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PubMed1979

Safety and efficacy of procainamide infusions.

Thirty-four patients who were resistant to conventional doses of lidocaine received procainamide intravenously according to a pharmacokinetically designed two infusion technique. A mean peak serum concentration of 7.1 mg/liter was achieved with an average loading dose of 989 mg administered over 1 hour. A mean steady state serum concentration of procainamide of 6.5 mg/liter was achieved with a mean dose of 64.4 mg/kg body weight for the first 24 hours of treatment. Dose, renal impairment, the degree of congestive heart failure and acetylator status influenced the steady state serum concentration of procainamide. Dangerous ventricular arrhythmias were abolished in 74% of the patients at a steady state level of 6.9 +/- 3.7 mg/liter (mean +/- standard deviation). Nonresponders to procainamide had a mean steady state serum concentration of procainamide of 4.2 +/- 2.1 mg/liter (P less than 0.05). Systolic and diastolic blood pressures decreased moderately (10 and 8%, respectively), and heart rate decreased 11%. The infusion was interrupted in one patient because of hypotension. The duration of electrocardiographic conduction intervals was increased slightly in some patients. It is concluded that procainamide administered by this two infusion method is effective and well tolerated by most patients.

Arrhythmias, Cardiac↗
PubMed1980

Modification of ventricular tachycardia by procainamide in patients with coronary artery disease.

Fifteen consecutive patients with coronary artery disease had rapid (158 to 272 beats/min) and sustained ventricular tachycardia induced by the extrastimulus technique, and received procainamide infusion. Before the study, all but one patient had severe symptoms with tachycardia, and six had survived apparent sudden death. Procainamide consistently slowed ventricular tachycardia. However, in traditional doses (1 g infusion, plasma concentration greater than 4 micrograms/ml), it prevented induction of ventricular tachycardia in only 2 of the 15 patients. Induction of ventricular tachycardia was facilitated by procainamide in 10 patients. Larger doses of procainamide (plasma concentration 20.2 micrograms/ml +/- 9.7 [mean +/- standard deviation]) prevented induction of ventricular tachycardia in one of eight patients. Rapid ventricular rates (more than 210 beats/min) that were not slowed (by 50 percent or more) after a 1 g infusion of the drug predicted failure of procainamide to prevent ventricular tachycardia. Therefore, procainamide slowed but did not prevent induced ventricular tachycardia in most of these patients with coronary artery disease at risk of sudden death.

Adult↗
PubMed1983

Value of the ajmaline-procainamide test to predict the effect of long-term oral amiodarone on the anterograde effective refractory period of the accessory pathway in the Wolff-Parkinson-White syndrome.

In patients with the Wolff-Parkinson-White syndrome, intravenous ajmaline (50 mg administered over 3 minutes) or procainamide (10 mg/kg body weight administered over 10 minutes) is helpful in defining the duration of the anterograde effective refractory period of the accessory pathway. In this study the value of the ajmaline-procainamide test to predict the effects on the anterograde effective refractory period of the accessory pathway of long-term oral amiodarone were assessed. Thirty-six patients with the Wolff-Parkinson-White syndrome were studied. Twenty-four (Group A) had a negative result of the ajmaline-procainamide test and a mean duration of the anterograde effective refractory period of the accessory pathway of 237 +/- 24 ms. Twelve (Group B) had a positive result in the ajmaline-procainamide test (disappearance of preexcitation during sinus rhythm after administration of ajmaline and procainamide) and a duration of the anterograde effective refractory period of the accessory pathway of 284 +/- 25 ms (p less than 0.05 versus values in Group A). Amiodarone prolonged the anterograde effective refractory period of the accessory pathway by 53 +/- 35 ms in patients in Group A to 290 +/- 37 ms (p less than 0.001) and by 100 +/- 85 ms in patients in Group B to 384 +/- 94 ms (p less than 0.001). The difference in mean increase between both groups was not significant. In most patients (83%) in Group A amiodarone prolonged the anterograde effective refractory period of the accessory pathway to 260 to 330 ms. However, in most patients (83%) in Group B, amiodarone prolonged the anterograde effective refractory period of the accessory pathway to greater than or equal to 330 ms (p less than 0.01). Thus, an ajmaline-procainamide test is of value in predicting the results of oral amiodarone on the anterograde effective refractory period of the accessory pathway.

