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PubMed1992

Treatment of myotonia with antiarrhythmic drugs.

The effects of disopyramide, phenytoin, mexiletine, and tocainide were compared in 30 patients with myotonic disorders. The severity of myotonia was assessed by clinical and electromyographic criteria at the end of each treatment phase lasting four weeks. Mexiletine (MXT) and tocainide (TCD) were found to be the most potent antimyotonic agents. The antimyotonic efficacy of MXT and TCD is explained by their fast-blocking effect on voltage-dependent sodium channels in the muscle membrane. The benefits of myotonia control with pharmacological agents must be weight against the risk of therapy in the individual patient. Because of the risks of hematologic problems, TCD is not recommended by us for the treatment of myotonia.

Adolescent↗
PubMed1988

Effect of 711389-S, a new antiarrhythmic agent, on myocardial energy metabolism in guinea-pigs and rats.

The effect of 711389-S, a new antiarrhythmic agent, on myocardial energy metabolism was investigated using anaesthetized guinea-pigs and rats. 711389-S elevated the adenylate energy charge and phosphorylation potential in normal guinea-pig myocardium. Large doses also increased the myocardial lactate content with ECG abnormalities. The close relationship between rate-pressure product and the myocardial energy state under 711389-S treatments showed the suppression of energy consumption due to a decrease of work output. In guinea-pigs with arrhythmic myocardia induced by intravenous infusion of ouabain, 711389-S prevented the loss of high-energy phosphate compounds and the acceleration of anaerobic glycolysis concomitant with the effective antiarrhythmic property. In ischaemic myocardium produced by ligation of the coronary artery in rats, 711389-S suppressed the decreases of creatine phosphate, NAD+ and adenylate energy charge. Moreover, this agent effectively blocked the incidence of ventricular arrhythmias at an early stage following the ligation. In all of these actions, 711389-S was more effective than disopyramide, which is in the same class of antiarrhythmics. 711389-S was concluded to be a favourable antiarrhythmic agent offering beneficial action against arrhythmic and ischaemic metabolic changes in the myocardium.

Animals↗
PubMed1986

A new method for evaluating the effect of antiarrhythmic drugs on atrioventricular nodal conduction.

Electrophysiological variables were studied in 19 patients before and after one of three commonly used antiarrhythmic agents. The pacing rate at which alternating Wenckebach periods appeared in eight patients was significantly reduced by intravenous digoxin (0.01 mg/kg body weight). The atrioventricular nodal conduction time (A-H interval) and Wenckebach point were not significantly altered by digoxin. Intravenous propranolol (0.1 mg/kg body weight) in four patients did not affect the A-H interval, but it reduced the pacing rates at which the Wenckebach point and alternating Wenckebach periods occurred. Intravenous disopyramide (2 mg/kg body weight) significantly increased the pacing rate required to produce alternating Wenckebach periods but did not significantly alter the other indicators of atrioventricular conduction in seven patients. It is concluded that the pacing rate required to produce alternating Wenckebach periodicity may be a useful and sensitive variable in the evaluation of the effect of antiarrhythmic agents on atrioventricular nodal conduction.

Adult↗
PubMed1995

Favourable outcome in idiopathic ventricular fibrillation with treatment aimed at prevention of high sympathetic tone and suppression of inducible arrhythmias.

