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PubMed1977

Metabolism of procainamide and p-aminobenzoic acid in patients with chronic liver disease.

Procainamide acetylation and hydrolysis, procainamide-derived p-amino-benzoic acid acetylation, and plasma hydrolysis of procaine were studied in normal volunteers and in 20 patients with chronic liver disease, Impairment of procainamide acetylation was evident in the patients, but no correlations were demonstrable between the degree of impairment and the severity of the disease. On the other hand, procainamide hydroylsis was diminished in liver disease, and as indicated by depression of serum albumin levels and plasma prothrombin activity this alteration did correlate with the degree of impairment of liver function. Procaine hydrolysis in plasma was also affected, the mean in vitro plasma half-life being prolonged in the patients with liver disease and correlating with the degree of hepatic impairment. A correlation of procainamide hydrolysis with procaine hydrolysis was also observed. Finally, acetylation of procainamide-derived p-aminobenzoic acid appeared to increase in patients with liver disease, the degree of acetylation increasing with decreasing procainamide hydrolysis capacity.

4-Aminobenzoic Acid↗
PubMed1978

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Aged↗
PubMed1989

Chronopharmacokinetic studies of pranoprofen and procainamide.

There is increasing evidence demonstrating that plasma drug concentrations are affected by their time of administration. In the current study, the chronopharmacokinetic profiles of an antipyretic agent, pranoprofen, and an antiarrhythmic agent, procainamide, were examined. In the first study, 75 mg of pranoprofen was given orally in seven healthy subjects at 10:00 (morning trial) or 22:00 (evening trial). In the second study, 500 mg of procainamide was given orally in eight subjects with premature ventricular contractions at 10:00 or 22:00. Blood samples for plasma drug concentrations were taken for a 10-hour (pranoprofen study) or a 24-hour (procainamide study) post-drug period. In the first (pranoprofen) study, the mean time to maximum concentration was significantly shorter, and the mean maximum plasma concentration as well as absorption rate constant had a tendency to be greater after the morning than after the evening trial. The mean area under the plasma concentration-time curve, elimination half-life or oral clearance of the morning and evening dosages did not differ. In the second (procainamide) study, no significant difference was observed in any pharmacokinetic parameter concerning procainamide or its active metabolite, N-acetyl-procainamide (NAPA) between the morning and evening trials. These data indicate that plasma levels of pranoprofen are affected by its administration time while plasma concentrations of procainamide and NAPA do not vary with the time of dosage.

Acecainide↗
PubMed1994

The effects of programmed ventricular stimulation on plasma procainamide levels: an experimental model.

To evaluate the effects of programmed ventricular stimulation on resultant plasma concentrations of intravenously administered procainamide, drug dosing was performed with and without ventricular stimulation on two separate days (48 hours apart) in 12 dogs (13 dosing trials) at > or = 14 days after myocardial infarction (mean: 62 days). During infarct surgery, three bipolar electrodes were plunged into left ventricular epicardium, externalized, and later used for ventricular stimulation. On the first study day, procainamide was dosed to achieve two sequential plateau plasma levels (I and II), with a 20-minute equilibrium period at each plateau before ventricular stimulation. Plasma procainamide concentrations were measured before initiation of ventricular stimulation and at the completion of ventricular stimulation for each sequential plateau level. Stimulation involved delivery of one, two, and three extrastimuli at three paced cycle lengths at three left ventricular sites before procainamide dosing and at each of the two procainamide plateau levels. Three dogs were excluded from analysis due to induction of lethal ventricular arrhythmias. No ventricular arrhythmias were induced in the remaining nine animals. On the second study day, procainamide was dosed identically, but no ventricular stimulation was performed. Intravenous drug administration and collection of plasma concentration samples were performed with +/- 1 minute on both study days. Mean plasma procainamide concentrations at the end of ventricular stimulation at dosage Levels I & II were 10% and 12% greater (P < 0.02 and P < 0.005, respectively) than plasma concentrations measured at comparable times on the study day when no ventricular stimulation was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of amiodarone on the disposition of procainamide in the rat.

We examined the effect of amiodarone on the disposition of procainamide in the rat to determine the mechanism of a reported interaction between amiodarone and procainamide and to determine the effect of amiodarone on drug acetylation. Animals received a 5-d pretreatment with amiodarone hydrochloride (100 mg/kg) or diluent prior to the intravenous administration of 50 mg/kg of procainamide hydrochloride. The plasma clearance, volume of distribution, and half-life of procainamide did not significantly differ between the two groups. The urinary recovery of N-acetylprocainamide was increased by 31% (p less than 0.01) in amiodarone pretreated animals. However, there was no change in the partial clearance of procainamide to N-acetylprocainamide. Neither the renal clearance of procainamide nor N-acetylprocainamide was altered by amiodarone pretreatment. These data suggest that amiodarone interacts with procainamide by reduction of an alternate pathway of elimination, possibly oxidative metabolism.

