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PubMedDate not supplied

Interactions and non-interactions with ranitidine.

At present, there are two H2-receptor antagonists available for the treatment of peptic ulcer disease - cimetidine and ranitidine. Cimetidine is well known to interact with a number of concurrently administered drugs. Like cimetidine, ranitidine binds to cytochrome P-450 in the liver where it appears to exert an inhibitory effect, but to a lesser extent than cimetidine. Both H2-receptor antagonists may also reduce hepatic blood flow. Several drugs which are known to interact with cimetidine have been found not to interact significantly with ranitidine, including propranolol, lignocaine, phenytoin and diazepam. However, significant pharmacokinetic interactions between ranitidine and several other drugs have been established. These interactions may be attributed variously to an effect of ranitidine on hepatic metabolism or to an effect on the absorption of concomitantly administered drugs. For example, the bioavailability of midazolam is significantly increased due to the influence of ranitidine on gastric pH and thus on absorption of midazolam, leading to an increased soporific effect of this benzodiazepine; an effect of ranitidine on oxidative liver metabolism also appears to be a contributory factor in this interaction. Conversely, ranitidine distinctly reduced protein-bound cobalamin absorption from a mean of 7.66% prior to ranitidine administration to 0.84% during treatment with ranitidine 300 mg daily. A significant pharmacokinetic interaction has also been demonstrated between ranitidine and procainamide: the AUC of procainamide increased and the renal clearance fell significantly from a mean of 378 to 309 ml/min with ranitidine co-administration. However, this interaction is due to a different mechanism. In this case, ranitidine appears to compete with procainamide for the common renal proximal tubular secretion site. The reported interactions of ranitidine with warfarin, metoprolol, nifedipine, theophylline and fentanyl appear to be due to inhibition of cytochrome P-450. In a clinical study, warfarin clearance was significantly reduced from 66.7 to 48.7 ml/min by ranitidine, and by cimetidine to 42.9 ml/min. Similarly, the elimination half-lives of metoprolol and nifedipine were distinctly prolonged and the AUCs significantly increased by ranitidine. However, the latter pharmacokinetic interactions appear unlikely to be of clinical significance since the clinical effects of metoprolol and nifedipine were unaffected by ranitidine treatment. In therapeutic concentrations, ranitidine inhibited the disappearance of fentanyl from an in vitro microsomal preparation, indicating that it inhibits microsomal drug metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMedDate not supplied

Drug disposition in obese humans. An update.

Drug disposition for many drugs has now been studied in obese individuals and some general conclusions can be drawn. Absorption of drugs evaluated to date is unchanged due to obesity. Apparent volume of distribution is greatly increased for some drugs including most benzodiazepines, thiopentone, phenytoin, verapamil and lignocaine (lidocaine). Modest increases in volume of distribution have been noted for methylxanthines, aminoglycosides, vancomycin, ibuprofen, prednisolone and heparin. Distribution of digoxin, cimetidine and procainamide is unchanged in obesity. The mechanism for the increased distribution of some drugs and unchanged distribution of others in obesity is unclear at present. It may be in part due to the lipophilic character of the drug molecule; however, other complex and as yet poorly understood factors contribute to the variability in drug distribution in obese patients. Protein binding of drugs bound to albumin is not dramatically changed in obesity. In contrast, some studies report that drugs bound to alpha 1-acid glycoprotein (AAG) may have increased binding that is related to increased serum AAG concentration; however, this is not a consistent finding. Oxidative drug biotransformation is minimally changed in obesity with the exceptions of ibuprofen and prednisolone, for which clearance increases as a highly correlated function of total bodyweight. Drug conjugation uniformly increases as a function of bodyweight in obesity, with paracetamol (acetaminophen), lorazepam and oxazepam having been studied. Drug acetylation may be unchanged in obesity, with only procainamide evaluated at this time. High clearance drugs, including lignocaine, verapamil and midazolam, have no change in clearance in obese individuals compared to normal bodyweight controls. Renal clearance of drugs is little changed for some drugs evaluated (digoxin, cimetidine), and increased for others (aminoglycosides, unmetabolised procainamide). Characterisation of appropriate animal models of obesity is underway to clarify the mechanisms for these in vivo pharmacokinetic observations in obese man. Two models, the Zucker obese and the obese cafeteria-fed male Sprague-Dawley rat, have provided preliminary physiological pharmacokinetic data with evaluations of theophylline, phenobarbitone and verapamil.(ABSTRACT TRUNCATED AT 400 WORDS)

