A case of arrhythmogenic right ventricular dysplasia with prominent late potential.

A case of arrhythmogenic right ventricular dysplasia with frequent episodes of ventricular tachycardia (VT) in a 57-year-old man is reported. His electrocardiogram showed a normal axis and inverted T waves in V1-V3 during sinus rhythm and a left bundle branch block pattern during VT. The VT could be terminated by either intravenous administration of lidocaine or procainamide or by cardioversion. Echocardiogram and right ventriculography showed reduced wall motion of the apex and infundibulum of the dilated right ventricle. No evidence of ischemic heart disease was found by left ventriculography, coronary arteriography and RI scintigraphy. A prominent late potential following the QRS complex was recorded by averaging and magnifying the surface electrocardiogram. The combination of oral mexiletine and disopyramide partially suppressed the VT attacks and relieved the subjective symptoms, however the late potential remained almost unchanged.

Cardiac Pacing, Artificial↗
PubMed2005

Cough reflex by ventricular premature contractions.

A 72-year-old man was referred for further assessment of a chronic cough. He noticed an association between the episodes of coughing and palpitations. Electrocardiography (ECG) revealed normal sinus rhythm and sporadic unifocal ventricular premature contractions (VPCs). Each cough was preceded by a premature beat. Continuous wave Doppler echocardiography revealed a VPC-induced transient increase in the pulmonary artery blood flow. He was successfully treated for VPCs with oral disopyramide, resulting in subsidence of both the coughing and palpitations. We suspect that the VPC-induced hemodynamic changes in the pulmonary circulation might be responsible for coughing in our patient. Premature contractions should be considered as a possible cause of chronic dry cough in the clinical setting.

Anti-Arrhythmia Agents↗
PubMed1987

Antiarrhythmic effects of a novel diamine derivative, AN-132, on several animal models of cardiac arrhythmias.

The antiarrhythmic activities of AN-132, 3-(diisopropylaminoethylamino)-2',6'-dimethylpropionanilide X 2H3PO4, compared with three reference drugs, were examined in several arrhythmic models of rats, guinea-pigs and dogs. When compared on a weight basis, AN-132 given in oral or i.v. route proved to be more potent and longer-acting than disopyramide, propaphenone and mexiletine against supraventricular and ventricular arrhythmias induced by chloroform, aconitine, ouabain and halothane-adrenaline.

Aconitine↗
PubMed1998

Galanin inhibits glucagon-like peptide-1 secretion through pertussis toxin-sensitive G protein and ATP-dependent potassium channels in rat ileal L-cells.

The neuropeptide galanin is widely distributed in the gastrointestinal tract and exerts several inhibitory effects, especially on intestinal motility and on insulin release from pancreatic beta-cells. The presence of galanin fibres not only in the myenteric and submucosal plexus but also in the mucosa, prompted us to investigate the regulatory role of galanin, and its mechanism of action, on the secretion of the insulinotropic hormone glucagon-like peptide-1 (GLP-1). Rat ileal cells were dispersed through mechanical vibration followed by moderate exposure to hyaluronidase, DNase I and EDTA, and enriched for L-cells by counterflow elutriation. A 6- to 7-fold enrichment in GLP-1 cell content was registered after elutriation, as compared with the crude cell preparation (929 +/- 81 vs 138 +/- 14 fmol/10(6) cells). L-cells then accounted for 4-5% of the total cell population. Bombesin induced a time-(15-240 min) and dose- (0.1 nM-1 microM) dependent release of GLP-1. Glucose-dependent insulinotropic peptide (GIP, 100 nM), forskolin (10 microM) and the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA, 1 microM) each stimulated GLP-1 secretion over a 1-h incubation period. Galanin (0.01-100 nM) induced a dose-dependent inhibition of bombesin- and of GIP-stimulated GLP-1 release (mean inhibition of 90% with 100 nM galanin). Galanin also dose-dependently inhibited forskolin-induced GLP-1 secretion (74% of inhibition with 100 nM galanin), but not TPA-stimulated hormone release. Pretreatment of cells with 200 ng/ml pertussis toxin for 3 h, or incubation with the ATP-sensitive K+ channel blocker disopyramide (200 microM), prevented the inhibition by galanin of bombesin- and GIP-stimulated GLP-1 secretion. These studies indicate that intestinal secretion of GLP-1 is negatively controlled by galanin, that acts through receptors coupled to pertussis toxin-sensitive G protein and involves ATP-dependent K+ channels.

