Effect of subendocardial resection on sinus rhythm endocardial electrogram abnormalities.

BACKGROUND: Patients with sustained ventricular tachycardia after acute myocardial infarction frequently have characteristic abnormalities of left ventricular endocardial electrical activity, including fractionated (prolonged, multicomponent, low-amplitude), split (having discrete widely separated deflections), and late (extending after the end of the QRS complex) electrograms. The exact cause and source of these electrograms are not clear. METHODS AND RESULTS: In this study, endocardial electrograms from 18 patients were recorded with a 20-electrode array from the same area immediately before and immediately after resection of subendocardial tissue at the time of surgery for ventricular tachycardia. Electrograms could be compared before and after resection from 298 of 360 (83%) of the electrodes. Before resection, split electrograms were present in 130 (44%) and late components in 81 (27%) of the recordings. Recordings made after resection showed fewer abnormalities, including complete absence of split electrograms as well as all previously recorded late components (P < .02). Mean electrogram amplitude increased from 0.5 +/- 0.8 to 1.0 +/- 1.6 mV (P < .0001) because of removal of the attenuating effect of endocardial scar; mean duration decreased from 112 +/- 38 to 65 +/- 27 ms (P < .0001) mainly because of loss of late and split components. Overall electrogram contour was very similar aside from these changes. CONCLUSIONS: These data show that (1) some of the signal recorded on the endocardial surface is derived from deeper tissue layers and (2) split and late electrogram components appear to be generated by cells in the superficial endocardial layers, since they are eradicated by removal of this tissue. These findings correspond well with previous histological studies of resection specimens that show bundles of surviving muscle cells separated by layers of dense scar that act as an insulator.

Usefulness of the delta HA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias.

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HApace-HAsvt) was found to accurately distinguish AV nodal SVT (delta HA greater than 0 ms) from orthodromic SVT (delta HA less than -27 ms). An intermediate value of delta HA = -10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with delta HA intervals greater than -10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.

Sinus mapping in patients with cardiac arrest and coronary disease--results and correlation with outcome.

Electrophysiological testing and left ventricular endocardial mapping in sinus rhythm were performed in 61 patients with coronary artery disease who presented with cardiac arrest in an attempt to relate the results of these studies to clinical outcome. Forty-one patients (67%) had inducible sustained arrhythmias (18 uniform ventricular tachycardia, 23 polymorphic ventricular tachycardia/ventricular fibrillation) and 20 had no inducible arrhythmia. Patients with inducible arrhythmia had 45% abnormal and 6% fractionated electrograms versus 31% and 0% for those without inducible arrhythmia (P greater than 0.05 for both comparisons). Sixteen of 59 patients (27%) with adequate follow-up had arrhythmia recurrence (11/39 [31%] with inducible arrhythmia and 5/20 [25%] without inducible arrhythmia) over a mean follow-up period of 27 months. Of five patients without inducible arrhythmia who experienced recurrence, two did so despite the anti-ischemic therapy. In the 20 patients without inducible arrhythmia, the 15 who remained arrhythmia-free had a mean of 78 +/- 22% normal sites versus 46 +/- 24% normal sites in those with recurrence (P greater than 0.05). We conclude that in patients with coronary artery disease and cardiac arrest: 1) patients without inducible arrhythmia have less marked endocardial electrical abnormality than those with inducible arrhythmia, 2) those patients who have marked endocardial abnormality despite the lack of inducible arrhythmia are at risk for clinical recurrence which suggests that these abnormalities may represent an anatomic substrate for arrhythmia which cannot be identified by programmed stimulation. These patients are candidates for AICD implantation and 3) patients with relatively normal endocardial electrograms do well with anti-ischemic therapy alone.

Nonuniform recovery of excitability in the left ventricle.

The purpose of this study was to determine left ventricular activation, dispersion of refractoriness, and total recovery time in patients with coronary artery disease and ventricular tachycardia and in patients with the long QT syndrome and to compare these patients with a group of normal patients. Left ventricular endocardial catheter mapping and left ventricular refractory period determination were performed in 18 patients. Group 1 consisted of seven patients with no heart disease and no arrhythmia; group 2 consisted of six patients with previous infarction and sustained ventricular tachycardia; and group 3 consisted of five patients with prolonged QT interval and previous cardiac arrest. Total left ventricular endocardial activation was significantly longer in group 2 (75 +/- 23 msec, mean +/- SD) compared with group 1 (34 +/- 9 msec, p less than 0.01) and group 3 (42 +/- 5 msec, p less than 0.05). Dispersion of refractoriness was significantly greater in group 3 (87 +/- 27 msec) than in group 1 (40 +/- 14 msec, p less than 0.01) and group 2 (53 +/- 14 msec, p less than 0.05). Dispersion of total recovery time was significantly greater in group 2 (90 +/- 30 msec) than in group 1 (52 +/- 14 msec, p less than 0.05) as well as group 3 (114 +/- 43 msec) compared with group 1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anterior left ventricular aneurysm: factors associated with the development of sustained ventricular tachycardia.