Aminoglycosides↗
PubMed1976

[Experimental anti-arrhythmic effects of a new beta-adrenergic receptor blocking agent, dl-l-(tert. butylamino)-3-[(2-propinyloxy)phenoxy]2-propanol hydrochloride (dl Kö 1400-Cl)].

Antiarrhythmic property of a new adrenergic beta-blocking agent, dl-1-(tert.butylamino)-3[(2-propinyloxy) phenoxy]-2-propanol hydrochloride (Kö 1400-Cl) was studied, using 1) ouabain-induced arrhythmia in the guinea pig, 2) aconitine-induced arrhythmia in the rat, 3) arrhythmia induced by two-step ligation of coronary artery (Harris's method) in the dog and 4) halothane-adrenaline arrhythmia in the dog and was compared with those of propranolol, oxprenolol, procainamide and ajmaline. Procainamide and ajmaline produced a marked protective effect against aconitine-induced ventricular extrasystole, but were not so effective against aconitine-induced ventricular fibrillation, while oxprenolol and, to a lesser degree, propranolol were effective against the latter type of aconitine arrhythmias. Kö 1400-Cl proved to be ineffective. All the compounds tested produced a marked protective action against ouabain-arrhythmia. Whereas procainamide was most effective in abolishing the ventricular arrhythmia due to coronary-ligation even on the first postoperative day, Kö 1400-Cl and propranolol were almost ineffective on the first day. Even on the second postoperative day, the antiarrhythmic effects of these two beta-blockers were not remarkable, effective only in 2/4 animals in the case of Kö 1400-Cl and in 2/3 animals in the case of propranolol. On the contrary, all the beta-blockers tested produced a protective action against halothane-adrenaline arrhythmia at much lower doses than against coronary ligation arrhythmia. The potency ratio of Kö 1400-Cl and propranolol was 3 : 1, which paralleled with beta-blocking activity of these compounds.

Aconitine↗
PubMed1988

The role of newer antiarrhythmic drugs in the management of patients with ventricular arrhythmias.

The purpose of this review is to discuss the role of mexiletine, tocainide, flecainide, and amiodarone in the treatment of patients with symptomatic ventricular ectopy or sustained ventricular tachycardia (VT) and fibrillation (VF). The pharmacologic properties, electrophysiologic effects, clinical efficacy, adverse reactions, and costs of these new agents are compared with those of procainamide, quinidine, and disopyramide. With the exception of more convenient dosing intervals, these new agents do not afford novel or advantageous pharmacologic properties. The incidences and severity of adverse reactions are similar to those reported with conventional antiarrhythmic drugs. Results of clinical studies demonstrate that these newer drugs are comparable to procainamide, quinidine, and disopyramide in suppressing ventricular ectopy. Accordingly, the choice of an antiarrhythmic agent for patients with symptomatic ventricular ectopy can be based on the side-effect profile. The propensity for developing certain adverse effects can be defined if patients are subgrouped by age and left ventricular function. The adverse effects of amiodarone preclude its use in patients manifesting only ventricular ectopy. Treatment of patients with sustained VT/VF is more complex. Mexiletine and tocainide are generally not effective. The efficacy of flecainide is similar to that of procainamide, quinidine, and disopyramide. The negative inotropic effects of flecainide and disopyramide preclude their use in patients with severe ventricular dysfunction. Amiodarone is the most effective of these drugs for preventing recurrences of sustained VT/VF. Its use should, however, be restricted to patients refractory or intolerant to other antiarrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1982

A unique pharmacogenetic expression of the N-acetylation polymorphism in the inbred hamster.