OBJECTIVE: In the absence of an obvious cause for cardiac arrest, patients with idiopathic ventricular fibrillation are difficult to manage. A subset of patients has inducible arrhythmias. In others sympathetic excitation plays a role in the onset of the cardiac arrest. This study evaluates a prospective stepped care approach in the management of idiopathic ventricular fibrillation, with therapy first directed at induced arrhythmias and secondly at adrenergic trigger events. SETTING: University Hospital. PATIENTS: 10 consecutive patients successfully resuscitated from idiopathic ventricular fibrillation. INTERVENTIONS: Programmed electrical stimulation to determine inducibility, followed by serial drug treatment. Assessment of pre-arrest physical activity and mental stress status by interview, followed by beta blockade. Cardioverter-defibrillator implantation in non-inducible patients not showing significant arrest related sympathetic excitation. MAIN OUTCOME MEASURE: Recurrent cardiac arrest or ventricular tachycardia. RESULTS: Five patients were managed with serial drug treatment and four with beta blockade. In one patient a defibrillator was implanted. During a median follow up of 2.8 years (range 6 to 112 months) no patient died or experienced defibrillator shocks. One patient had a recurrence of a well tolerated ventricular tachycardia on disopyramide. CONCLUSIONS: Idiopathic ventricular fibrillation may be related to enhanced sympathetic activation. Prognosis may be favourable irrespective of the method of treatment. Whether the present approach enhances prognosis of idiopathic ventricular fibrillation remains to be determined. However, it may help to avoid potentially hazardous antiarrhythmic drugs or obviate the need for implantation of cardioverter-defibrillators.

Adult↗
PubMed1996

Effects of blockade of fast and slow inward current channels on ventricular fibrillation in the pig heart.

OBJECTIVE: To determine the contribution of fast and slow inward channels to the electrocardiogram (ECG) of ventricular fibrillation. METHODS: Ventricular fibrillation was induced by endocardial electrical stimulation in pigs anaesthetised with pentobarbitone sodium (30 mg/kg intravenously). ECGs simultaneously recorded from the body surface (lead II) and from the endocardium were studied by power spectrum analysis (0-40 Hz). RESULTS: The mean (SEM) dominant frequency of fibrillation (9.0 (1.1) Hz in lead II at 0-40 s) did not change significantly with time in pigs given intravenous saline. However, the dominant frequency was significantly reduced by intravenous pretreatment with the class I antiarrhythmic drugs, lignocaine (3 mg/kg, 6.5 (0.5) Hz; 10 mg/kg, 4.2 (0.6) Hz), mexiletine (3 mg/kg, 6.2 (0.4) Hz; 10 mg/kg, 5.5 (0.4) Hz), and disopyramide (2.5 mg/kg, 5.4 (0.6) Hz). After flecainide (3 mg/kg, 6.9 (0.5) Hz) the reduction in frequency was not significant. Similar data were obtained with endocardial recordings. In contrast pre-treatment with verapamil (0.2 mg/kg, 11.7 (0.8) Hz; and 1.0 mg/kg, 12.9 (1.6) Hz) produced a significantly higher dominant frequency of fibrillation than saline and widened the bandwidth of frequencies around the dominant frequency. CONCLUSIONS: These results indicate that voltage-dependent sodium channel currents contribute to the rapid frequencies of ventricular fibrillation. Blockade of L-type inward calcium channel activity increases the fibrillation frequency and fractionates the frequencies of the fibrillation wavefronts.

Animals↗
PubMed1996

Regulation of cholecystokinin secretion in STC-1 cells by nitric oxide.

In the present study we evaluated the effects of agents anticipated to change NO levels on the secretion of cholecystokinin (CCK) from STC-1 cells. After a 15-min treatment with the nitric oxide (NO) generating agent sodium nitroprusside (SNP; 10 microM), a 24% inhibition in basal CCK release and an increase in cellular guanosine 3',5'-cyclic monophosphate (cGMP) levels were noted. By contrast, SNP (10 microM) had no effect on CCK release stimulated by L-phenylalanine (20 mM). Inhibition of NO synthase (NOS) with NG-nitro-L-arginine methyl ester (L-NAME) produced dose-dependent stimulation in CCK release. L-NAME (100-400 microM) also inhibited ATP-sensitive potassium (KATP) channels in cell-attached patches. Pretreatment of cells with disopyramide (200 microM), a KATP channel blocker, blocked L-NAME stimulation of CCK release. After inhibition of potassium channel activity by L-NAME, addition of the nonhydrolyzable cGMP analogue 8-bromo-cGMP (1-2 mM) reactivated potassium channels. NO-generating agents had no effect on channel activity in inside-out membrane patches. It is concluded that NO may serve as an important regulator of basal CCK release.

