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PubMed2001

Evidence for the possible involvement of Ca2+ entry blockade in the relaxation by class I antiarrhythmic drugs in the isolated pig coronary smooth muscle.

Effects of several Na+ channel blockers (i.e., class I antiarrhythmic agents), procainamide, quinidine, lidocaine, mexiletine, propafenone, were investigated in the isolated endothelium-denuded pig coronary artery focusing on the possible involvement of the blockade of Ca2+ channels and/or opening of K+ channels in the relaxant responses. All drugs except procainamide induced a concentration-dependent full relaxation of the coronary artery precontracted with high-KCl (30 mM, 80 mM). Inhibitions by procainamide of both high-KCl-induced contractions were less than 50% even at a concentration of 3 x 10(-2) M. Both high-KCl contractions were diminished by an L-type Ca2+ channel blocker, diltiazem, in a concentration-dependent manner. In contrast, cromakalim failed to inhibit 80 mM KCl-induced contraction. Tetrodotoxin (3 x 10(-5) M) did not affect the relaxant actions of the tested class I antiarrhythmic agents in high-KCl (80 mM)- or prostaglandin F2alpha-contracted muscle. The inhibitions by these class I antiarrhythmic agents of high-KCl-induced contraction were significantly attenuated when extracellular CaCl2 was increased from 2 mM to 20 mM. Furthermore, procainamide, quinidine, lidocaine, mexiletine as well as diltiazem decreased both cytoplasmic Ca2+ level ([Ca2+](cyt)) and muscle tension elevated by high-KCl in fura-2-loaded coronary preparations. These findings suggest that blockade of voltage-gated Ca2+ channels is involved in the relaxing action of these class I antiarrhythmic drugs in pig coronary artery. Blockade of Na+ channel and/or opening of K+ channels does not seem to play the principal role in the mechanism by which these antiarrhythmic drugs relax coronary artery.

Animals↗
PubMed1992

Effects of quinidine on vascular resistance and sympathetic nerve activity in humans.

OBJECTIVES: The purpose of the present study was to test the hypothesis that intravenous quinidine, unlike procainamide, causes direct vasodilation and reflexly mediated increases in sympathetic nerve activity. BACKGROUND: Intravenous quinidine can cause significant hypotension. Animal experiments have suggested that quinidine blocks alpha-receptors and also relaxes vascular smooth muscle by a nonadrenergic mechanism. In a recent study we showed that intravenous procainamide causes peripheral vasodilation, hypotension and inhibition of sympathetic nerve activity in humans. Intraarterial procainamide, however, did not cause vasodilation. METHODS: Postganglionic muscle sympathetic nerve traffic was recorded from the peroneal nerve at the fibular head with tungsten microelectrodes, and forearm blood flow was measured with venous occlusion plethysmography. Central venous pressure was measured directly. The direct effects of quinidine on vascular resistance were determined with brachial artery quinidine infusions and measurement of ipsilateral forearm blood flow. RESULTS: In eight normal subjects intravenous quinidine (8 mg/kg body weight infused for 27 min) decreased mean arterial pressure from 87 +/- 3 (mean +/- SE) to 83 +/- 3 mm Hg, central venous pressure from 6.3 +/- 0.6 to 5.0 +/- 0.7 mm Hg and forearm vascular resistance from 32.2 +/- 5.5 to 25.3 +/- 4.7 U (all p < 0.05). Heart rate increased from 67 +/- 4 to 77 +/- 5 beats/min and muscle sympathetic nerve activity from 288 +/- 70 to 660 +/- 151 U/min (both p < 0.05). In five subjects intravenous nitroprusside that caused similar hemodynamic effects produced similar increases in sympathetic nerve activity. In eight subjects graded infusions of quinidine into the brachial artery (0.37, 0.74 and 1.48 mg/min) produced dose-dependent decreases in ipsilateral forearm vascular resistance and marked attenuation of forearm vasoconstriction caused by the cold pressor test. CONCLUSIONS: These data show that quinidine, unlike procainamide, causes vasodilation directly and, when given intravenously, is associated with baroreflex-mediated increases in sympathetic nerve activity.