Liver N-acetyltransferase (NAT) preparations (105,000 x g cytosol) were obtained from both sexes of 26 strains of inbred hamsters. Liver NAT activity levels were determined for six arylamine substrates; isoniazid, p-aminobenzoic acid (PABA), p-aminosalicylic acid (PAS), sulfamethazine (SMZ), procainamide and 2-aminofluorene. The N-acetylation of isoniazid, SMZ, procainamide and 2-aminofluorene exhibited a monomorphic expression in the hamster as the genetic variation in NAT activity levels between hamster strains was only about 2-fold for each substrate. In contrast, the N-acetylation of PABA and PAS showed a polymorphic expression in the hamster. Two inbred hamster lines (Bio 1.5 and Bio 82.73) had over 400-fold lower PABA NAT and over 20-fold lower PAS NAT activity levels than did the other inbred strains. In addition, the genetically determined N-acetylation differences between the rapid and slow acetylator hamster strains were also demonstrated in vivo for PABA but not for SMZ. Comparison of Michaelis-Menten kinetic constants of PABA NAT activity in a rapid and slow acetylator strain showed a 20-fold lower Km in the rapid acetylator strain suggesting an intrinsic structural difference in rapid and slow acetylator hamster liver NAT. Thus, the pharmacogenetic expression of the N-acetylation polymorphism is quite unique in the inbred hamster, in that PABA and PAS are genetically polymorphic substrates, whereas isoniazid, SMZ, procainamide and 2-aminofluorene are monomorphic, in direct contrast to man and rabbit.

Acetylation↗
PubMedDate not supplied

Influence of selected antiarrhythmic drugs on the hemodynamic parameters in rabbits during anesthesia. Part III. Ketamine anesthesia.

The influence of procainamide, N-acetylprocainamide, verapamil or propranolol on hemodynamic parameters in rabbits was studied during ketamine anesthesia. Using radioisotopic methods the following parameters were estimated: cardiac output, stroke volume, total peripheral resistance, renal and hepatic blood flows, arterial pressure and heart rate. During ketamine anesthesia the inhibitory effect of verapamil on peripheral resistance was intensified; after administration of the rest of antiarrhythmic drugs the decrease of peripheral resistance was not observed in the animals without general anesthesia. During ketamine anesthesia the negative chronotropic effect of N-acetylprocainamide was decreased, but the negative chronotropic effect of procainamide was intensified. Procainamide administration during ketamine anesthesia markedly decreased renal blood flow. Propranolol given without anesthetic, as well as given together with ketamine markedly decreased hepatic blood flow.

Anesthesia↗
PubMed1997

Mechanisms of the atrium-specific positive inotropic activities of quinidine- and atropine-like agents in rats.

This study investigated the mechanism of the positive inotropic effects of class 1 antiarrhythmic agents using electrically stimulated right atria (sinoatrial node excised), left atria and right ventricles of rats. Quinidine, disopyramide and procainamide produced concentration-dependent positive inotropic effects on right and left atria; effects on the right atria were greater than on left atria. At concentration producing positive inotropic effects on atria, the contractions of right ventricles were slightly increased by quinidine, unaffected by disopyramide and decreased by procainamide. The positive inotropic effects of quinidine were inhibited by propranolol, reserpine and mecamylamine but not by cocaine, hexamethonium and d-tubocurarine; propranolol also antagonized the positive inotropic effects of disopyramide and procainamide. Bupivacaine, which like quinidine blocks transient outward potassium current, slightly increased the contractions of right atria but not of left atria and ventricles. The atrium-specific positive inotropic effects of quinidine were mimicked by atropine, pirenzepine and dimethylphenylpiperazinium but not by nicotine, cytisine and butyrylcholine; the effects of atropine, dimethylphenylpiperazinium and pirenzepine were also blocked by propranolol. Quinidine increased the release of norepinephrine from atria but not from the ventricles; this release was greater from the right than from the left atria. It is concluded that quinidine- and atropine-like agents exert atrium-specific positive inotropic effects by blocking muscarinic receptors and permitting a dominance of acetylcholine effects via a release of norepinephrine from sympathetic nerve terminals.

Animals↗
PubMed1993

An estimate of the rate of direct drug diffusion from the surface of heart and kidney--implications for their representation as compartments.