Adolescent↗
PubMed1983

Effect of procainamide on dispersion of ventricular refractoriness.

Ventricular arrhythmias after Q-T prolongation by drugs could result from a nonhomogeneous increase in refractoriness (dispersion). Dispersion of effective refractory periods (ERP) was measured before and after infusion of 1 g of procainamide using twice-threshold extrastimuli applied in sinus rhythm and with 500 ms ventricular drive cycle length at 3 right ventricular sites (2 patients) or 2 right and 1 left ventricular site (10 patients). Procainamide prolonged ERP. In drive, average ERP was 247 +/- 5 ms (standard error of the mean) before and 277 +/- 7 ms after procainamide (p less than 0.001). The Q-T interval was prolonged by 50 ms in drive (p less than 0.001), but Q-T prolongation did not reflect the increased ERP (r =-0.05). However, procainamide did not alter measured dispersion (54 +/- 16 to 44 +/- 14 ms in sinus, 48 +/- 14 to 47 +/- 13 ms in drive). Polymorphic ventricular tachycardia (VT) was induced in 6 patients in whom drive itself generally failed to reduce dispersion, and failure to induce tachycardia or shorter runs after procainamide was associated with narrowed dispersion. Polymorphic VT was not induced after procainamide in 2 patients with clinical episodes of torsades de pointes caused by type I agents. The mechanism of torsades de pointes was not explained by dispersion of refractoriness or by polymorphic VT initiated by premature beats after a type I drug.

Aged↗
PubMed1986

Effects of quinidine versus procainamide on the QT interval.

Eighteen patients were given quinidine and procainamide separately to evaluate whether prolongation of the QT interval by type Ia antiarrhythmic agents is a drug-specific phenomenon. Doses were titrated to achieve standard trough therapeutic levels of quinidine (2 to 5 micrograms/ml) and procainamide (4 to 12 micrograms/ml). In 16 of the 18 patients, the increase in corrected QT interval (QTc) was greater with quinidine than with procainamide, averaging 78 +/- 10 ms (+/- standard error of the mean) with quinidine and 39 +/- 7 ms with procainamide (p less than 0.001). The greater degree of QTc prolongation with quinidine than with procainamide was not due to differences in sinus cycle length, QRS duration, serum potassium level or concomitant drug therapy. Differences in relative drug level did not appear to account for the greater effect of quinidine. Thus, at frequently used plasma levels, quinidine prolongs QTc to a greater degree than does procainamide. This effect does not appear to be due to the comparison of "nonequivalent" drug levels.

Adult↗
PubMed1990

Value of a revised procainamide test in the Wolff-Parkinson-White syndrome.

A shortest preexcited RR interval less than 250 ms during atrial fibrillation identifies the patient with Wolff-Parkinson-White syndrome potentially at risk for ventricular fibrillation. Loss of preexcitation after infusion of up to 10 mg/kg of procainamide during sinus rhythm has been reported to correlate with a slow ventricular response during atrial fibrillation and has been proposed as a noninvasive test to establish risk of sudden death in these patients. Others have failed to establish this relation and have questioned the usefulness of the procainamide test. Such conflicting results were hypothesized to be a result of differing dosages and methodology. Consequently, this study tested the effect of incremental doses of procainamide (to a cumulative dose of 1 g) on the anterograde effective refractory period of the accessory pathway and related the reliability of the procainamide test to the dose at which preexcitation was lost. The effect of procainamide on the anterograde effective refractory period of the accessory pathway was dose dependent; patients who lost preexcitation had a steeper dose-response curve. Loss of preexcitation by a cumulative dose of 550 mg provided the best balance for sensitivity (60%) and specificity (89%) in identifying patients with preexcited shortest RR greater than 250 ms. Specificity fell steeply after this dosage and higher doses were not useful. The diagnostic accuracy of the procainamide test is critically related to dosage and method of infusion.