Adult↗
PubMed1994

The electrophysiological effects of dicentrine on the conduction system of rabbit heart.

1. The electrophysiological effects of dicentrine, an aporphine alkaloid isolated from the root of Lindera megaphylla, were examined in the Langendorff perfused rabbit heart and rabbit isolated cardiac cells. 2. Standard electrophysiological characters were measured in the Langendorff perfused rabbit heart (control study) and after 5 min exposure to 1, 3 and 9 microM of dicentrine and during the subsequent recovery phase sequentially (n = 7). The same study protocols were performed in 0.5 to 4.5 microM quinidine (n = 7), 18 to 162 microM procainamide and N-acetylprocainamide (n = 7) for comparison. 3. The results showed that the spontaneously beating heart rate and the sinoatrial (SA) and atrioventricular nodal (AH) conduction time were not significantly affected by dicentrine but were significantly suppressed by the higher doses of quinidine (4.5 microM) and procainamide (162 microM). 4. The His-Purkinje conduction time was significantly increased by the higher dose of dicentrine, quinidine and procainamide. 5. The ventricular repolarization time and its effective refractory period were significantly increased by the higher dose of dicentrine and the other agents. 6. The effective refractory period of the atrium, AV node and His-Purkinje system were also significantly increased by dicentrine and the other agents. 7. A voltage clamp study revealed that the prolongation of atrial action potential duration by dicentrine (9 microM) was associated with a significant inhibition of the transient potassium outward current. As well as inhibition of the transient outward current, a significant inhibition of the sodium inward current by dicentrine was found. 8.We conclude that (1) dicentrine is potentially a useful antiarrhythmic agent with type Ia and type III antiarrhythmic action; (2) the relative potency of dicentrine on the electrophysiological function of cardiac tissue is 10-20 times more than that of procainamide.

Action Potentials↗
PubMed1993

Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs.

OBJECTIVE: To test the hypothesis that female prevalence is greater than expected among reported cases of torsades de pointes associated with cardiovascular drugs that prolong cardiac repolarization. DATA SOURCES: A MEDLINE search of the English-language literature for the period of 1980 through 1992, using the terms torsade de pointes, polymorphic ventricular tachycardia, atypical ventricular tachycardia, proarrhythmia, and drug-induced ventricular tachycardia, supplemented by pertinent references (dating back to 1964) from the reviewed articles and by personal communications with researchers involved in this field. STUDY SELECTION: Ninety-three articles were identified describing at least one case of polymorphic ventricular tachycardia (with gender specified) associated with quinidine, procainamide hydrochloride, disopyramide, amiodarone, sotalol hydrochloride, bepridil hydrochloride, or prenylamine. A total of 332 patients were included in the analysis following application of prospectively defined criteria (eg, corrected QT [QTc] interval of 0.45 second or greater while receiving drug). DATA EXTRACTION: Clinical and electrocardiographic descriptors were extracted for analysis. Expected female prevalence for torsades de pointes associated with quinidine, procainamide, disopyramide, and aminodarone was conservatively estimated from gender-specific data reported for antiarrhythmic drug prescriptions in 1986, as derived from the National Disease and Therapeutic Index, a large pharmaceutical database; expected female prevalence for torsades de pointes associated with sotalol, bepridil, and prenylamine was assumed to be 50% or less since these agents are prescribed for male-predominant cardiovascular conditions. RESULTS: Women made up 70% (95% confidence interval, 64% to 75%) of the 332 reported cases of cardiovascular-drug-related torsades de pointes, and a female prevalence exceeding 50% was observed in 20 (83%) of 24 studies having at least four included cases. When analyzed according to various descriptors, women still constituted the majority (range, 51% to 94% of torsades de pointes cases), irrespective of the presence or absence of underlying coronary artery or rheumatic heart disease, left ventricular dysfunction, type of underlying arrhythmia, hypokalemia, hypomagnesemia, bradycardia, concomitant digoxin treatment, or level of QTc at baseline or while receiving drug. When cases of torsades de pointes were analyzed by individual drug, observed female prevalence was always greater than expected, representing a statistically significant difference (P < .05) for all agents except procainamide. CONCLUSIONS: These findings strongly suggest that women are more prone than men to develop torsades de pointes during administration of cardiovascular drugs that prolong cardiac repolarization. The pathophysiological basis for, and therapeutic implications of, this gender disparity should be further investigated.