In many regional pharmacokinetic experiments and models, the anatomical boundaries of the heart and kidney are intrinsically assumed to be barriers for drug diffusion such that these organs can be represented as one or more compartments. To test this, an experimental preparation was developed in which the heart and kidney of anaesthetized sheep were surrounded with 0.9% saline. The rate of drug diffusion from the surface of the organs into the saline was examined during constant-rate i.v. drug infusions. It was found that the maximum clearances of lidocaine and procainamide into the pericardial saline were 10.3-11.6 and 0.6-2.1 ml min-1 respectively, and the values for the kidney were 0.3-0.6, 0.1-1.0 and 0.4-1.3 ml min-1, for lidocaine, procainamide, and meperidine respectively. These corresponded to calculated times of 4-481 min to reach the steady-state saline concentration depending on the drug and the organ. The steady-state ratio of the saline concentrations over the arterial blood drug concentrations usually ranged from 0.5-1.0. It is concluded that drugs can rapidly enter regions of low or no perfusion surrounding these organs, and that the concept of treating the heart and kidney as compartments may not be valid in certain 'worst-case' situations.

Animals↗
PubMedDate not supplied

Comparison of standard chromatographic procedures for the optimal purification of soluble human brain acetylcholinesterase.

With the view of purifying soluble human brain acetylcholinesterase (AChE) into its separate isoforms, various preparative chromatographic procedures were compared. Chromatofocusing of cerebrospinal fluid (CSF) AChE revealed two major activity peaks, whilst that of caudate nucleus AChE showed one major peak. Both CSF and caudate nucleus AChE eluted at isoelectric points (pI) of between 5.5 and 5.2. Chromatofocusing failed to separate AChE into its individual isoforms, based on qualitative isoelectric focusing. Preparative purification by affinity chromatography showed a better AChE yield with the use of procainamide as a ligand, vis-à-vis acridinium. Maximum recovery for CSF and caudate nucleus AChE was 10 and 43% using acridinium and procainamide, respectively. Qualitative analysis by SDS-PAGE of affinity-purified AChE revealed four major bands between 50 and 62 kDa, corresponding to the catalytic subunits of AChE as verified by an anti-AChE polyclonal antibody. A size-exclusion column also allowed brain AChE purification, with the latter eluting at a putative molecular mass of 310 kDa. Unfortunately, cation-exchange using the state-of-the-art SMART system failed to separate AChE into its isoforms. AChE aggregation is given as one major obstacle precluding good resolution of isoforms.

Acetylcholinesterase↗
PubMed2003

Effect of losartan microinjections into the NTS on the cardiovascular components of chemically evoked reflexes in a rabbit model of acute heart ischemia.

In the acute phase of myocardial infarction (MI) there are modifications of the autonomic outflow with an increase in the sympathetic tone and changes in cardiovascular reflexes. Activation of angiotensin AT1 receptors in the nucleus tractus solitarii (NTS) inhibits the baroreceptor and enhances the carotid chemoreflex. In this study, we investigated the role of NTS-AT1 receptors on the cardiovascular reflex responses evoked on stimulation of carotid chemoreflex and cardiac chemosensitive fibres in the acute phase of MI. We also test the hypothesis that changes in cardiovascular responses to activation of carotid chemo and cardiac chemosensitive reflexes are secondary to changes in haemodynamic conditions due to infarction or to the activation of nociceptors of the heart. Rabbits were anaesthetised, paralysed and artificially ventilated. Carotid chemoreceptors and cardiac chemosensitive fibres were stimulated with lobeline and ATP, respectively. Arterial blood pressure, electrocardiogram and heart rate were monitored. A craniotomy was made to expose the caudal portions of the medulla and a multibarreled glass microelectrode was inserted in order to allow the identification of NTS and the microinjection of losartan (an angiotensin AT1 receptor antagonist). The heart was exposed by a midline thoracotomy and cardiac ischemia was produced by ligating the left descending coronary artery. The carotid chemoreflex and cardiac chemosensitive reflexes were evoked before and following the coronary ligation. The effect of losartan injection into the NTS on these reflexes was also assessed. In control experiments reflexes were assessed before and after the administration of capsaicin and procainamide. Results show that the activation of carotid chemoreflex elicited a greater increase of blood pressure and bradycardia after MI and that this was partially reversed by losartan microinjection after MI. Also the stimulation of cardiac chemosensitive fibres evoked a larger decrease on blood pressure and heart rate after MI and these were also partially reversed by losartan. The same enhancement of cardiovascular carotid chemo and cardiac chemosensitive receptors was observed after administration of capsaicin on the ventricular surface but not after procainamide. In conclusion, this study strongly suggests that, at NTS level, angiotensin AT1 receptors are involved in the modifications of autonomic outflow observed in the acute phase of MI.

