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PubMed1990

Facilitation of ventricular tachycardia initiation by procainamide during programmed ventricular stimulation in patients with heart failure.

Antiarrhythmic drugs occasionally facilitate, rather than prevent, ventricular tachycardia. The purpose of this study was to assess the incidence of procainamide facilitation of ventricular tachycardia initiation during programmed electrical stimulation in patients with no history of spontaneous sustained ventricular tachycardia but who are at high risk. Twenty patients with advanced heart failure (mean left ventricular ejection fraction 0.19 +/- 0.09) and nonsustained ventricular tachycardia and in whom sustained ventricular tachycardia was not inducible by programmed electrical stimulation in the basal state were studied. Six patients had coronary artery disease, 13 had idiopathic dilated cardiomyopathy, and 1 had valvular heart disease. All patients received programmed stimulation from the right ventricular apex with one to three extra-stimuli before and after the intravenous infusion of 10 mg/kg of procainamide (serum level 6.6 +/- 2.4 mcg/l). In two patients (10%) sustained monomorphic ventricular tachycardia was initiated only after the administration of procainamide. One of these patients later died in ventricular tachycardia during hyperkalemia. Of the noninducible patients, during a follow-up period of 6 +/- 5 months, two died suddenly and one developed symptomatic ventricular tachycardia. Thus, procainamide can unmask potential reentry circuits in some patients who have not had spontaneous sustained ventricular tachycardia. In patients with heart failure, this risk, as assessed by programmed stimulation after a single dose of procainamide, appears to be low.

Adult↗
PubMed1990

Effects of procainamide hydroxylamine on generation of reactive oxygen species by macrophages and production of cytokines.

A series of experiments was conducted to examine the effects of the N-oxidized metabolite of procainamide, procainamide hydroxylamine (PAHA), on reactive oxygen species (ROS) production by macrophages in vitro, as well as on the release of the cytokine interleukin-1 (IL-1). Results with PAHA were compared with those from the parent compound, procainamide, and in some cases with other procainamide metabolites such as N-acetylprocainamide or nitrosoprocainamide. The effects of PAHA on ROS production by mouse and rat macrophages were complex, resulting in both stimulatory and inhibitory activity depending upon the PAHA concentration and whether macrophages were resting or elicited. The primary effect of PAHA appeared to be a stimulation of ROS production. Monocytes pretreated with PAHA (20 microM) depressed the responsiveness of lymphocytes in co-culture to a T-cell mitogen (conconavalin A) but not a B-cell mitogen (lipopolysaccharide). This effect was inhibited when monocyte pretreatment with PAHA was accompanied by the antioxidants, catalase or superoxide dismutase. IL-1 production by rat adherent splenocytes was unaffected by PAHA in concentrations that were not cytotoxic. These observations suggest that the oxidative metabolism of procainamide to PAHA may result in enhanced production of ROS by macrophages contributing its toxicity to lymphocytes.

Animals↗
PubMed1988

Differential effects of procainamide, lidocaine and acetylstrophanthidin on body surface potentials and epicardial conduction in dogs with chronic myocardial infarction.

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecting the more subtle effects on conduction caused by lidocaine and acetylstrophanthidin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Termination of acute atrial fibrillation in the Wolff-Parkinson-White syndrome by procainamide and propafenone: importance of atrial fibrillatory cycle length.

The effects of intravenous procainamide (n = 30) or propafenone (n = 25) were evaluated in 55 patients with acute atrial fibrillation and the Wolff-Parkinson-White syndrome. All patients received either procainamide (12 to 15 mg/kg body weight) or propafenone (1 to 2 mg/kg) during sustained (greater than 10 min) atrial fibrillation or after termination of nonsustained atrial fibrillation. Termination of atrial fibrillation was attributed to a drug if it occurred less than or equal to 15 min after infusion. Measurements included mean cycle length of fibrillatory electrograms (mean AA interval) as measured at the high right atrium and shortest RR interval between pre-excited cycles during atrial fibrillation. Atrial fibrillation terminated more frequently after procainamide administration (65%) than after propafenone (46%), although this difference was not significant. Procainamide prolonged the shortest pre-excited RR interval (228 +/- 41 to 339 +/- 23 ms, p = 0.0001) as did propafenone (215 +/- 40 to 415 +/- 198 ms, p = 0.0001) and the magnitude of increase was greater for propafenone (p = 0.048). Patients with sustained atrial fibrillation had shorter mean AA intervals than did their counterparts with nonsustained atrial fibrillation (123 +/- 25 versus 186 +/- 35 ms, p = 0.0001). Termination of sustained atrial fibrillation by either drug was accompanied by prolongation of the mean AA interval but not necessarily by the shortest pre-excited RR interval. Termination of atrial fibrillation was heralded by a 68% increase in the mean AA interval after procainamide administration compared with a 30% increase when the arrhythmia persisted. For propafenone the increases were 90% and 68%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Hemodynamic effects of intravenous procainamide during ventricular tachycardia.