Adolescent↗
PubMed1976

Antiarrhythmic efficacy of N-acetylprocainamide in patients with premature ventricular contractions.

Oral administration of a 1.5-gm dose of N-acetylprocainamide (NAPA) to 9 patients with premature ventricular contractions (PVCs) confirmed previous indirect evidence that this metabolite of procainamide has antiarrhythmic efficacy and potency comparable to those of procainamide. Although the mechanism by which NAPA acts as an antiarrhythmic drug is not known, it was found that the 6 patients with coupled PVCs responded to NAPA therapy and that the 3 patients without coupled PVCs failed to respond. Coupling interval prolongation also occurred during NAPA therapy in 4 of the 6 responding patients. These observations suggest that NAPA may terminate coupled PVCs by slowing and then interrupting conduction of re-entrant impulses, as has been proposed for procainamide. NAPA plasma concentrations of 7.4-17.2 mug/ml were well tolerated by the patients and produced an average fall of 3 mm Hg in mean arterial pressure and a 7.6% mean increase in corrected QT interval.

Aged↗
PubMed1977

Clinical consequences of polymorphic acetylation of basic drugs.

The clinical consequences (therapeutic and toxic) of drug acetylation polymorphism are reviewed for procainamide, hydralazine, phenelzine, isoniazid, and salicylazosulfapyridine. Genetic slow acetylators are more likely than rapid acetylators to experience the following adverse drug reactions: (1) earlier development of procainamide-induced antinuclear antibody; (2) earlier and more frequent development of procainamide-induced systemic lupus erythematosus (SLE); (3) hydralazine-induced SLE; (4) spontaneous SLE; (5) drowsiness and nausea from phenelzine; (6) cyanosis, hemolysis, and transient reticulocytosis from salicylazosulfapyridine; and (7) polyneuropathy after isoniazid therapy. The incidence of isoniazid hepatitis may, however, be more common in rapid than than in slow acetylators. Genetic slow acetylators are also more likely than rapid acetylators to experience greater therapeutic responses from similar doses of the following: phenelzine, hydralazine provided beta blockers are concurrently used, and isoniazid if once weekly therapy is used. Thus, knowledge of the acetylator phenotype of a patient can help determine the relative risk for some drug-related toxic and therapeutic responses.

Acetylation↗
PubMed1990

Cytotoxic interactions of cardioactive cationic amphiphilic compounds in primary rat hepatocytes in culture.