Acute Disease↗
PubMed1982

Electrophysiologic drug testing in prophylaxis of sporadic paroxysmal atrial fibrillation: technique, application, and efficacy in severely symptomatic preexcitation patients.

Electrophysiologic drug testing was performed in nine patients with severely symptomatic sporadic (2 to 13 [mean 4.2] attacks/24 months) paroxysmal atrial fibrillation (PAF). All patients had control inductions of sustained (greater than 30 seconds) AF by high right atrial stimulation, and attempted inductions following serial administration of drugs. Drugs tested were intravenous procainamide (1.0 to 1.5 gm) (five patients), intravenous propranolol (0.1 mg/kg) (three patients), oral quinidine (1.6 to 2.4 gm/day) six patients), oral disopyramide (1.2 to 1.6 gm/day) (four patients), and oral aprindine (100 to 250 mg/day) (four patients). In all patients, one or more drugs prevented induction of sustained AF: procainamide (one patient), quinidine (five patients), disopyramide (four patients), and aprindine (four patients). All patients were treated with drugs which prevented induction of sustained AF and followed for 8 to 40 (mean 24) months. Seven patients tolerated their drugs: six had no AF and one had several short nonsustained attacks. Two patients did not tolerate their drugs: one had paroxysmal palpitation (on decreased aprindine dosage), and one had AF (while off of aprindine). In conclusion, electrophysiologic drug testing is feasible in patients with sporadic PAF. Inability to induce sustained AF following drug administration suggests successful prophylaxis of spontaneous PAF with the same drug.

Administration, Oral↗
PubMed1983

Electrophysiologic properties and antiarrhythmic mechanisms of intravenous N-acetylprocainamide in patients with ventricular dysrhythmias.

To define electrophysiologic properties and antiarrhythmic mechanisms of N-acetylprocainamide (NAPA), we studied 16 patients with symptomatic ventricular dysrhythmias. Electrophysiologic studies were performed before and after intravenous infusion of NAPA at 20 mg/kg over 20 minutes, achieving plasma concentrations of 24 +/- 3.2 to 35.5 +/- 4.5 micrograms/ml. NAPA did not significantly change sinus cycle length or atrioventricular (AV) conduction times (PA, AH, HV, and QRS), but it lengthened the QTc interval (p less than 0.001) during sinus rhythm. Programmed atrial stimulation revealed that NAPA had no discernible effects on AV nodal conduction; however, it exerted depressive effects on the His-Purkinje system in 9 of 16 patients. In 7 of 16 patients who manifested frequent ventricular premature beats (VPBs), NAPA abolished VPBs in only three of them; NAPA induced progressive prolongation of the premature coupling interval before complete abolition of VPBs. In 8 of 16 patients who had inducible repetitive ventricular response (RVR) because of reentry within the His-Purkinje system, NAPA narrowed or abolished the RVR zone in 3 patients and slowed the RVR rate with widening of the RVR zone in the remaining 5 patients. In 2 of 16 patients with slow ventricular tachycardia (VT), NAPA had no antiarrhythmic effects. By contrast, in the other 2 of 16 patients in whom sustained VT could be reproducibly elicited with programmed ventricular stimulation, NAPA slowed the rate of VT and suppressed VT inducibility. We conclude that electrophysiologic properties of NAPA are slightly different from those of procainamide and that NAPA is not uniformly effective for suppressing ventricular dysrhythmias, but its antiarrhythmic mechanisms are similar to those of procainamide.

Acecainide↗
PubMed1984

Evaluation of noninvasive tests for identifying patients with preexcitation syndrome at risk of rapid ventricular response.