Radionuclide angiography was used to study the hemodynamic effects of intravenous procainamide during stable monomorphic ventricular tachycardia. In four patients studied without procainamide, the ejection fraction was 25% +/- 2.4% during normal sinus rhythm, dropped to 11.3% +/- 2.2% (p less than 0.05) at the onset of ventricular tachycardia, increased to 16.7% +/- 1.7% after remaining in ventricular tachycardia for 10 minutes, and returned to 25.3% +/- 3.7% in sinus rhythm. In the 10 study patients, ejection fraction dropped from 36% +/- 5.8% in sinus rhythm to 25% +/- 5.1% in ventricular tachycardia (p less than 0.2). Ejection fraction decreased further (23% +/- 5.0%) following low doses of procainamide (140 +/- 52 mg) despite cycle length prolongation (354 +/- 18 msec versus 373 +/- 21 msec, p less than 0.5). In 8 of 10 patients, there was a progressive increase in the ejection fraction (28.8% +/- 4.1%). Ventricular tachycardia onset also resulted in a decrease in cardiac output and end-diastolic and end-systolic volumes. Two patients who tolerated procainamide in sinus rhythm showed hemodynamic collapse secondary to procainamide during ventricular tachycardia. We conclude that in some patients hemodynamic intolerance to an antiarrhythmic drug may only become evident during ventricular tachycardia.

Adult↗
PubMed1996

Effects of verapamil, propranolol, and procainamide on adenosine-induced negative dromotropism in human beings.

Adenosine, verapamil, propranolol, and procainamide are widely used antiarrhythmic drugs. The interactions among them are still not known in human beings. Adenosine-induced negative dromotropic effects were assessed by rapid bolus injection of adenosine during constant high right atrial pacing in each patient. The initial dose of adenosine was 0.5 mg and was followed by a stepwise increment of 0.5 mg until atrioventricular (AV) nodal block occurred. The negative dromotropic actions of adenosine were examined in the control state and in the following three protocols in three groups of patients: (1) In 12 patients (group 1), intravenous verapamil, 0.15 mg/kg, was given; (2) In 12 patients (group 2), intravenous propranolol, 0.1 mg/kg, was given; and (3) in 10 patients (group 3), intravenous procainamide, 15 mg/kg, was given. The dose-response curves of adenosine on AV nodal conduction were almost identical in the control state and after verapamil, propranolol, or procainamide injection. However, verapamil, in contrast to propranolol, significantly reduced the dose of adenosine required to produce AV nodal block, from 4.4 +/- 0.7 mg to 2.7 +/- 0.3 mg (p < 0.01). Of note, procainamide exerted no significant effects on adenosine-induced negative dromotropism on AV nodal conduction or AV nodal block. In conclusion, the negative dromotropic effects of adenosine are preserved and independent even in the presence of verapamil, propranolol, or procainamide. Both verapamil and propranolol can exhibit additive effects with adenosine in prolonging AV nodal conduction time; however, only verapamil can reduce the dose of adenosine required to produce AV nodal block. This finding indicates that the dose of adenosine may be reduced for patients who have already been treated with verapamil.

Adenosine↗
PubMed1998

Prospective comparison of intravenous quinidine and intravenous procainamide in patients undergoing electrophysiologic testing.