Animals↗
PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗
PubMed1980

Effects of antiarrhythmic drugs on atrioventricular conduction in patients with acute myocardial infarction.

Three hundred fifty-eight of 429 (83%) consecutive patients with acute myocardial infarction (MI) and a normal PR interval received various antiarrhythmic drugs (AD), including lidocaine and/or procainamide, quinidine, digoxin, propranolol or disopyramide. There was no significant difference in the incidence of progression to any degree of atrioventricular (AV) block or to higher degrees of AV block (Mobitz II or third-degree AV block) between those treated and not treated with AD: 38 of 358 (11%) and six of 358 (1.7%) with AD vs 11 of 71 (15%) and two of 71 (2.8%) in the untreated group, respectively. Similarly, there was no significant difference in progression between treated and untreated patients with anterior MI, 14 of 144 (10%) vs five of 32 (16%); inferior MI, 21 of 111 (19%) vs five of 26 (19%), or subendocardial MI, three of 103 (3%) vs one of 12 (8%). Bundle branch block (BBB) (without AV block) was initially present in 89 of 249 (21%). The incidence of AV block (seven of 24, 30%) was higher in treated patients with newly acquired BBB (27 patients) than in the untreated patients (none of three, p less than 0.05). The commonly used ADs did not adversely affect AV conduction in patients with acute MI with narrow QRS and either normal, first-degree, or Mobitz I AV block. Moreover, no subset of patients grouped by infarct location, specific AD used, or BBB (except perhaps for those with newly acquired BBB) appeared to be at risk of development of AV block during AD therapy.

Aged↗
PubMed1981

Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients.

Torsade de pointes, also called atypical ventricular tachycardia (AVT), was diagnosed in 10 patients, nine on antiarrhythmic therapy and one with acute central nervous system damage. Four patients received quinidine and five disopyramide, either alone or in combination with amiodarone. AVT was dose-dependent in some, but in others, it started shortly after initiation of drug therapy (idiosyncrasy). All patients had QT prolongation longer than 0.60 second immediately before the onset of AVT. This measurement appeared to be a more sensitive predictor of the development of AVT than QTc prolongation or QRS widening. All patients also showed bradycardia before AVT onset. After therapy, the QT immediately decreased, while QTc and QRS remained prolonged for longer periods. Isoproterenol was effective in five of seven patients, but was contraindicated in two others. Ventricular pacing was used in four patients, including the two who did not respond to isoproterenol, and this abolished AVT promptly. Isoproterenol or pacing appear to be the therapy of choice for AVT, while the conventional drugs used to treat the usual form of ventricular tachycardia are not only ineffective, but even contraindicated.

Adult↗
PubMed1983

Direct endocardial recording from an accessory atrioventricular pathway: localization of the site of block, effect of antiarrhythmic drugs, and attempt at nonsurgical ablation.

We recorded a discrete 0.95 mV potential consistent with accessory atrioventricular pathway (AP) activation during serial electrophysiologic studies in a patient with Ebstein's anomaly and Wolff-Parkinson-White syndrome. Bipolar pacing from the catheter electrode in which the AP potential was recorded resulted in a stimulus-ventricle interval identical to the AP-ventricle interval during antegrade conduction, and a stimulus-atrium interval identical to the AP-atrium interval during retrograde conduction. With the patient in the drug-free state, antegrade AP block during atrial pacing and retrograde AP block during ventricular pacing occurred distal to the AP potential (AP-ventricle junction and AP-atrium junction, respectively), supporting the "impedance mismatch" hypothesis. Procainamide and disopyramide each lengthened the antegrade AP effective refractory period by affecting the AP-ventricle junction (possibly by decreasing the current generated by the AP). Both drugs also lengthened the retrograde AP effective refractory period but produced a greater effect on the ventricle-AP junction than on the AP-atrium junction, suggesting marginal geometry of the former. R wave synchronous shocks of 160 and 320 W-sec delivered between the catheter electrode recording the largest unipolar AP potential and a skin electrode produced transient, complete, antegrade block over the AP, suggesting the feasibility of this new nonsurgical technique for AP ablation.