Animals↗
PubMedDate not supplied

Reliability of antiarrhythmic drug plasma concentration monitoring.

Measurement of drug levels is becoming increasingly popular to optimise the dosage of various drugs. In the case of antiarrhythmic drugs, the narrow therapeutic margin of most of these agents and a direct relationship between their pharmacological effects and plasma concentrations would justify more widespread use of monitoring. Optimum plasma concentration ranges have been described for lignocaine (lidocaine), procainamide, quinidine and, more recently, also for disopyramide, mexiletine, tocainide and other new antiarrhythmics. A critical analysis of the original data shows, however, that therapeutic and toxic levels are not so well defined as often assumed: small numbers of patients, marked interindividual variability, sometimes inadequate documentation of arrhythmias and lack of standardised blood sampling characterise many of these studies. Uncertainty about the reliability of concentration-effect relationships also arises when active drug metabolites are identified or there are marked concentration-dependent changes of drug protein-binding. In addition, abolition of various types of arrhythmias might require different drug concentrations. Nevertheless, therapeutic monitoring can be of practical value in patients with life-threatening ventricular arrhythmias and can also greatly facilitate dosage adjustment in cases with renal hepatic or severe cardiac failure. For a correct interpretation of drug levels, the time of blood sampling, dosage regimen, duration of treatment, pharmacokinetic principles, and the clinical condition of the patient must be taken into account. Further studies are needed to define the optimum therapeutic range for several drugs and to evaluate the usefulness of plasma concentration measurements in routine antiarrhythmic treatment.

Amiodarone↗
PubMed1985

Haemodynamic effects of class I antiarrhythmic agents.

In order to choose the most appropriate antiarrhythmic agent, the basic haemodynamic characteristics of class I antiarrhythmic agents must be known. Class Ia agents, quinidine and procainamide, have minor haemodynamic effects, while disopyramide causes serious left ventricular depression. Class Ib drugs are exceptionally well tolerated, and class Ic agents have the potential for adverse haemodynamic effects in patients with left ventricular dysfunction. In this article, haemodynamic effects of class I antiarrhythmic agents are described, with particular emphasis on their clinical implications.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Efficacy of sequential antiarrhythmic treatment in sinus rhythm maintenance after successful electrocardioversion in patients with chronic non-valvular atrial fibrillation.

BACKGROUND: Sequential use of antiarrhythmic drugs may improve prognosis in chronic atrial fibrillation (AF). We conducted a prospective study of the efficacy of sequential antiarrhythmic drug therapy in sinus rhythm (SR) maintenance after a successful electrocardioversion (CV) in pts with chronic AF. MATERIAL AND METHODS: 58 pts (64.3 +/- 4.3 years old) with chronic AF underwent CV. After SR restoration (Group I) pts received one of the following antiarrhythmic drugs (Drug I): propafenone, sotalol or disopyramide. In case of arrhythmia recurrence, second CV was performed and pts received another drug from those mentioned above (Drug II). If treatment proved to be unsuccessful pts received amiodarone (Drug III) and third CV was attempted. After first unsuccessful CV (Group II) pts received a loading dose of amiodarone and another CV was attempted. In case of SR restoration amiodarone was administered continuously. RESULTS: After 12 months 81% pts were on SR; 85% pts received amiodarone continuously. After 1 year 6 (10%) pts presented with SR treated with Drug I (median 71 days); Drug II proved to be ineffective in all patients (median 27 days). 28 pts continued to receive amiodarone (no median). CONCLUSIONS: Sequential antiarrhythmic drug therapy improves arrhythmia prognosis in AF within a 12-month observation period. Amiodarone seems to be the most effective antiarrhythmic drug also in pts who required second CV proceeded by amiodarone treatment to restore SR.

Aged↗
PubMedDate not supplied

The effect of commonly used drugs on angiogenesis.