BACKGROUND: Intravenous procainamide hydrochloride is frequently used in the acute care setting and during electrophysiologic testing, but intravenous quinidine gluconate is rarely used because of concerns about its safety. This study prospectively compares the hemodynamic and electrophysiologic effects of these agents in patients undergoing electrophysiologic testing. METHODS AND RESULTS: Sixty-five consecutive patients with inducible ventricular tachyarrhythmias were prospectively treated with either intravenous quinidine gluconate or intravenous procainamide hydrochloride in an alternating unblinded fashion. The hemodynamic and electrophysiologic effects of these two drugs were compared. Seven (22%) patients assigned to intravenous quinidine gluconate and eight (24%) patients assigned to intravenous procainamide hydrochloride were rendered noninducible for ventricular tachyarrhythmias. Four (13%) patients assigned to intravenous quinidine gluconate were unable to complete the infusion compared with none (p = 0.05) assigned to intravenous procainamide hydrochloride. Otherwise, the overall hemodynamic and electrophysiologic effects of the two drugs were similar. CONCLUSIONS: Intravenous quinidine gluconate is a reasonable alternative to intravenous procainamide hydrochloride in patients requiring a parenteral type IA antiarrhythmic agent.

Aged↗
PubMed1993

Dual actions of procainamide on batrachotoxin-activated sodium channels: open channel block and prevention of inactivation.

We have investigated the action of procainamide on batrachotoxin (BTX)-activated sodium channels from bovine heart and rat skeletal muscle. When applied to the intracellular side, procainamide induced rapid, open-channel block. We estimated rate constants using amplitude distribution analysis (Yellen, G. 1984. J. Gen. Physiol. 84:157). Membrane depolarization increased the blocking rate and slowed unblock. The rate constants were similar in both magnitude and voltage dependence for cardiac and skeletal muscle channels. Qualitatively, this block resembled the fast open-channel block by lidocaine (Zamponi, G. W., D. D. Doyle, and R. J. French. 1993. Biophys. J. 65:80), but procainamide was about sevenfold less potent. Molecular modeling suggests that the difference in potency between procainamide and lidocaine might arise from the relative orientation of their aromatic rings, or from differences in the structure of the aryl-amine link. For the cardiac channels, procainamide reduced the frequency of transitions to a long-lived closed state which shows features characteristic of inactivation (Zamponi, G. W., D. D. Doyle, and R. J. French. 1993. Biophys J. 65:91). Mean durations of kinetically identified closed states were not affected. The degree of fast block and of inhibition of the slow closures were correlated. Internally applied QX-314, a lidocaine derivative and also a fast blocker, produced a similar effect. Thus, drug binding to the fast blocking site appears to inhibit inactivation in BTX-activated cardiac channels.

Animals↗
PubMed2000

Involvement of K(+) channel in procainamide-induced relaxation of bovine tracheal smooth muscle.

The relaxant effect of procainamide, a class Ia antiarrhythmic agent, was examined in bovine tracheal smooth muscle. Procainamide produced concentration-dependent decreases in tension and full relaxation in the preparations contracted with methacholine (0.3 microM). By comparison, in preparations contracted with 40 mM K(+), procainamide had only slight relaxant effects. The relaxant effects of cromakalim and salbutamol on 40 mM K(+)-contracted preparations were significantly (P<0.01) smaller than those on 0.3 microM methacholine-contracted ones. On the other hand, the concentration-response relationships for quinidine, lidocaine, mexiletine and propafenone were not so dramatically different between 0.3 microM methacholine- and 40 mM K(+)-contracted preparations. Tetraethylammonium (300 microM), iberiotoxin (30 nM) and Ba(2+) (1 mM) significantly (P<0.05) attenuated the relaxant effects of procainamide on methacholine-induced contractions, whereas apamin (100 nM), 4-aminopyridine (300 microM), and glibenclamide (10 microM) did not affect them. The inhibitory effect of a combination of iberiotoxin and Ba(2+) was greater than that of iberiotoxin or Ba(2+) alone (P<0.01). These results suggest that the activation of at least two types of K(+) (maxi-K(+) and inward rectifier K(+)) channels contributes to the procainamide-induced relaxation of bovine tracheal smooth muscle.

Albuterol↗
PubMed1985

Limitations of failure of procainamide during electrophysiologic testing to predict response to other medical therapy.