Adult↗
PubMed1987

Idiopathic ventricular fibrillation: inducibility and beneficial effects of class I antiarrhythmic agents.

Ventricular fibrillation in patients without recognizable heart disease is uncommon and electrophysiologic data on such patients is limited. Over a 7 year period, five patients (three men and two women, ranging in age from 24 to 52 years) without demonstrable heart disease underwent electrophysiologic studies with pharmacologic drug testing because of single (four patients) or multiple (one patient) documented episodes of ventricular fibrillation. The arrhythmic event was unrelated to myocardial ischemia or infarction, metabolic or electrolyte disturbances, drug toxicity, preexcitation, or prolonged QT syndromes. In all three patients receiving no antiarrhythmic drugs and in two pretreated with amiodarone, a rapid poorly tolerated ventricular tachyarrhythmia requiring cardioversion was induced by programmed ventricular stimulation with up to two extrastimuli. In all instances, addition of either oral quinidine or oral disopyramide prevented the induction of sustained ventricular arrhythmias. All five patients were placed on antiarrhythmic drug regimens found effective during electrophysiologic studies and remained asymptomatic during follow-up periods ranging from 12 to 93 (mean 52) months. We conclude that in the patients with idiopathic ventricular fibrillation in our study: programmed ventricular stimulation reliably replicated the spontaneous arrhythmia, class I antiarrhythmic agents effectively prevented induction of the arrhythmia in the laboratory, and in contrast to the severity of the presenting arrhythmia, a benign clinical course was observed during long-term therapy with class I antiarrhythmic agents.

Adult↗
PubMed1982

Intravenous antiarrhythmic drugs: newer aspects of therapy.

The use of the intravenous form of antiarrhythmic drugs from the perspective of prophylaxis, urgency of therapy, and rapid assessment of effectiveness is reviewed. Examples of clinical relevance for each of these 3 variables are used to illustrate the relevance of these approaches. 1) In the human model of acute myocardial infarction, prophylaxis with lidocaine is proved and is safe, with toxicity minimized when accurate determinations of blood levels of drug are readily available. 2) When reversion is unsuccessful and ventricular response cannot be controlled with conventional therapy, rapid supraventricular tachyarrhythmias will often normalize in response to intravenous verapamil therapy, a calcium-blocking agent soon available for clinical use. 3) A long-term outpatient antiarrhythmic drug program guided by target blood levels can be defined rapidly by intravenous administration of drug; this approach enhances safety and simplifies the definition of an ongoing antiarrhythmic program. Disopyramide responsiveness can be defined using this technique.

Anti-Arrhythmia Agents↗
PubMed1983

Quantitative analysis of the antiarrhythmic effect of drugs on canine ventricular arrhythmias by the determination of minimum effective plasma concentrations.

Antiarrhythmic effects and minimum antiarrhythmic plasma concentrations (min PC) were examined using three canine ventricular arrhythmia models, i.e., two-stage coronary ligation arrhythmia (Cor), halothane-adrenaline arrhythmia (Adr) and digitalis arrhythmia (Dig). Disopyramide suppressed these three arrhythmias and its min PCs were 5.3 +/- 1.8 (Cor), 4.2 +/- 1.1 (Adr) and 1.7 +/- 0.4 micrograms/ml (Dig). Procainamide suppressed coronary ligation arrhythmia and its min PC was 27.1 +/- 4.0 micrograms/ml, but was not effective on adrenaline arrhythmia. Aprindine was effective on three arrhythmias and its min PCs were 1.6 +/- 0.3 (Cor), 1.0 +/- 0.4 (Adr) and 0.8 +/- 0.4 micrograms/ml (Dig). Lidocaine was not effective on coronary ligation arrhythmia, but was effective on adrenaline arrhythmia and its min PC was 15 micrograms/ml. Phenytoin was effective on three arrhythmias and its min PCs were 9.8 +/- 2.0 (Cor), 12.1 +/- 3.1 (Adr) and 11.3 +/- 3.0 micrograms/ml (Dig). It was not specifically effective on canine digitalis arrhythmia. Propranolol and other beta-blockers were effective on adrenaline arrhythmia, but very high doses were necessary for suppressing coronary ligation and digitalis arrhythmias. Verapamil was only effective on adrenaline arrhythmia and its min PC was 0.03 +/- 0.01 microgram/ml. Canine min PCs of drugs were almost the same as those reported in man except for procainamide and lidocaine. Membrane stabilizing effects seem to be important for suppressing canine ventricular arrhythmias.