Intermittent preexcitation, block in the accessory pathway after intravenous injection of ajmaline or procainamide, and block in the accessory pathway during exercise usually exclude a short antegrade refractory period of an accessory pathway in patients with the Wolff-Parkinson-White syndrome. This report describes three patients with these findings suggestive of a relatively long antegrade effective refractory period of the accessory pathway in whom life-threatening ventricular response occurred during atrial fibrillation. In the first patient with a pattern of intermittent preexcitation, rapid ventricular response with wide QRS was present during atrial fibrillation. In the second patient in whom preexcitation disappeared after intravenous injection of ajmaline or procainamide as well as during exercise testing, atrial pacing showed 1:1 conduction over the accessory pathway at a cycle length of 220 msec and the shortest R-R interval during induced atrial fibrillation was 190 msec. The third patient, with no evidence of preexcitation during sinus rhythm, presented antidromic reciprocating tachycardia and atrial fibrillation with life-threatening ventricular response, the minimal R-R interval being 220 msec. Noninvasive tests in the preexcitation syndrome lack sufficient prognostic sensitivity. The evaluation of ventricular response during induced atrial fibrillation represents the most reliable means of identifying such patients at risk.

Adult↗
PubMed1986

Antiarrhythmic efficacy of ethmozine in patients with ventricular tachycardia as determined by programmed electrical stimulation.

The antiarrhythmic properties of ethmozine were studied in 27 patients with a history of a cardiac arrest or symptomatic ventricular tachycardia. Programmed electrical stimulation studies were performed in 20 men and seven women with a mean age of 62 years and a mean left ventricular ejection fraction of 43%. All patients had inducible ventricular tachycardia by programmed electrical stimulation while off all antiarrhythmic therapy. Patients were then tested on procainamide if their treatment with this drug orally had not previously failed. Procainamide, 1000 and 1500 mg, was administered intravenously, and ventricular tachycardia could be provoked in 14 of 18 patients. Ethmozine was given in an oral loading regimen starting 24 to 36 hours later. After 500 mg oral ethmozine, patients were given 15 mg/kg ethmozine every 8 hours for seven to nine doses prior to drug testing. Ethmozine did not significantly change the baseline heart rate, blood pressure, and QTc interval from the initial drug-free values. The PR and QRS intervals were significantly prolonged. Seven patients were protected on oral ethmozine; 14 patients still had ventricular tachycardia inducible at programmed electrical stimulation testing, and six patients developed ventricular tachycardia spontaneously on ethmozine and were not tested in the programmed electrical stimulation laboratory. One patient had gastrointestinal complaints and was not discharged on the drug. The five patients who tolerated the oral protocol without side effects and who were protected against programmed stimulation induction of ventricular tachycardia were discharged on oral therapy. One patient on long-term therapy appeared to develop an allergic reaction to the agent with unexplained fevers and was switched to amiodarone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Electrophysiologic and clinical factors influencing response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia.

Clinical and electrophysiologic data from 51 consecutive patients with sustained monomorphic ventricular tachycardia inducible during programmed ventricular stimulation were evaluated to determine what variables predict the response to intravenous class IA antiarrhythmic agents. All patients received acute drug testing in the electrophysiologic laboratory with either intravenous procainamide or intravenous quinidine. Ventricular tachycardia suppression was achieved in 9 out of 51 patients (18%). The age, gender, left ventricular ejection fraction, baseline right ventricular effective refractory period, baseline HV interval, and baseline ventricular tachycardia cycle length were not predictive of ventricular tachycardia suppression with intravenous procainamide or quinidine during programmed ventricular stimulation. The degree of prolongation of the right ventricular effective refractory period after drug administration did not predict success or failure to suppress inducible ventricular tachycardia. The degree of prolongation of the HV interval was also not predictive. In addition, the degree of prolongation of the right ventricular effective refractory period or the HV interval did not predict the change in the ventricular tachycardia cycle length after drug administration in patients who remained inducible. These data indicate that the response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia cannot be predicted on the basis of various clinical and electrophysiologic parameters.

Arrhythmias, Cardiac↗
PubMed1988

Prolongation of the conduction time of early premature beats: a marker of ventricular action potential duration.