To determine whether failure of procainamide to prevent initiation of ventricular tachyarrhythmias during electrophysiologic testing predicted failure of other antiarrhythmic regimens, 81 consecutive patients with coronary artery disease whose ventricular tachyarrhythmias remained inducible during procainamide administration were studied. Overall, 26 (12%) of 216 subsequent drug studies were successful and at least one effective drug regimen was identified in 22 (27%) of the 81 patients. Drug success was significantly related to the arrhythmia induced at baseline study; 7% of drug studies were successful in patients with sustained ventricular tachycardia, 24% in patients with ventricular fibrillation, and 29% in patients with nonsustained ventricular tachycardia. An effective drug regimen was found in 11 (19%) of 59 patients with sustained ventricular tachycardia, 4 (50%) of 8 patients with ventricular fibrillation and 7 (50%) of 14 patients with nonsustained ventricular tachycardia. In patients with sustained ventricular tachycardia, failure of procainamide to suppress the arrhythmia correlated with failure of other agents used singly but not in combination. This study supports the view that when procainamide fails to prevent initiation of the arrhythmia in patients with inducible sustained ventricular tachycardia it is unlikely that other individual standard agents will be effective. However, combination regimens may suppress the arrhythmia and should be evaluated. In patients with nonsustained ventricular tachycardia, all agents should be evaluated because failure to respond to procainamide does not predict subsequent responses to other agents either alone or in combination.

Adult↗
PubMed1985

Rate-dependent effects of intravenous lidocaine, procainamide and amiodarone on intraventricular conduction.

In this study, the duration of the QRS complex during ventricular pacing was used as an index of intraventricular conduction to quantitate the rate-dependent effects of intravenous lidocaine, procainamide and amiodarone. Right ventricular apical pacing (15 to 20 beats) was performed at cycle lengths of 600, 500, 400, 350, 300, 275 and 250 ms, before and 5 minutes after the intravenous administration of lidocaine in 11 patients (serum level 3.2 +/- 0.8 micrograms/ml [mean +/- SD] ), procainamide in 14 patients (serum level 8.2 +/- 1.9 micrograms/ml) and amiodarone in 12 patients (serum level 3.9 +/- 1.2 micrograms/ml). Electrocardiographic recordings were made at a paper speed of 150 mm/s. QRS duration was measured in a blinded fashion, with reproducibility within 5%. In the control state, QRS duration was the same at all paced cycle lengths. After lidocaine, procainamide and amiodarone administration, the shortest paced cycle length with complete ventricular capture was 250 +/- 0, 275 +/- 38 and 264 +/- 20 ms, respectively. At a paced cycle length of 600 ms, the increase in QRS duration compared with the control state was 1 +/- 2% with lidocaine (p greater than 0.05), 21 +/- 7% with procainamide (p less than 0.001) and 6 +/- 6% with amiodarone (p less than 0.05). At the shortest paced cycle length with complete capture, the increase in QRS duration compared with the control state was 20 +/- 6% with lidocaine (p less than 0.001), 42 +/- 11% with procainamide (p less than 0.001) and 26 +/- 4% with amiodarone (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Antiarrhythmic activity of p-hydroxy-N-(2-diethylaminoethyl) benzamide (the p-hydroxy isostere of procainamide) in dogs and mice.

p-Hydroxy-N-(2-diethylaminoethyl)benzamide (2), the p-hydroxy isostere of procainamide (1), shows antiarrhythmic activity against acontine-induced atrial arrhythmia and lowers mean arterial blood pressure after iv infusion in dogs. In isolated canine Purkinje fibers, phenolic 2 in a bath concentration of 20 mug/ml significantly reduced the rate of phase O depolarization, prolonged the repolarization time, and reduced automaticity. These in vitro and the above in vivo activities of phenolic 2 were similar to those observed for procainamide (1). Bioisosters, phenolic 2 and procainamide (1), have almost identical respective 13C NMR chemical shifts indicating that electron densities on the respective carbons are very similar. This may explain their similar antiarrhythmic and hypotensive effects. Phenolic 2 and procainamide (1) therapeutic ratios in ICR male mice (acute LD50/ED50 against chloroform hypoxia induced ventricular fibrillation) are 2.1 and 1.8, respectively. Procainamide analogues with electron-donating groups [OH, NH2, NHC(=O)CH3] on the aromatic ring possess more antiarrhythmic activity in mice than the analogue with an electron-withdrawing group (NO2). This indicates that a shift in electron density toward the amide region in the former analogues, as determined by 13C NMR spectroscopy, is one of the factors influencing antiarrhythmic potency in this series.

Action Potentials↗
PubMed1998

Conversion of atrial fibrillation to sinus rhythm using acute intravenous procainamide infusion.