Animals↗
PubMed1988

Therapeutic effectiveness and plasma levels of single or combination use of class I antiarrhythmic agents for ventricular arrhythmias.

The efficacy of disopyramide (DP), mexiletine (MX), aprindine (AP) and cibenzoline (CZ) on ventricular arrhythmias was compared (single drug therapy). In addition, the efficacy of the combination therapy of DP with MX was also studied (combination therapy). One hundred of the 106 patients completed the protocol of the single drug therapy. Fifty percent or more reduction in the frequency of ventricular premature contractions (VPCs) was obtained in 24 of 43 patients (56%) with DP, in 24 of 44 (55%) with MX, in 18 of 29 (62%) with AP and 10 of 18 (56%) with CZ. AP was comparatively more effective than the other drugs tested. DP was significantly effective on VPCs with organic heart disease as compared to idiopathic VPCs (p less than 0.05), while the other 3 drugs did not have such a tendency. With MX therapy, 10 of the 12 patients with fast VT rate (greater than or equal to 150 beats/min) showed a significant effect while only 4 of the 12 patients with non-fast VT rate (greater than or equal to 100 and 150 beats/min) had a significant one (p less than 0.05). On the other hand, DP, AP and CZ showed almost the same efficacy at any cycle length of VT. Six patients withdrew from the study, 4 because of digestive troubles with MX therapy, 1 because of micturition disturbances with DP and 1 because of skin rash with AP. The average therapeutic plasma levels of DP, MX, AP and CZ were 1.76 +/- 0.54 microgram/ml, 1.08 +/- 0.41 microgram/ml, 0.85 +/- 0.43 microgram/ml and 268.2 +/- 123.3 ng/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Clinical study on coupling interval of ventricular premature contraction in patients with organic heart disease.

The characteristics of the coupling interval (CI) of ventricular premature contraction (VPC) were studied in 100 patients with frequent VPCs using 24 h ambulatory ECG recording. All R-R intervals were registered on computer to determine the mean value of CIs (Mean CI) and the standard deviation of CIs (SD-CI). We compared the Mean CI and the SD-CI between idiopathic VPCs and VPCs with organic heart disease (OHD). In addition, we evaluated the efficacy of disopyramide (DP) and mexiletine (MX) and we examined the relationship between the efficacy of these drugs and the characteristics of CI. The Mean CI of VPCs with OHD was longer than that of idiopathic VPCs (530 vs. 494 msec, p less than 0.05). The SD-CI of VPCs with OHD was larger than that of idiopathic VPCs (54.1 vs. 39.3 msec, p less than 0.01). In all treated cases, the drug efficacy was not different between DP (11/18, 61%) and MX (9/19, 47%). However when we isolated cases of OHD, we found a tendency that DP (9/12, 75%) was more effective than MX (7/16, 44%). In cases where DP was administered, the Mean CI of VPCs was not different between effective and ineffective cases, while in cases where MX was administered, the Mean CI of ineffective cases had a tendency to be longer than that of effective cases (552 vs. 506 msec, p less than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1992

The effect of pretreatment with moricizine on early arrhythmia resulting from myocardial ischemia in rats.