Hepatocytes from adult male Sprague-Dawley rats were isolated by the two-stage collagenase perfusion technique; 1 x 10(6) cells/plate were incubated in primary cell culture in Leibovitz's L-15 medium for 24 hr with or without various concentrations (12.5 to 400 mumol/L) of cardioactive cationic amphiphilic compounds such as propranolol, verapamil, sotalol, atenolol and procainamide. Propranolol and verapamil caused a significant release of lactate dehydrogenase (used as cytotoxic index in this study) in the culture media in a concentration-dependent manner, with LC50 values of 220 +/- 10 and 224 +/- 7 mumol/L, respectively. Atenolol, sotalol and procainamide had no effect on lactate dehydrogenase release. Electron microscopy of the hepatocytes showed that subtoxic concentrations of propranolol (12.5 to 125 mumol/L) and verapamil (12.5 to 100 mumol/L) induced multilamellar inclusion bodies after 24 hr of incubation. The two higher concentrations of propranolol (50 and 125 mumol/L) and 100 mumol/L of verapamil produced a significant decrease in the percentage of volume density of the mitochondria as quantitated by morphometrical analysis. An unusual feature of the electron microscopical changes with propranolol and verapamil was the presence of mitochondria within the multilamellar inclusion bodies. When these two drugs were used together or with subtoxic concentrations of amiodarone or desethylamiodarone, release of lactate dehydrogenase was significantly enhanced. No correlation was evident between the cytotoxic response and the volume density of cellular inclusions in hepatocytes treated with different concentrations of propranolol, verapamil, amiodarone or desethylamiodarone. Sotalol, atenolol and procainamide in concentrations up to 400 mumol/L did not produce any ultrastructural changes in hepatocytes after 24 hr of incubation. These results show that (a) cationic amphiphilic structure per se is not the only requirement for induction of multilamellar inclusions, (b) propranolol and verapamil can induce the formation of multilamellar inclusion bodies and cause a concentration-dependent release of lactate dehydrogenase from hepatocytes and (c) combination of different cationic amphiphiles in subtoxic concentrations can enhance cytotoxicity and increase the volume density of multilamellar inclusions.

Amiodarone↗
PubMed1998

Postoperative junctional ectopic tachycardia.

PURPOSE: To report the management of junctional ectopic tachycardia after cardiac surgery in an infant. Postoperatively, the patient suffered profound cardiac decompensation secondary to the accelerated rhythm and required extracorporeal membrane oxygenation (ECMO) for haemodynamic support. CLINICAL FEATURES: A 14-day-old, 3.5 kg boy exhibited junctional ectopic tachycardia after cardiopulmonary bypass. Left atrial pressure was 25-28 mmHg. No impact on the tachycardia was seen after rapid overdrive atrial pacing or after 20 micrograms fentanyl i.v., 45 micrograms digitalis, 100 mg magnesium or procainamide (loading dose 15 mg, then 30 mg.kg-1.min-1). Active cooling decreased the nasopharyngeal temperature to 35.2 degrees C, when the heart rate decreased below 180 bpm with a left atrial pressure of 8-10 mmHg. Dopamine (2 micrograms.kg-1.min-1) and dobutamine (5 micrograms.kg-1.min-1) were added to improve the cardiac output. Sodium nitroprusside (0.25 to 1 microgram.kg-1.min) maintained the systolic pressure < 100 mmHg. On arrival in ICU, heart rate increased to 200 bpm. The patient received cardiac massage for severe hypotension 75 min after surgery. Emergency ECMO was instituted for circulatory support. Procainamide, digoxin, dopamine, dobutamine, sodium nitroprusside and hypothermia were continued. Sinus rhythm resumed on the first postoperative day, but procainamide and induced hypothermia at 34 degrees C were maintained for 36 hr after normalization of the rhythm to prevent recurrence of the tachycardia. Total duration of ECMO was three and a half days. Recovery was uneventful. CONCLUSION: The use of ECMO, as a first line of defence, is suitable for the emergency support of patients with JET because of the ease of support of circulation and precise control of hypothermia.

Anesthetics, Intravenous↗
PubMed1985

Long-term lorcainide therapy in patients with ventricular tachycardia.

One hundred patients inducible at electrophysiologic studies underwent serial drug testing with procainamide, lidocaine, and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic drug. Lorcainide prevented ventricular tachycardia (VT) induction in 69% of the 100 patients studied, procainamide was effective in 50% of the 75 patients studied, and lidocaine prevented VT induction in 30% of 53 patients. Following PES and serial drug testing, 46 patients were started on lorcainide, nine patients on procainamide, and 45 patients were started on other antiarrhythmic drug regimens. Seventy percent of the patients have remained on lorcainide therapy, while 47% have continued on other drug therapies started over a 20.5 +/- 3.2-month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was tolerated well in this population and remained an effective antiarrhythmic with prolonged administration.