The efficacy and safety of intravenous procainamide in the conversion of atrial fibrillation was investigated. A total of 114 patients without severe heart failure were randomized to receive either intravenous procainamide (1 g over 30 minutes, followed by an infusion of 2 mg/min over 1 hour) or placebo in a double-blind trial. Digoxin (0.5 mg intravenously) was administered to all patients who had not previously been receiving digoxin. Treatment was considered successful if sinus rhythm was restored within 1 hour after starting the infusion. Conversion to sinus rhythm was achieved in 29 (50.9%) of the 57 patients treated with procainamide and in 16 (28.1%) of the 57 who received placebo (P approximately 0.012). When the duration of the atrial fibrillation was < or = 48 hours, conversion to sinus rhythm was achieved in 29 (69%) of the 42 patients receiving procainamide and in 16 (38.1%) of those receiving placebo (P approximately 0.004). None of the patients with atrial fibrillation lasting > or = 48 hours converted to sinus rhythm in either group. Another factor that played a role in the restoration of sinus rhythm was the size of the left atrium: the smaller the left atrium, the larger the success rate. The results of the study suggest that intravenous procainamide is an effective and safe means for the rapid termination of atrial fibrillation of recent onset and that its success rate is inversely related to the size of the left atrium. However, the drug is ineffective in the conversion of atrial fibrillation lasting more than 48 hours.

Adult↗
PubMed1997

Activity of Procanbid, procainamide twice-daily formulation, to suppress ventricular premature depolarizations. The Study Group Investigators.

Procainamide is a class IA antiarrhythmic drug indicated for the treatment of life-threatening or symptomatic ventricular arrhythmias. The current sustained-release formulation requires 6-hour dosing (qid). To improve patient compliance, a new sustained-release formulation for twice-daily (bid) administration has been developed (Procanbid, Parke-Davis). This study assesses the pharmacologic equivalence of the bid and qid formulations in the suppression of symptomatic ventricular premature depolarizations (VPDs). Fourteen centers enrolled a total of 99 patients with frequent symptomatic VPDs (average > or = 20 VPDs/hr) who previously responded to and tolerated the procainamide qid formulation. During the first week of the double-blind phase, patients were randomized to either placebo or procainamide dosages of 1000, 2000, or 4000 mg/d (bid or qid formulations). In the second week, the patients were crossed over to the alternate formulation. Seventy-seven patients qualified for the primary activity analysis. The bid and qid formulations showed comparable effectiveness in the suppression of mean VPDs with a linear dose-response relationship. The VPD suppression was not attenuated towards the end of the dosing interval for either formulation. Sixty-eight of these patients entered an optional 1-year extension to receive the bid formulation. Thirty-seven (54%) patients had adverse effects. Of those, 15 (22%) had side effects considered treatment related. Most of the adverse events occurred during the first 6 weeks of treatment. Only a few patients (8%) withdrew as a consequence of treatment with the bid formulation. The overall safety profile of the bid formulation was similar to other formulations, and the procainamide bid formulation has a low proarrhythmic rate (< 3%). In conclusion, the effectiveness of the twice-daily formulation of procainamide in the suppression of VPDs is comparable to the currently available qid formulation.

Aged↗
PubMed1980

Aging and renal clearance of procainamide and acetylprocainamide.

Thirty-two patients had blood and urine collected simultaneously for measurement of procainamide, acetylprocainamide, and creatinine. The ratios of drug clearance to creatinine clearance were calculated for each. The procainamide:creatinine clearance ratio averaged 2.9 +/- 1.6 (SD) and fell as age of the patients rose (r = 0.5, p < 0.01). The acetylprocainamide:creatinine clearance ratio averaged 1.7 +/- 0.8 and also fell with age. The combination of decline in overall renal function with age with this decrease in the rate of renal tubular secretion of these drugs led to a progressive age-related rise in the steady-state serum level of procainamide (r = 0.56, p < 0.01) and acetylprocainamide (r = 0.36, p < 0.1) achieved by any dose of procainamide. Thus, the dosage of procainamide must be individualized for both overall renal function (GFR) and the age-related variations in renal tubular secretion that are of most note in children and the elderly.

Acecainide↗
PubMed1988

Metabolites of procainamide and practolol inhibit complement components C3 and C4.