Adolescent↗
PubMed1993

Usefulness of the response to intravenous procainamide during electrophysiologic study in predicting the response to oral quinidine in patients with inducible sustained monomorphic ventricular tachycardia associated with coronary artery disease.

The response to intravenous procainamide (15 to 20 mg/kg) and to oral quinidine 324 to 648 mg every 8 hours for 3 to 5 days was prospectively studied in 50 consecutive patients (43 men and 7 women, aged 38 to 83 years old [mean 64 +/- 11]) with coronary artery disease and baseline-inducible sustained monomorphic VT. Mean procainamide and trough quinidine serum levels were 10.5 +/- 2.6 and 2.6 +/- 0.8 micrograms/ml, respectively. Mean left ventricular ejection fraction was 37 +/- 12%. Sustained monomorphic VT was suppressed by intravenous procainamide in 18 patients (36%); 8 of these patients (44%) also had suppression with oral quinidine, but 10 (56%) did not. Of the 32 patients (64%) who continued to have inducibility with intravenous procainamide, 12 (38%) responded to oral quinidine and 22 (62%) did not. The overall concordant response rate to intravenous procainamide and oral quinidine was 56% (28 of 50 patients). It is concluded that the response (i.e., the presence or absence of inducible sustained monomorphic VT) to intravenous procainamide does not adequately predict the response to oral quinidine in patients with coronary artery disease and sustained monomorphic VT.

Adrenergic beta-Antagonists↗
PubMed1980

Procainamide-induced lupus erythematosus pericarditis encountered during coronary bypass sugery.

Procainamide is probably the most common offending drug responsible for the drug-induced lupus erythematosus syndrome today. Pericarditis has been reported to occur in from 14 to 18 per cent of the cases of procainamide-induced lupus erythematosus, and occasional reports of massive pericardial effusion, pericardial tamponade and constrictive pericarditis have appeared in the literature. We describe a patient who presented with features of procainamide-induced lupus erythematosus without any clinical evidence of pericarditis. He underwent coronary bypass surgery 12 days after administration of the drug was stopped and was found to have a significant pericardial effusion at the time of surgery; histologic examination of pericardial tissue and pericardial fluid confirmed that the pericardial effusion was related to the procainamide-induced lupus syndrome. The incidence of pericarditis in procainamide-induced lupus erythematosus may be higher than presently accepted figures would indicate. Symptoms and signs related to procainamide-induced lupus pericarditis may cause diagnostic confusion with common postoperative bypass complications; the full implications of this disease entity to the patient undergoing coronary bypass are unknown.

Biopsy↗
PubMed1992

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms.

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infused at a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 +/- 4 vs. 7.4 +/- 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 +/- 78 vs. 450 +/- 81 ms, p = NS) and QRS duration (184 +/- 38 vs. 185 +/- 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1992

Differential effect of intravenous procainamide on anterograde and retrograde accessory pathway refractoriness.

Although procainamide may markedly impair or abolish anterograde conduction over an accessory atrioventricular (AV) pathway, orthodromic AV reentry may remain inducible. This difference may be related to a systemic differential effect of procainamide on anterograde and retrograde accessory pathway refractoriness. To examine this phenomenon, an infusion of procainamide producing five incremental blood levels over 75 min was administered to 15 patients with the Wolff-Parkinson-White syndrome. At each procainamide level, accessory pathway effective refractory period and accessory pathway block cycle length were determined in the anterograde and retrograde directions. At baseline, there were no significant differences between anterograde and retrograde accessory pathway effective refractory periods (282 +/- 7 vs. 266 +/- 9 ms, p = 0.08) and block cycle lengths (288 +/- 15 vs. 283 +/- 9 ms, p = 0.66). The concentration of procainamide resulting in 50% prolongation of accessory pathway refractoriness was less in the anterograde direction than in the retrograde direction (27.5 [log concentration -4.56 +/- SE 0.13] vs. 64.6 [-4.19 +/- 0.11] mumol/liter, p = 0.02). Similarly, the concentration of procainamide resulting in 50% prolongation of accessory pathway block cycle length in the anterograde direction (25.1 [-4.60 +/- 0.13] mumol/liter) was less than in the retrograde direction (52.5 [-4.28 +/- 0.07] mumol/liter, p = 0.01). The probability of persistence of accessory pathway conduction in the anterograde direction was less than in the retrograde direction by Kaplan-Meier analysis (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of procainamide on the signal-averaged electrocardiogram in relation to the results of programmed ventricular stimulation in patients with sustained monomorphic ventricular tachycardia.