Benzeneacetamides↗
PubMed1985

Antiarrhythmic effects of cibenzoline.

Thirty-three patients with ventricular tachyarrhythmias were referred for evaluation of their arrhythmias using programmed electrical stimulation to guide antiarrhythmic therapy. Cibenzoline succinate, a new antiarrhythmic agent, was compared to procainamide in patients with ventricular tachycardia. Cibenzoline was given intravenously, initially 1.0 mg/kg, then in 1 mg/kg increments to a maximum of 3.0 mg/kg, during electrophysiologic testing. The results were compared to procainamide, which was also administered intravenously to 1000 and then to 1500 mg. Cibenzoline provided protection against ventricular tachycardia induction in 16 of 33 patients. The PR interval increased 13%, QRS duration widened 26%, and QTc interval was prolonged by 7%. There was a 9% fall in mean arterial blood pressure. Procainamide prevented ventricular tachycardia induction in 21 out of 31 patients tested. The PR interval increased 11%, QRS duration widened 27%, and QTc interval prolonged by 8%. Cibenzoline was given orally to 13 patients for chronic treatment. Chronic oral cibenzoline therapy after a mean follow-up of 8.8 months caused a reduction of ventricular ectopy from 666 to 190 beats/hr. Ventricular tachycardia events decreased per Holter monitor recording from 6 to 0.6. Cibenzoline therapy was discontinued in 5 of 13 patients due to break-through arrhythmias (nonsustained ventricular tachycardia on Holter monitor and recurrence of symptoms). Cibenzoline may be an effective antiarrhythmic agent in selected patients.

Adult↗
PubMed1986

Lorcainide therapy in a cardiac arrest population.

Thirty-eight patients with prior history of cardiac arrest underwent programmed electrical stimulation (PES) studies and serial drug testing. Lorcainide was tested acutely in all 38 patients and prevented ventricular tachycardia (VT) or ventricular fibrillation (VF) induction in 14 patients and failed in 24 (efficacy rate 37%). Procainamide had failed clinically (cardiac arrest or breakthrough VT) in 16 patients, seven patients had previously severe adverse side effects, and thus only 15 were tested on procainamide at PES testing with seven protected. Following initial studies, 14 patients were started on lorcainide oral therapy and 24 on other therapy determined effective at PES testing (N-acetylprocainamide-two, flecainide-nine, bethanidine-three, slow-release procainamide hydrochloride-three, quinidine-two, cibenzoline-one, amiodarone-four). After 29 +/- 7 months follow-up, three are alive on lorcainide therapy, five discontinued therapy due to side effects; six died--three sudden deaths (33%) and two cardiac deaths (both myocardial infarctions). Twenty out of 24 patients are alive who were started on PES predicted effective therapy other than lorcainide; four died--three sudden deaths (13%) and one cardiac nonsudden death. Antiarrhythmic therapy guided by PES studies gives overall encouraging results in a cardiac arrest group of patients. Lorcainide, however, is not tolerated well and affords less protection against a sudden death recurrence than is noted in a population on other antiarrhythmic therapy predicted effective at PES testing.

Arrhythmias, Cardiac↗
PubMed1982

Long-term intravenous infusion of antiarrhythmic drugs using a totally implanted drug delivery system.

In vitro and in vivo testing was performed to establish the feasibility of a totally implantable pump system to deliver antiarrhythmic agents. In vitro flow characteristics suggested predictable day to day delivery with acceptably small variations in flow with changes in reservoir volume or temperature. During 3 months of in vitro testing, procainamide and bretylium were found suitable for long-term delivery. Delivery of lidocaine was limited by high viscosity and corrosion of steel elements within the pump. The pump was implanted in a subcutaneous pocket in four dogs. Procainamide (0.5 g/ml), delivered at 4 ml/day (70 mg/kg body weight per day), provided a mean steady state drug concentration of 5.3 micrograms/ml. Bretylium (50 mg/ml), delivered at 8 ml/day (13 mg/kg per day), provided a steady state concentration of 0.8 micrograms/ml (range 0.4 to 1.4). Long-term intravenous administration of therapeutic doses of bretylium and procainamide with this delivery system has been demonstrated in dogs and appears to be feasible in human subjects.