Administration, Oral↗
PubMed1976

Comparison of the acetylation of procainamide and sulfadimidine in man.

The acetylation of procainamide and sulfadimidine has been measured simultaneously in plasma and urine in 20 healthy human volunteers by a specific G.L.C. method, after single and multiple oral dral doses of procainamide retard tablets. A distinct bimodality (9 rapid and 11 slow acetylators) was apparent from the concentrations of procainamide and N-acetylprocainamide both in urine and plasma, which was in complete agreement with data about sulfadimidine acetylation. The influence of acetylator phenotype on the relative concentrations of procainamide and N-acetylprocainamide in plasma as cn 5 additional healthy subjects after a single oral dose of procainamide. The present results show that acetylator phenotype can now be determined using procainamide as the test substance, and for this purpose multiple doses offer hardly any advantage over a single dose of the drug. However, because the separation between rapid and slow acetylators is less pronounced for procainamide than for sulfadimidine, precise criteria must be established for the conditions of the test, and the influence of diseases, such as renal insufficiency, should be taken into consideration.

Acetylation↗
PubMed1989

A comparison of sotalol and procainamide in symptomatic ventricular tachycardia.

UNLABELLED: The effects of oral sotalol were compared with 1000 and 1500 mg of procainamide in 23 patients with sustained ventricular tachycardia. The predictive value of an induction study after procainamide was assessed. The mean age of the study group was 62 +/- 12 years, and the mean ejection fraction was 32 +/- 16%. The cycle length (CL) of the induced tachycardia, the coupling interval (CI) of the first extrastimulus (in ms), and the number of noninducible (NI) patients are given in the table below. (table; see text) One patient developed torsades during the loading period of sotalol and is included in the number requiring cardioversion (DC). Important proarrhythmic effects (spontaneous occurrence of tachycardia) were seen twice after procainamide. Induction suppression by procainamide predicted success with sotalol (p = 0.0013). CONCLUSION: Ventricular tachycardia seems to be less often inducible after oral sotalol than after procainamide. The success of procainamide during programmed electrical stimulation predicts the same for sotalol. If ventricular tachycardia remains inducible after oral sotalol, it is faster than after procainamide but slower than the baseline tachycardia. Both drugs slightly prolong refractoriness.

Aged↗
PubMedDate not supplied

Procainamide for rate control of postsurgical junctional tachycardia.

This study was conducted to determine the efficacy of procainamide therapy for rapid rate control of postoperative junctional tachycardia (JT). Postoperative JT is one of the most difficult forms of tachycardia to manage. Reported success with a variety of treatments of JT in infants and children has been inconsistent and limited. Rate control using procainamide was achieved in 17 children having rapid JT (heart rate >200 beats/min) between 1986 and 1997. In the first 5 patients (protocol A), following a loading dose of 3 mg/kg over 20 minutes, a continuous procainamide infusion was initiated at a rate of 20 microg/kg/min. The infusion dose was increased in 10 microg/kg steps every 30 minutes to 40-120 microg/kg/min until the heart rate decreased below the target rate of 180 beats/min. In the other 12 patients (protocol B), after a higher loading dose of 10 mg/kg the infusion rate was increased every 10-15 minutes until the heart rate decreased below the target rate of 180 beats/min. Procainamide decreased JT rates in all patients but the response was significantly faster in protocol B. In the patients treated with protocol A, pretreatment JT rates ranged from 203 to 240 (213+/-17) beats/min and decreased to 195+/-10 beats/min at 2 hours (p = ns), 186+/-8.8 at 4 hours (p<0.02), and 179+/-8 at 6 hour postinitiation of PA. In protocol B, pretreatment JT rates ranged from 201 to 240 (218+/-17) beats/min and decreased to 183+/-20 beats/min at 2 hours (p<0.001) and 171+/-12 at 4 hours after starting the procainamide therapy. The mean duration to decrease JT rates below the target rate of 180 beats/min was 3.2+/-1.1 hours in protocol B compared to 6.4+/-3.8 hours in protocol A (p<0.02). Eight of 12 patients in protocol B achieved rate control below the target rate of 180 beats/min within 4 hours despite remaining on significant inotropic support. The procainamide infusion rates to maintain heart rates below 180 beats/min were 40-120 (68.4+/-22.1) microg/kg/min. No proarrhythmia, bradycardia, or significant hypotension was observed. In this series procainamide provided safe, effective, and rapid rate control of JT occurring in the immediate postoperative period.