OBJECTIVES: The aim of this study was to assess the ability of the signal-averaged electrocardiogram (ECG) to predict the efficacy of procainamide. BACKGROUND: The main role of the signal-averaged ECG has been the identification of postinfarction patients at risk of sudden death. Prediction of the efficacy of antiarrhythmic drugs represents another potential clinical application of this technique. METHODS: The study examined the effects of procainamide on the time domain and spectral temporal analysis of the signal-averaged ECG in relation to the results of programmed ventricular stimulation studies in 31 patients with inducible sustained monomorphic ventricular tachycardia. RESULTS: Procainamide significantly prolonged the total and the initial QRS complex and low amplitude signal durations (mean +/- SD 135 +/- 30 vs. 161 +/- 46 ms, p < 0.0001; 87 +/- 16 vs. 98 +/- 20 ms, p < 0.0001, and 48 +/- 23 vs. 63 +/- 36 ms, p < 0.001, respectively) whereas the root-mean-square voltage of the total QRS complex and of the last 40 ms of the QRS complex was significantly reduced (mean +/- SD 112 +/- 36 vs. 87 +/- 36 microV, p < 0.0001; 21 +/- 19 vs. 13 +/- 12 microV, p < 0.002, respectively). The results of spectral temporal mapping of the signal-averaged ECG were similar before and after procainamide administration. Procainamide prevented the inducibility of sustained ventricular tachycardia or prolonged the cycle length of ventricular tachycardia by > or = 100 ms in 16 patients (52%) (responders). The fractional prolongation of the total QRS duration was significantly greater in responders (26 +/- 15%) than in nonresponders (10 +/- 10%) (p < 0.002) and, when this prolongation was > or = 15%, identified responders with a sensitivity of 94%, a specificity of 87% and an overall predictive accuracy of 90%. CONCLUSIONS: The effects of procainamide on inducibility of ventricular tachycardia during programmed ventricular stimulation can be predicted by the degree of drug-induced prolongation of the signal-averaged QRS complex.

Aged↗
PubMed1996

Efficacy and safety of procainamide in preventing arrhythmias after coronary artery bypass surgery.

Arrhythmias are common after cardiac surgery and are associated with hemodynamic compromise, stroke, and prolonged hospitalization. Beta blockers prevent atrial fibrillation postoperatively, but there are few data regarding the prophylactic use of type 1 antiarrhythmic agents or the prevention of ventricular arrhythmias. Accordingly, we performed a randomized, double-blind, placebo-controlled study of the effects of oral procainamide on 100 patients undergoing elective coronary artery bypass surgery. Procainamide was received for 4 days; the dosage was adjusted for body weight. Patients receiving procainamide had a significant reduction in atrial fibrillation (16 vs 29 patient-days, p < 0.05) and ventricular tachycardia (2% vs 20%, p < 0.01). However, the incidence of atrial fibrillation was not significantly reduced (38% vas 26%). In the group achieving therapeutic serum procainamide levels, there was reduction in all measured postoperative arrhythmias. No serious cardiac or noncardiac adverse events were noted during procainamide therapy, although there was a significant increase in the incidence of nausea. We conclude that procainamide reduces arrhythmias in the early postoperative period after coronary artery bypass surgery, most prominently in patients who achieve therapeutic serum levels. This was associated with no serious cardiac adverse reactions.

Administration, Oral↗
PubMed1979

Lymphocyte alteration by procainamide: relation to drug-induced lupus erythematosus syndrome.