BACKGROUND: Within the last decade, there has been much interest in the area of tumor angiogenesis, with the advent of many new anti-angiogenic drugs undergoing testing in cancer clinical Phases II and III. Many of the cancer patients also take multiple medications for a variety of chronic illnesses. Because of possible drug-drug interactions, it is important to investigate the effect that commonly prescribed medications may have on angiogenesis. MATERIALS AND METHODS: In this pilot study, we assessed the effect of the following drugs on in vitro angiogenesis: atenolol, diltiazem, enalapril, disopyramide, mexiletine, coumadin, cimetidine and omeprazole. RESULTS & CONCLUSION: We observed that, although some of these drugs at massive doses inhibited endothelial proliferation, they did not affect in vitro angiogenesis at human therapeutic ranges.

Angiogenesis Inhibitors↗
PubMed2003

[Anti-arrhythmic therapy: diagnostic possibilities of signal-averaged electrocardiography and heart rate variability].

Effects of monotherapy with class IC, II and III antiarrhythmic drugs on parameters of signal averaged (SA) ECG and heart rate variability were studied in 88 patients (mean age 45.6+/-7.8 years). Class IC drugs (ethacizine, disopyramide) caused worsening of qualitative parameters of SA ECG and appearance of ventricular late potentials. Therapy with beta-adrenoblockers, amiodarone and sotalol in patients with ventricular arrhythmias was associated with improvement of parameters of SA ECG, lowering of sympathetic and augmentation of parasympathetic activity without sings of arrhrythmogenic and negative inotropic effects. Combination of noninvasive diagnostic methods including SA ECG, temporal and spectral analysis of heart rate variability, Holter ECG monitoring can facilitate selection of appropriate antiarrhythmic therapy and control of its efficacy.

Adrenergic beta-Antagonists↗
PubMed1992

[Ion channels and drugs: what can be learned from their interactions?].

The study of the interaction between drugs and the sodium channel is important to understand the functioning of the channel at the molecular level. The affinity of a drug to bind depends on the channel's state: rested, activated or inactivated state. Since the probability of these three states depends on the membrane potential and the drug itself may carry a charge, there are two reasons for a modulation of the effect by the membrane potential. Drugs like lidocaine and tertiary amines bind preferentially to the inactivated state. Others like disopyramide and penticainide block only the open or activated channel and do not bind to the channel in the rested or inactivated state. The same rule has to be applied for the unblocking. The consequences of these differences are discussed.

Anesthetics, Local↗
PubMed2004

Atrial fibrillation: rate control often better than rhythm control.

(1) The treatment aims in atrial fibrillation are to reduce patients' symptoms and to prevent both embolism and deterioration of any underlying heart disease. Therapy consists of anticoagulant or antiplatelet drugs, treatment of any underlying heart disease, and heart rate control. (2) Digoxin, betablockers, diltiazem and verapamil slow the heart rate but rarely restore sinus rhythm. Amiodarone, disopyramide, flecainide, quinidine and sotalol can be used to prevent relapse of atrial fibrillation after electrical cardioversion, but they all have potentially serious adverse effects. New trials of antiarrhythmic treatments have been published since our last review of this subject. (3) In one trial in 403 patients, amiodarone was more effective than sotalol and propafenone in restoring and maintaining sinus rhythm. After 15 months of follow-up, there were fewer strokes among patients treated with amiodarone, but there was no difference between the three drugs in the overall incidence of cardiovascular events. (4) A clinical trial with 4060 patients compared rhythm control (mainly with amiodarone, sotalol or propafenone; sometimes combined with electrical cardioversion) and rate control (with digoxin, betablocker, diltiazem or verapamil; systematically combined with anticoagulant therapy). The antiarrhythmic treatment restored sinus rhythm in more than half the patients in the long term. But rhythm control did not reduce the risk of death or serious cardiovascular events during a mean follow-up period of 3.5 years. Rhythm control caused more adverse events than rate control; subgroup analyses (weak evidence) suggest that rhythm control may also have caused more deaths among patients over 65 and among patients with coronary heart disease. (5) In another trial, electrical cardioversion followed by antiarrhythmic therapy (mainly sotalol) sustainably restored sinus rhythm in more than one-third of 522 patients. But, compared with rate control treatment plus anticoagulant therapy, rhythm control did not reduce the risk of cardiovascular events, and was associated with a larger number of serious adverse cardiac effects. (6) Other recent trials confirm the risk of serious adverse effects, including severe arrhythmia with sotalol (especially at the start of treatment), and adverse thyroid and pulmonary effects with amiodarone. (7) Combined radiofrequency ablation and cardiac stimulation improved symptoms in some patients with incapacitating atrial fibrillation who had not responded to other treatments. However, this approach carries a risk of serious adverse effects, and its impact on the risk of cardiovascular events and death is not known. (8) In practice, an attempt should be made to restore sinus rhythm with amiodarone and/or electrical cardioversion, in symptomatic, recent or paroxysmal atrial fibrillation in patients under 65 who have no signs or symptoms of coronary heart disease. In other situations, rate control is the first-line option, using digoxin, betablockers (other than sotalol) or calcium channel blockers (diltiazem or verapamil). Whatever the option, treatment must be combined with anticoagulant or antiplatelet therapy, and with treatment of any underlying heart disease.