Analysis of Variance↗
PubMed1976

Electrophysiologic effects of procainamide in subtherapeutic to therapeutic doses on human atrioventricular conduction system.

The effects of single intravenous infusions of 50 to 400 mg of procainamide on the functional properties of the atrioventricular (A-V) conduction system were studied in 36 patients and correlated with plasma concentrations. A 50 mg dose of procainamide resulted in a plasma concentration of less than 1.0 mug/ml and produced no electrophysiologic changes. Doses of 100, 200, 300 and 400 mg resulted in progresively increasing plasma concentrations (1.2, 1.8, 3.5 and 4.2 mug/ml, respectively). The effects of procainamide on the sinus rate were variable and not dose-related. The effects of doses of up to 300 mg on A-V nodal conduction were variable and not dose-related. Only in a dose of 400 mg did procainamide prolong A-V nodal conduction in six of seven patients. Whereas 100 mg had no effect on His-Purkinje system conduction, doses of 200, 300 and 400 mg prolonged His-Purkinje system conduction time by 6, 8 and 9 msec, respectively. Dose-related increases in atrial refractoriness started with a dose of 200 mg and became statistically significant with doses of 300 and 400 mg. The effects of procainamide on A-V nodal functional refractoriness were variable and not dose-related, but in doses of 100 to 400 mg, procainamide produced significant and progressively dose-related increases in His-Purkinje system refractoriness. Suppression of some types of ventricular arrhythmia by small doses of this drug may be explained by changes in refractoriness of the His-Purkinje system produced by doses of procainamide as small as 100 mg.

Atrioventricular Node↗
PubMed1980

Efficacy, plasma concentrations and adverse effects of a new sustained release procainamide preparation.

To assess the efficacy, plasma drug concentrations and adverse effects of a new sustained release preparation of procainamide, 33 patients with heart disease were studied in an acute dose-ranging protocol and a chronic treatment protocol. Patients initially received a daily dose of 3 g of sustained release procainamide; this dose was increased by 1.5 g daily until ventricular premature depolarizations were suppressed by 75 percent or more, adverse drug effects occurred or a total daily dose of 7.5 g of sustained-release procainamide was reached. Twenty-five patients (76 percent) had at least a 75 percent reduction (range 75 to 100percent [mean +/- standard deviation 91 +/- 8.2]) in ventricular permature depolarization frequency at a dosage of 4.8 +/- 1.46 g/day (range 3.0 to 7.5). Despite the 8 hour dosing interval, the variation between maximal and minimal plasma procainamide and N-acetylprocainamide concentrations under steady state conditions was very small. Mean maximal procainamide and N-acetylprocainamide plasma concentrations were 10.4 +/- 6.02 and 12.0 +/- 7.40 micrograms/ml, respectively. The respective mean minimal concentrations were 6.8 +/- 4.50 and 8.7 +/- 5.99 micrograms/ml. In nine patients (27 percent) treatment with sustained release procainamide resulted in conversion of the antinuclear antibody test from negative to positive. Adverse drug effects occurred in 17 (52 percent) of the subjects. In general, adverse effects were minor and abated within 24 hours after administration of the drug was stopped. One patient had the procainamide-induced systemic lupus erythematosus-like syndrome.

Acecainide↗
PubMed1985

Rate-dependent effects of procainamide on His-Purkinje conduction in man.

Microelectrode studies in isolated cardiac tissues have shown that the depressant effect of several antiarrhythmic drugs on the maximal upstroke velocity of the cardiac action potential is rate-dependent. To determine whether this effect of antiarrhythmic drugs is seen in humans, 14 patients undergoing atrial pacing at several rates were prospectively studied before and after the infusion of procainamide (15 mg/kg). The HV interval (His-Purkinje conduction rate) and the QRS duration (intraventricular conduction rate) were measured. Before procainamide infusion, atrial pacing did not significantly prolong the maximal HV interval (from 54 +/- 15 to 58 +/- 13 ms). After procainamide infusion (mean serum level 10.0 +/- 3 micrograms/ml) atrial pacing at an average of 5 pacing rates significantly prolonged the HV interval (from 67 +/- 18 to 80 +/- 20 ms, p less than 0.001). The extent of HV prolongation with atrial pacing after procainamide infusion was independent of the HV interval at rest before procainamide. The duration of the QRS complex also tended to prolong with atrial pacing after procainamide infusion, but this prolongation was not statistically significant. Thus, procainamide produces a rate-dependent depressant effect on His-Purkinje and intraventricular conduction, confirming observations made in isolated tissue preparations.