Sera from 11 (65%) of 17 patients with newly diagnosed procainamide-induced lupus contained cold-reactive lymphocytotoxic antibodies to normal human lymphocytes in titres of 1/2 to 1/128. In contrast, only 3 of 15 patients on long-term procainamide therapy without lupus and 3 of 65 normal men had serum lymphocytotoxic antibodies, none at a titre higher than 1/2. Antibody levels in the lupus patients declined quickly after procainamide was stopped, in parallel with their clinical improvement. Procainamide (3.75 x 10(-3) mol/l) suppressed by more than 80% in-vitro phytohaemagglutinin-induced 3H-thymidine incorporation by normal human blood lymphocytes. At 3.75 x 10(-4) mol/l, procainamide enhanced the mitogenic response to 160 +/- 20% of normal. Thus procainamide may interact with the lymphocyte membrane, possibly producing a lupus syndrome directly, by altering lymphocyte function, or indirectly, by generating autoantibodies reactive with normal membrane structures.

Aged↗
PubMed1986

Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure.

Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 +/- 1.0, 2.5 +/- 0.9 and 2.6 +/- 0.8 hours, respectively), volume of distribution (1.9 +/- 0.7, 1.8 +/- 0.4 and 1.8 +/- 0.5 liters/kg, respectively), clearance (11.3 +/- 7.5, 9.3 +/- 3.6 and 9.1 +/- 3.5 ml/min per kg, respectively) and unbound drug fraction (66 +/- 9, 66 +/- 9 and 69 +/- 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 micrograms/ml in patients with acute myocardial infarction and 3.3 micrograms/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

Aged↗
PubMedDate not supplied

Metabolism of procainamide to a hydroxylamine by human neutrophils and mononuclear leukocytes.

The chronic use of procainamide is associated with a high incidence of drug-induced lupus and also agranulocytosis. We have previously demonstrated that procainamide is metabolized in the liver to reactive hydroxylamine (PAHA) and nitroso (nitroso-PA) metabolites which covalently bind to protein and are toxic to lymphocytes. We proposed that these metabolites were responsible for the toxicities of procainamide. However, PAHA and nitroso-PA do not appear to escape the liver in significant concentrations. In this paper we describe the metabolism of procainamide to a reactive hydroxylamine by neutrophils and mononuclear leukocytes. Such metabolism only occurs if the cells have been stimulated to have a respiratory burst. These observations have obvious possible implications for the mechanism of procainamide-induced agranulocytosis (formation of a reactive metabolite by neutrophils) and procainamide-induced lupus (formation of a reactive metabolite by monocytes). The metabolism of drugs to reactive metabolites by monocytes may be a general mechanism for hypersensitivity reactions because monocytes play a key role in the processing of antigen and stimulation of antibody synthesis.

Biotransformation↗
PubMed2005

A comparison of the covalent binding of clozapine, procainamide, and vesnarinone to human neutrophils in vitro and rat tissues in vitro and in vivo.

Covalent binding of drug reactive metabolites to neutrophils or their precursors is thought to play a role in the development of drug-induced agranulocytosis. In this study, we used immunochemical techniques to compare the covalent binding of clozapine, vesnarinone, and procainamide (three drugs associated with agranulocytosis) to phorbol-12,13-myristate acetate (PMA)-activated human neutrophils in vitro and rat tissues in vivo. In PMA-activated human neutrophils in vitro, clozapine and procainamide modified neutrophil proteins with molecular masses ranging from 30 to 200 kDa, while vesnarinone predominately formed adducts with molecular masses greater than 70 kDa. All three drugs formed adducts at 126, 98, and 58 kDa, and they all covalently bound to human myeloperoxidase when incubated with this enzyme and H2O2 in vitro. Covalent binding to PMA-activated neutrophils was inhibited by nucleophiles, such as glutathione and N-acetylcysteine, but not by N-acetyllysine. In the presence of the PMA, all three drugs covalently bound to activated rat bone marrow cells in vitro, while in its absence only clozapine did. Covalently modified liver proteins were observed in rats treated for 6 weeks with clozapine (25 or 50 mg/kg/day), vesnarinone (300 mg/kg/day), or procainamide (50 mg/kg/day). Clozapine extensively modified proteins in all subcellular fractions; procainamide formed a 99 kDa adduct in a membrane-containing fraction and 57, 47, and 36 kDa adducts in a cytosolic fraction, while vesnarinone formed liver-protein adducts with molecular masses of 82, 62, 49, and 40 kDa in membrane, cytosolic, and S9 fractions. In addition, clozapine and procainamide, but not vesnarinone, formed a 49 kDa drug-protein adduct in the bone marrow of treated rats. Furthermore, procainamide covalently bound to a 58 kDa protein in neutrophils of a patient treated with the drug. We suspect that covalent modification of common targets in the neutrophils by these three drugs plays a role in the development of drug-induced agranulocytosis.