Adult↗
PubMed2005

Deglutition-induced atrial fibrillation.

We present the case of 38-year-old woman who experienced palpitations on swallowing, which were later found to be atrial fibrillation. Her symptoms improved on treatment with disopyramide and verapamil. Within 9 months, she was weaned from both medications without recurrence of symptoms.

Adult↗
PubMed1990

[Assessment of anti-arrhythmic activity of palpitin and cardio-hemodynamic effects of its administration].

Palpitin, an agent of the disopyramide series, was evaluated for its antiarrhythmic potency in the treatment of ventricular and supraventricular arrhythmias and for its effects of ECG and central hemodynamic parameters in 108 patients (91 had coronary heart disease, 8 presented with postmyocardial cardiosclerosis, 5 had hypertensive disease, and 4 suffered from neurocirculatory dystonia). 24-hour ECG monitoring and echocardiography were employed in the study. It was concluded that the drug possessed a high antiarrhythmic potency. No substantial changes were found in the mean values of echocardiographic parameters, as well as of atrioventricular and intraventricular conduction.

Adolescent↗
PubMed2006

Pathophysiology of hypertrophic cardiomyopathy determines its medical treatment.

Physicians treating hypertrophic cardiomyopathy (HCM) are faced with unique management challenges. Understanding pathophysiology and overall good prognosis forms the basis for medical treatment. Treatment is tailored by the presence or absence of outflow tract gradient and individual symptoms. In all patients, formal stratification for sudden death risk is necessary, with consideration of defibrillator implantation in patients deemed to be at high risk. In patients with no or only mild symptoms the approach of watchful waiting is often appropriate. For symptomatic patients with non-obstructed disease medical treatment with calcium channel blockers and beta-blockers is aimed to improve heart failure symptoms, and ischemia. Verapamil is the most often used, with likely benefit of relieving ischemia. Obstruction, most commonly due to systolic anterior motion of the mitral valve (SAM) and mitral-septal contact, occurs in >/=50% of all HCM patients, worsening symptoms and increasing mortality. Successful medical treatment of obstruction with negative inotropes slows acceleration of left ventricular ejection with delay in SAM, ultimately yielding a lower pressure gradient. Beta -blockers are the first line treatment in obstructive HCM predominantly by mitigating provocable gradients. The magnitude of symptom relief with verapamil is similar to the effect of beta -blockade. Disopyramide combined with beta -blockade is thought by some to be the most effective medical treatment of obstruction, and has been shown to be safe and not pro-arrhythmic. Most symptomatic HCM patients with significant obstruction at rest or provocation can be successfully managed with long-term medication alone.

Adrenergic beta-Antagonists↗
PubMed1991

[Comparative effectiveness of class I anti-arrhythmia drugs and the algorithms of their selection in patients with ventricular arrhythmia].

The efficacy of 7 well-known Class I antiarrhythmic agents were retrospectively and by+crossover compared in 2 groups of patients treated in hospital in different years for ventricular arrhythmias. Class IC agents proved to be the most potent in the two groups of patients. The following algorithm is proposed to choose Class I agents: if quinidine or mexiletine is beneficial in the same patients, the other drugs will be also effective. If disopyramide fails to be beneficial, allapinin , ethacizine , propaphenon will be the most effective. When allapinin produces effects, ethacizine and propaphenon show their highest potency, but when each of them fails, a combination of antiarrhythmic agents should be used.

Adolescent↗