Drug-induced systemic lupus erythematosus arises from toxic side-effects of administration of hydralazine, isoniazid, procainamide and practolol. Hydralazine and isoniazid are nucleophilic drugs and inhibit the covalent binding reaction of complement components, C3 and C4, an effect likely to lead to deposition of immune complexes (a feature of systemic lupus erythematosus). Procainamide and practolol do not themselves inhibit C3 and C4. A range of metabolites and putative metabolites of procainamide and practolol were synthesized, and tested for their ability to inhibit the covalent binding reactions of C3 and C4. The highly nucleophilic hydroxylamine metabolite of procainamide was strongly inhibitory in both tests, as was a putative hydroxylamine metabolite of practolol. These studies indicate a potential role for the hydroxylamine metabolites in mediating the toxic side-effects of procainamide and practolol, and emphasize the need for adequate measurements of hydroxylamine metabolites in human tissue.

Acecainide↗
PubMed2001

New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives.

AIMS: Sudden unexplained death syndrome occurs in previously healthy South-east Asian young adults without any structural cause of death. The common electrocardiographic (ECG) change in sudden unexplained death syndrome survivors is right bundle branch block and ST elevations in leads V(1) to V(3), which are similar to the ECG pattern in the Brugada syndrome (Brugada sign). It is difficult to diagnose the Brugada sign with the 12-lead ECG in sudden unexplained death syndrome survivors and their family members because the ECG could be transiently normalized. We proposed using the higher intercostal space V(1) to V(3) lead ECG, together with procainamide to detect the Brugada sign. METHODS AND RESULTS: Among 20 ventricular fibrillation cardiac arrest patients, 13 sudden unexplained death syndrome survivors and their relatives (n=88) were studied using the single standard 12-lead ECG and the new six higher intercostal space V(1) to V(3) lead ECG (-V(1) to -V(3) and -2V(1) to -2V(3)). Ten sudden unexplained death syndrome survivors and relatives (n=48) who had a normalized ECG were also infused with procainamide (10 mg x kg(-1)i.v.) to unmask the Brugada sign and both ECG methods were recorded. Forty healthy individuals and 13 spouses served as the control group. Prior to the procainamide infusion, the Brugada sign could be detected in nine sudden unexplained death syndrome survivors (69.2%) and three (3.4%) relatives with the standard ECG and in 12 (92.3%) and nine (10.2%) with the new six-lead ECG. After the procainamide infusion, the Brugada sign could be demonstrated in seven sudden unexplained death syndrome survivors (70%) and seven (14.6%) relatives with the standard ECG and in nine (90%) (P=0.26) and 23 (47.9%) (P=0.0004) with the new six-lead ECG, respectively. All the controls were negative for the Brugada sign. CONCLUSIONS: Our data suggest that the new higher intercostal space lead ECG, with or without the procainamide test is helpful in detecting the Brugada sign in sudden unexplained death syndrome survivors and their relatives.

Anti-Arrhythmia Agents↗
PubMed1978

Exacerbation of coronary occlusion induced ventricular arrhythmias by the vagolytic effect of procainamide.

The influence of the vagolytic effect of procainamide on the early ventricular arrhythmias induced by left anterior descending coronary (LAD) occlusion was studied in chloraloseanaesthetised cats. All control animals developed a ventricular arrhythmia (1119 +/- 166 PVCs per hour), with a consistent onset time, duration, and overall mortality due to ventricular fibrillation (ie 20%). In 18 animals pretreated with procainamide (0.5 mg.kg-1.min-1 for 50 min), there was no effect on the ventricular arrhythmia in terms of ectopic frequency (1020 +/- 180 PVCs per hour), time to onset of arrhythmia, duration of arrhythmia, and mortality incidence (ie 16.7%). However, subdividing the data according to whether or not vagal blockade had been produced by procainamide revealed that animals exhibiting complete vagal blockade demonstrated significantly more ectopic beats (1606 +/- 310 PVCs per hour) and 33% developed ventricular fibrillation. Treated animals without complete vagal blockade exhibited an ectopic frequency rate of 620 +/- 98 PVCs per hour and none of the animals developed ventricular fibrillation. The haemodynamic parameters were similar between both procainamide treated subgroups. These results suggest that an important factor in response of the ischaemic heart to the cardiac rhythm effects of procainamide is the degree of vagal blockade induced by this agent.

Animals↗