Animals↗
PubMed1998

Cardiac anticholinergic effects of procainamide and its N-acetylated metabolite: experimental pharmacological and radioligand binding studies.

1. The cardiac anticholinergic effects of procainamide (1 mg kg(-1) min(-1)) and its N-acetylated metabolite (NAPA) at equimolar dose (1.16 mg kg(-1) min(-1)) were studied using in vivo experimental pharmacological and in vitro radioligand binding studies. 2. Procainamide and NAPA progressively reduced vagal stimulation-induced bradycardia in chloralose-anaesthetized dogs. As indicated by the ED50, the vagolytic activity of NAPA is 1.5-2.0 times weaker than that of procainamide. Both drugs increased heart rate, with lowering of mean blood pressure during the second part of procainamide infusion, but not during NAPA infusion. 3. Binding studies on rat heart membranes yielded Ki values that were 1.5 times higher for NAPA than for procainamide. 4. These results show that NAPA exerts a weaker cardiac vagolytic action than procainamide, which is probably linked to a lower ability to bind to cardiac muscarinic receptors.

Acecainide↗
PubMed2001

Effect of procainamide on the postrepolarization refractoriness in cardiac muscle: evaluation using the block coupling interval in the artificial isthmus model in the canine right atrium.

The post-repolarization refractoriness (PRR) is an important factor to determine the conduction block in cardiac muscle. Recently, we proposed the block coupling interval (BCI) as an useful electrophysiological index for evaluating the PRR. In the present study, the effect of procainamide on PRR was evaluated using the BCI and the effective refractory period (ERP). In five beagle dogs, radiofrequency linear ablation was performed on the right atrial surface parallel to the AV groove, forming an artificial isthmus (8-10 mm width and 15-20 mm length). Bipolar recordings were performed in the isthmus at a resolution of 1.2 mm and single extrastimuli with eight basic drive trains were delivered to cause conduction blocks in the isthmus. When a conduction block occurred, the recorded coupling interval at the recording site just proximal to the site of block was defined as BCI. At the site of the block, the ERP and duration of the monophasic action potential (MAP) at each drive cycle length was measured. The PRR was calculated using two different formulas: (1) [ERP-MAP] and (2) [BCI-MAP]. Procainamide was administrated intravenously at a dose of 15 mg/kg after the control study and the whole study protocol was repeated. The site of the block in an individual dog was always the same. BCI, ERP, and MAP were all shortened in accordance with the shortening of the basic drive cycle length, and the BCI was always the longest, ERP the middle, and the MAP was the shortest. The administration of procainamide prolonged each parameter, but the order of BCI > ERP > MAP remained unchanged. The PRR calculated as [BCI-MAP] was prolonged from 15 +/- 10 ms to 29 +/- 8 ms by the administration of procainamide (P = 0.048), but [ERP-MAP] was unchanged (8 +/- 10 ms vs 8 +/- 4 ms). In the conduction block model in the canine right atrium, procainamide prolonged the [BCI-MAP], but did not change the [ERP-MAP]. The procainamide effect of prolonging the PRR might be expressed better by the change in the BCI than the ERP.

Animals↗