Adult↗
PubMed1989

Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia.

Transient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval). The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9% (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = -0.08, p = NS). The effect of procainamide on the difference between correlated strongly with changes in the cycle length of ventricular tachycardia (r = 0.97, p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed2006

Study of feasibility of the treatment with procainamide hydrochloride and cisplatin in pregnant mice.

Cisplatin is one of the most widely utilized anticancer drugs; nevertheless its use is often hampered by the onset of serious side effects. In spite of its tight binding to DNA, great teratogenic effects do not characterize cisplatin, although its embryolethal and growth retardation activities are quite remarkable. On the basis of our previous observations, demonstrating the usefulness of procainamide hydrochloride for the protection against cisplatin toxic effects in adult mice and rats, we now analyze the feasibility of the combined treatment with cisplatin and the antiarrhythmic drug procainamide hydrochloride in pregnant mice and the possible protective action of procainamide against the embryotoxic activity of cisplatin. Our data, obtained in CD-1 dams after treatment with 8 or 12 mg/kg cisplatin ip, with or without 50 mg/kg procainamide hydrochloride iv, confirm the embryotoxic effects of cisplatin. We also demonstrate that procainamide may be administered with cisplatin without causing an increase in its embryotoxic effects, but slightly improving some embryotoxicity parameters in living embryos such as the fetal weight, the percentage of fetuses with skeletal anomalies, and the number of ossification centres. The mechanism of action of this partially protective activity seems to be linked in part to the lower cisplatin accumulation in fetal tissue, probably due to an interaction of drugs at the level of placenta, in part to the protection of procainamide against maternal toxicity of cisplatin. A relevant result of this research is the suggestion that procainamide hydrochloride might be administered in case of pregnancy to protect against the maternal toxic effects of cisplatin without an increased embryotoxic/teratogenic risk for the offspring.

Animals↗
PubMed1976

Facilitation of A-V nodal reciprocation by procainamide.

Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.

Animals↗
PubMed1976

Maintenance therapy with a new retard tablet preparation of procainamide.

The procainamide plasma concentration was followed during maintenance therapy with a new procainamide retard tablet preparation in 23 hospitalized patients suffering from acute or chronic coronary heart disease with complicating ventricular arrhythmias. After initial individually adjusted treatment with Pronestyl every third hour, either orally or intramuscularly, for at least eight dose intervals, the retard tablets were given at 6 hour intervals for 2 to 12 days, or more. In 19 patients with no major fluctuations in their circulatory or renal state, adequate and relatively stable plasma procainamide concentration was obtained upon a constant dose of the retard preparation. On an average, the difference from minimum to maximum concentration was 55 per cent within the 6 hour dose intervals. In four patients with unstable circulation and/or renal function, procainamide therapy had to be disrupted in two because of severe side effects and toxic concentrations, and the dose was adjusted in the remaining two. It is concluded that the formulation of procainamide tablet preparations has simplified procainamide therapy within and outside hospital and improved our possibilities to perform short-and long-term studies on the risk/ benefit ratio of procainamide treatment in patients with severe ventricular arrhythmias.

Adult↗
PubMed2002

Reduction of cisplatin hepatotoxicity by procainamide hydrochloride in rats.