Animals↗
PubMed1984

Evaluation of lorcainide in patients with symptomatic ventricular tachycardia.

One hundred patients with inducible ventricular tachycardia (VT) on electrophysiologic studies underwent serial drug testing with procainamide, lidocaine and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic agent. Lorcainide prevented VT induction in 69% of the 100 patients studied, procainamide in 50% of the 75 patients studied and lidocaine in 30% of 53 patients. After PES and serial drug testing, 46 patients were started on lorcainide, 9 on procainamide and 45 on other antiarrhythmic drug regimens. Eighty percent of the patients have remained on lorcainide therapy, whereas 47% have continued on other drug therapies started over 17.5-month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was well tolerated in this population and remained an effective antiarrhythmic agent with prolonged administration.

Anti-Arrhythmia Agents↗
PubMed1985

Electrophysiologic evaluation of the antiarrhythmic effects of N-acetylprocainamide for ventricular tachycardia secondary to coronary artery disease.

Antiarrhythmic properties of N-acetylprocainamide (NAPA), an active metabolite of procainamide, were studied in 12 patients with coronary artery disease who presented with cardiac arrest or documented sustained ventricular tachycardia (VT). Programmed electrical stimulation (PES) studies were performed in 10 men and 2 women, aged 52 to 80 years (mean 63), who had a left ventricular ejection fraction of 16 to 69% (mean 33). All patients tested had inducible VT provoked by PES without antiarrhythmic therapy. Patients were then tested with procainamide, 1,000 mg administered intravenously. VT could be provoked after procainamide treatment in 8 of 10 patients. Twenty-four to 36 hours later NAPA was administered, 18 mg/kg body weight intravenously, and PES was performed after 20 minutes. NAPA did not significantly change heart rate, mean arterial blood pressure, electrocardiographic intervals and AH or HV conduction times. The QT interval lengthened, but not significantly. The mean serum NAPA levels were 15.7 +/- 4 micrograms/ml in the group protected by NAPA and 16.2 +/- 4 micrograms/ml in the group not protected by NAPA. Five patients were discharged with NAPA therapy, 1.5 g orally every 8 hours. Two patients have been maintained with chronic NAPA therapy (10 +/- 3 months), and 2 patients had breakthrough VT on follow-up Holter monitoring and alternative therapy was given. One patient died while taking oral therapy. NAPA demonstrates antiarrhythmic efficacy in preventing induction of VT by PES in a high-risk group of patients. During chronic oral therapy in some patients, NAPA appears to be well tolerated, with antiarrhythmic efficacy that may be enhanced with further upward dose titration.

Acecainide↗
PubMed1989

Evaluation of antifibrillatory effects of drugs.

Several electrical stimulation techniques have been used to measure ventricular fibrillation (VF) threshold such as single pulse stimulation, train of pulses stimulation, continuous 50-Hz stimulation and sequential pulse stimulation. This study was undertaken to clarify the difference in VF threshold values obtained by each method. The development of VF was classified into 4 stages. Stage 1 is the phase in which fragmented activities are generated at the stimulated area of the ventricular muscle. In stage 2, the local activities propagate to surrounding ventricular muscle, causing ventricular excitation. Stage 3 is characterized by repetitive ventricular excitations. In state 4, repetitive ventricular responses in a form of accelerating tachycardia induce disorganized excitations that finally degenerate into fibrillation. Based on this classification of stages between local excitation and fibrillation, single pulse stimulation is considered to measure VF threshold for stages 1 to 4, continuous 50-Hz stimulation for stages 2 to 4 and sequential pulse stimulation for stages 3 and 4. Thus, the antifibrillatory effect of drugs can be interpreted with some significance by using different stimulation methods. The sequential pulse stimulation method revealed that some antiarrhythmic agents caused a dissociation between repetitive nonstimulated excitation (RE) threshold and VF threshold. Procainamide and disopyramide increased RE threshold while decreasing VF threshold. Mexiletine and lidocaine elevated both RE and VF thresholds. Local infusion of procainamide at the site of test stimulation reduced both thresholds. However, after the application of procainamide to the whole heart, RE threshold remained decreased but VF threshold was elevated. It is likely that the antifibrillatory effect of the drug includes 2 different processes: antireentrant and antimultiple reentrant effects.