Moricizine (moracizine) is a new class I antiarrythmic drug which is undergoing a large scale clinical trial at present. A rat model was used to compare the effects of moricizine (5 mg/kg i.v.), disopyramide (DSP 5 mg/kg i.v.) and mexiletine (MXT 5 mg/kg i.v.) on early ventricular arrhythmias occurring within 30 min after ligation of the left coronary artery. After intravenous administration, all three drugs slowed the heart rate significantly (p less than 0.01), and compared to the control group only moricizine significantly increased the systolic, diastolic and mean arterial blood pressures. The total number of premature ventricular complexes were as follows; control group (n = 9); 1666 +/- 250 beats, moricizine group (n = 7); 1645 +/- 417 beats (NS), DSP group (n = 10); 325 +/- 155 beats (p less than 0.01 vs control) and MXT group (n = 10); 733 +/- 147 beats (p less than 0.01 vs control). The incidence of primary ventricular fibrillation, was significantly reduced by DSP and MXT (10% reduction and 20% reduction respectively) (p less than 0.05), while moricizine (incidence 80%) had no effect in comparison to the control group (incidence 90%). Death due to arrhythmia was completely abolished by DSP and MXT; although moricizine showed a slight tendency to increase the mortality rate, but the difference was not significant. In conclusion, moricizine has no obvious protective effect on early ventricular arrhythmias resulting from coronary artery occlusion in rats.

Animals↗
PubMed1985

Effect of l-carnitine chloride and its acetyl derivative on the electrophysiological derangement induced by palmityl-l-carnitine in isolated canine ventricular muscle.

Using the microelectrode technique, the effects of l-carnitine (LC) and acetyl-l-carnitine (ALC) on the changes in the transmembrane action potential of the canine ventricular muscle induced by palmityl-l-carnitine (PLC) were studied in comparison with those of disopyramide (D). LC (5 X 10(-3) M) itself had no effect on the electrophysiological parameters of the ventricular muscle. ALC (5 X 10(-3) M) increased the maximum rate of rise (dV/dt max) slightly and decreased the action potential duration (APD), although these changes were not statistically significant. D (1.5 X 10(-3) M) decreased dV/dt max and prolonged APD and the absolute refractory period (ARP). PLC (3 X 10(-4) M) decreased the resting membrane potential, action potential amplitude and dV/dt max, and it shortened APD and ARP. LC and ALC (5 X 10(-3) M) improved the electrophysiological derangement produced by PLC to the same degree. On the other hand, application of D (1.5 X 10(-5) M) resulted in no improvement of the electrophysiological derangement produced by PLC.

Acetylcarnitine↗
PubMed1995

Antiarrhythmic effects of bisaramil on triggered arrhythmias produced by intracoronary injection of digitalis and adrenaline in the dog.

Antiarrhythmic effects of bisaramil were examined by using new in vivo triggered arrhythmia models, and they were compared with those of other antiarrhythmic drugs. Bisaramil (3-10 micrograms, i.c.) suppressed triggered ventricular arrhythmias that were produced during pauses between trains of rapid ventricular stimulation (cycle length: 250 msec, train number: 15) in anesthetized open-chest dog hearts administered with subtoxic doses of digitalis or adrenaline to the anterior descending coronary artery. The potencies of bisaramil, disopyramide, lidocaine and flecainide suppressing digitalis-induced triggered ventricular arrhythmias were similar to those suppressing adrenaline-induced ones. The potency of verapamil for suppressing digitalis-induced triggered ventricular arrhythmias were weaker than that for suppressing the adrenaline-induced ones. Bisaramil was the most effective among the antiarrhythmic drugs used in the present experiment. Since bisaramil has been reported to be effective in suppressing other canine automatic ventricular arrhythmias, and the triggered ventricular arrhythmias occur in clinical situations, bisaramil may become a useful drug for the treatment of clinical arrhythmias.

Animals↗