In preceding papers, we proposed that procainamide hydrochloride, a class I antiarrhythmic agent, was able to protect mice and rats from cisplatin-induced nephrotoxicity and that it could exert its action through accumulation in kidneys followed by coordination with cisplatin (or its hydrolysis metabolites) and formation of a less toxic platinum compound similar to the new platinum(II) triamine complex cis-diamminechloro-[2-(diethylamino)ethyl 4-amino-benzoate, N4]-chlorideplatinum(II) monohydrochloride monohydrate, obtained by the reaction of cisplatin with procaine hydrochloride. Hepatotoxicity is not considered as a dose-limiting toxicity for cisplatin, but liver toxicity can occur when the antineoplastic drug is administered at high doses. Here, we report that procainamide hydrochloride, at an i.p. dose of 100 mg/kg, reduces cisplatin-induced hepatotoxicity, as evidenced by the normalization of plasma activity of glutamic oxalacetic transaminase and gamma-glutamyl transpeptidase, as well as by histological examination of the liver tissue. Twenty-four hours after i.p. treatment with the combination of 7.5 mg/kg cisplatin and 100 mg/kg procainamide, a significant increase of procainamide (+56%, P<0.05), total platinum (+31%, P<0.05), platinum-DNA adducts (+31%, P<0.05) and percent DNA-DNA interstrand cross-links (+69%, P<0.02) was found in liver tissue, as compared to animals treated with cisplatin alone. Moreover, in accordance with these findings, we also observed a slightly lower concentration and cumulative excretion of platinum in the feces. Since mitochondrial injury is considered a central event in the early stages of the nephrotoxic effect of cisplatin, the distribution of platinum in these subcellular organelles obtained from hepatocytes was determined after treatment with cisplatin with or without procainamide hydrochloride, together with platinum concentration in their cytosolic fraction. Our data show that the coadministration of procainamide hydrochloride produced a rearrangement of subcellular platinum distribution in hepatocytes with a slight decrease in mitochondria (-15%, P<0.10) and a slight increase in the cytosolic fraction (+40%, P<0.10) of platinum content, compared to the treatment with cisplatin alone. In analogy with our previous results in the kidney, confirmed here by our data in vitro, we suggest that the hepatoprotective activity of procainamide hydrochloride is linked to the formation of a less toxic platinum complex, which leads to inactivation of cisplatin itself and/or its highly toxic hydrolysis metabolites and to a different subcellular distribution of platinum.

Animals↗
PubMed1996

Application of computer-assisted radiotelemetry in the pharmacokinetic and pharmacodynamic modeling of procainamide and N-acetylprocainamide.

The cardiovascular pharmacodynamics (PD) of procainamide and N-acetylprocainamide have not been well characterized in small rodents without the presence of anesthesia or restraint. This study was undertaken to examine the pharmacokinetics (PK) and PD relationship of procainamide and N-acetylprocainamide by use of electrocardiogram (ECG) telemetry in unrestrained rats. Male Sprague Dawley rats received the following treatments: vehicle, procainamide 50 and 100 mg/kg and N-acetylprocainamide 50 and 100 mg/kg via intraperitoneal (i.p.) administration. Blood samples were collected over 8 h and subsequently analyzed. PD measurements (PQ, QS, QR, QT, RR, and HR) were collected prior to dosing and over a 24 h period. Mean PK parameters after the 50 mg/kg dose were as follows: Cls/Fprocainamide = 86.42 mL min-1 kg-1, Cls/FN-acetylprocainamide = 36.62 mL min-1 kg-1, Vdprocainamide = 10.42 L/kg, and VdN-acetylprocainamide = 5.91 L/kg. The relationship between concentration (procainamide or N-acetylprocainamide) and effect (percent change QT interval) was best described by an Emax model for procainamide (EC50 = 445 ng/mL; Emax = 30.09%). These results approximate ECG changes noted in procainamide clinical studies, suggesting that telemetry can be used as a predictive tool of efficacy. Furthermore, the proposed PK-PD model describes the electrophysiological effects associated with procainamide.

Acecainide↗
PubMed1999

The effect of intravenous procainamide on the HV interval at electrophysiologic study.

The His bundle electrogram recorded at electrophysiologic study clearly differentiates atrioventricular (AV) node disease from distal conduction system disease. The distal conduction system may be tested further by infusing procainamide (10-15 mg/kg) intravenously. High-grade distal AV block or prolongation of the HV interval <80 ms was defined as an abnormal response to this test. We retrospectively reviewed the medical records of 79 patients who underwent electrophysiologic study with intravenous procainamide. An abnormal response to procainamide was observed in only 3% of 37 patients with a normal baseline HV (</= ms), in 48% of 27 patients with mild HV prolongation (56 to 70 ms), and in all 15 patients with moderate HV prolongation (<70 ms) (P <0.0001 for the trend). Procainamide induced high-grade AV block in 4 of 28 patients (14%) studied for syncope and in 1 of 51 patients (2%) studied for ventricular tachycardia. Syncope as the indication for electrophysiologic study (P = 0.05) and left bundle branch block morphology (P = 0.03) were predictors of high-grade AV block; baseline HV and QTc intervals were significantly prolonged in patients who developed AV block with procainamide. We identified a strong linear correlation (R = 0.85) between post-drug and baseline HV intervals, with a regression slope of 1.17 +/- 0.09 and an intercept (+/- standard error) of 5.8 +/- 5.0 ms. This linear response to procainamide and published prospective studies support pacing syncope patients with baseline HV <70 ms. Therefore, procainamide infusion during the electrophysiologic study of patients with undifferentiated syncope should be reserved for those with mild HV prolongation from approximately 55 to 70 ms.

Aged↗