The conduction time of premature ventricular complexes, which are generally quite constant throughout late diastole, abruptly prolongs during repolarization as the refractory period of the ventricle is approached (conduction time breakpoint). The relationship between the conduction time breakpoint and the recovery properties of the ventricle was examined by relating the conduction time of premature ventricular complexes to the effective refractory period and the monophasic action potential derived from the ventricular suction electrode signal. In five anesthetized dogs during ventricular drive (cathode; 2.5 Hz; three times diastolic threshold), effective refractory period and conduction times of premature ventricular complexes were derived from computerized strength-interval curves. The recovery properties of the ventricle were altered by infusion of norepinephrine, calcium, and quinidine and by cooling (29 degrees to 34 degrees C). In these circumstances, the moment of conduction time breakpoint changes correlated well (r = 0.93) with the end of the negative slope of the ventricular suction electrode signal, which suggests that the conduction time breakpoint may be an indirect marker of the ventricular action potential duration. In seven additional dogs the interval between the effective refractory period and the conduction time breakpoint, which defines the relative refractory period, was increased by 5 to 8 minutes of ischemia (coincident with height of ventricular vulnerability) and was reversed by procainamide. Procainamide is known to diminish spontaneous and induced ventricular arrhythmias by reducing the disparity between the effective refractory period and the action potential duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Prolongation of ventricular refractoriness by class Ia antiarrhythmic drugs in the prevention of ventricular tachycardia induction.

The effects of class la antiarrhythmic drugs (procainamide, quinidine) on the right ventricular effective refractory period (VERP) and intraventricular conduction time were assessed during serial invasive electrophysiologic studies for sustained monomorphic ventricular tachycardia (VT). In 47 patients with remote myocardial infarction, sustained VT was inducible by up to two extrastimuli after the basic drive at one of two basic cycle lengths at the right ventricular apex. With oral drug administration, sustained VT was no longer inducible (group I) in 27 patients but remained inducible (group II) in 20 with the same protocol. Class la drugs prolonged the VERP in both groups, but there was greater lengthening when drugs were effective (e.g., +32 +/- 14 msec in group I vs +12 +/- 19 msec in group II; p less than 0.005, basic cycle length 600 to 700 msec). Prolongation of the VERP by greater than 30 msec had an 88% positive predictive value for prevention of sustained VT induction. In all except one patient in group I, drugs prolonged the VERP such that the coupling intervals that had resulted in sustained VT induction under control conditions were no longer attainable. In contrast, conduction time through the ventricle (surface QRS duration) in sinus rhythm and during right ventricular pacing was prolonged similarly regardless of efficacy (e.g., +33 +/- 21 msec vs +27 +/- 27 msec at a cycle length of 400 msec). The presence of similar plasma levels of drug did not imply equivalent prolongation of the VERP in the two groups. These results suggest that greater prolongation of the VERP by oral procainamide or quinidine correlates with drug efficacy against VT induction and is a better predictor of drug effect than achievement of a "therapeutic plasma level."

Adult↗
PubMed1995

Conversion of atrial flutter in pediatric patients by transesophageal atrial pacing: a safe, effective, minimally invasive procedure.

Atrial reentry tachycardia, often termed atrial flutter, is an arrhythmia that is uncommon in the general pediatric population but is seen frequently in patients with congenital heart disease. One goal in treating the arrhythmia is to terminate it, returning the atrium to its underlying rhythm. This report describes the use of transesophageal atrial pacing to attempt termination of atrial reentry in 102 pediatric patients (158 episodes). The patients ranged in age from 1 hour to 41.5 years. Conversion was successful for 112 (71%) of 158 episodes. Six of the 112 episodes required an infusion of procainamide after initial attempts at pacing led to atrial fibrillation. There were no significant differences between the ages of patients or the duration of the tachycardia in comparing successful versus unsuccessful conversions. In contrast, the atrial cycle lengths for the successfully converted tachycardias were significantly greater than for unsuccessful attempts. Transesophageal atrial pacing is a safe and effective means of terminating atrial flutter in the pediatric population. It is minimally invasive, it can often be performed in an outpatient setting, and the technique may occasionally be facilitated by infusion of intravenous procainamide.

Adolescent↗