Animals↗
PubMed1990

Effect of empiric antiarrhythmic therapy in resuscitated out-of-hospital cardiac arrest victims with coronary artery disease.

The effect of empiric antiarrhythmic therapy with quinidine and procainamide on long-term mortality was examined in 209 patients with coronary artery disease resuscitated after out-of-hospital cardiac arrest. The antiarrhythmic agent used was determined by the patient's private physician without knowledge of the study ambulatory electrocardiogram. Of the 209 patients, procainamide was prescribed in 45 (22%), quinidine in 48 (23%) and no antiarrhythmic therapy in 116 (55%). Digoxin therapy was initiated in 101 patients. The 2-year total survival rate for the quinidine, procainamide and nontreated patients was 61, 57 and 71% (p less than 0.05), and for sudden death was 69, 69 and 89% (p less than 0.01), respectively. These observations suggest that empiric antiarrhythmic therapy in survivors of out-of-hospital cardiac arrest did not affect total mortality and was associated with an increased frequency of sudden death.

Aged↗
PubMed1983

Aromatic amines and the pathogenesis of lupus erythematosus.

The acetylation pathway of drug metabolism is the pathway by which aromatic amines and hydrazines are metabolized. Hydralazine and procainamide are aromatic amines or hydrazines that are metabolized by this pathway. Persons who are genetically slow acetylators are predisposed to development of lupus from these two drugs, suggesting that the free amine or hydrazine moiety is the inciting agent. When acetylprocainamide was given as an antiarrhythmic drug to patients with procainamide-induced lupus, the disease went into remission, indicating that the free amine group on procainamide had induced the disease. The genetic acetylator phenotypes of persons with idiopathic lupus were studied, and an excess of genetic slow acetylators was observed. This suggests amines or hydrazines induce some cases of this disease. One patient was identified with a lupus-like illness due to occupational exposure to hydrazine itself.

Acecainide↗
PubMed1988

Direct treatment of fetal supraventricular tachycardia after failed transplacental therapy.

Digitalization by direct intramuscular injection of the fetus successfully controlled supraventricular tachycardia at 24 weeks' gestation after more traditional intensive trials of transplacental therapy with digoxin, verapamil, and procainamide, either separately or in combination, had failed. The fetal pharmacokinetics were calculated from fetal blood samples obtained by cordocentesis. No clear evidence of placental transfer of digoxin administered to the mother could be found despite a digoxin concentration in the mother that ranged from 1.8 to 2.6 ng/ml for 4 days. After direct fetal digitalization we calculated that the coefficient of elimination for digoxin from the fetus was 0.0463 h-1, and digoxin elimination half-life was 15.9 hours. The latter time span is substantially less than the 50-hour half-life previously reported in newborn infants with low birth weight. The fetal/maternal concentration ratio of procainamide was 0.914. However, maternal clearance of procainamide (9.7 ml/kg-1/min-1) was twice as long as the clearance reported for nonpregnant patients undergoing fast acetylation. We conclude first, that at least in the dose of this ill fetus, little digoxin administered to the mother crossed the placentae; and second, that while direct fetal therapy with digoxin is effective, the necessary frequent number of injections render this therapy impractical. Direct fetal digitalization should probably be reserved for the preterm fetus who has evidence of heart failure and has not responded to maternally administered therapy other than digoxin.

Adult↗