Fifty patients with anteroapical left ventricular aneurysm secondary to prior myocardial infarction underwent aneurysmectomy, at which time endocardial sinus rhythm mapping was performed. Forty patients had a history of recurrent sustained monomorphic ventricular tachycardia, and 10 had an aneurysm but no history of spontaneous sustained tachycardia. A comparison of the clinical, angiographic and sinus rhythm endocardial electrographic characteristics of these two groups revealed that the patients without spontaneous ventricular tachycardia had more severe coronary artery disease (2.6 +/- 0.5 versus 1.9 +/- 0.8 coronary arteries having greater than 70% stenosis; p less than 0.03), underwent surgery earlier after infarction (3 +/- 2 versus 46 +/- 53 months; p less than 0.03) and had less extensive wall motion abnormalities on contrast ventriculography (0 of 8 versus 13 of 35 patients assessed had an abnormally contracting ventriculographic segment length greater than 60%; p less than 0.04). During intraoperative programmed electrical stimulation, all 40 patients with and 4 of 10 without a history of spontaneous ventricular tachycardia had inducible tachycardia. The patients with inducible tachycardia had a larger area of endocardium from which abnormal electrograms (duration greater than 70 ms or amplitude less than 0.7 mV) were recorded (62 +/- 17 versus 45 +/- 20% of electrograms; p less than 0.03) as well as fractionated (duration greater than 90 ms, amplitude less than 0.3 mV) electrograms (20 +/- 14 versus 9 +/- 7% of electrograms; p less than 0.04) than did patients without inducible tachycardia, but there were no angiographic differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental myocardial cryoinjury: local electromechanical changes, arrhythmogenicity, and methods for determining depth of injury.

To characterize the electromechanical effects of acute and 2-week-old cryoinjury, programmed stimulation and epicardial M-mode echo mapping (7.5 mHz) were performed prior to, at 15 minutes and 15 +/- 2 days after cryoinjury in 10 dogs. Epicardial and intramural bipolar and unipolar electrograms were recorded in five of the dogs. Cryoinjury was produced with a 5 mm in diameter flat cryoprobe at -60 degrees C applied to the left ventricular epicardium for 10 minutes at each of six contiguous sites. Cryoinjury, acutely and at 2 weeks, was characterized by a loss of normal intramural systolic thickening and a decrease in echo density. The maximum depth of cryoinjury determined by echo ranged from .55 to .85 cm acutely, and .50 to .80 cm chronically and it correlated acutely and chronically (r = .80; r = .85) with pathologically documented depth of cryoinjury at 2 weeks. Acutely, the presence of either an abnormal intramural unipolar or bipolar electrogram also defined the depth of cryoinjury within .16 cm. In contrast, epicardial electrograms were not useful for judging depth of cryoinjury. A QS complex on the epicardial unipolar electrogram was recorded over the cryoinjury acutely and at 2 weeks in four of five dogs despite preserved subendocardial systolic wall thickening and normal histology extending 40 to 65% of the wall thickness. Epicardial bipolar electrograms uniformly showed a marked decrease in amplitude and slope of the intrinsic deflection, a small but insignificant increase in width and no multicomponent activity. Ventricular fibrillation was reproducibly initiated with three ventricular extrastimuli in five of 10 dogs at 2 weeks. No ventricular tachycardia was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'.

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.

Amiodarone versus amiodarone and a type IA agent for treatment of patients with rapid ventricular tachycardia.

Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 +/- 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 +/- 2.0 micrograms/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 +/- 30 to 352 +/- 46 msec (p less than .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p less than .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 +/- 10 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Improved results in the operative management of ventricular tachycardia related to inferior wall infarction. Importance of the annular isthmus.

Ventricular tachycardia associated with inferior wall myocardial infarction has had a lower surgical cure rate with localized subendocardial resection than ventricular tachycardia related to anterior infarction. Some investigators have advocated visually directed extensive subendocardial resection, including resection of the papillary muscles and mitral valve replacement, even without documenting the origin of ventricular tachycardia at these sites. We have operated on 46 patients (43 men and three women) for ventricular tachycardia associated with inferior wall myocardial infarction. Thirty-one consecutive patients (Group I) had standard localized subendocardial resection. Two patients in this group had mitral valve replacement for mitral insufficiency. Fifteen consecutive recent patients (Group II) underwent subendocardial resection plus focal endocardial cryoablation (3 minutes at -70 degrees C) of the annular isthmus. The annular isthmus is defined as the ventricular muscle between the basal end of the ventriculotomy and the mitral valve anulus. In Group I there were four operative deaths (13%). Ventricular tachycardia was noninducible in 15 of 27 operative survivors (56%) at postoperative electrophysiologic studies. In Group II there was one operative death (7%) and 13 of 14 survivors (93%) had no inducible ventricular tachycardia at postoperative electrophysiologic studies (p less than 0.01 versus Group I). No Group II patient required mitral valve replacement. Six operative survivors in Group II had intraoperative activation maps consistent with macroreentry incorporating the annular isthmus. Group I and Group II were indistinguishable in terms of preoperative hemodynamics, number of coronary arteries diseased, or the presence of left ventricular aneurysm. These results suggest that subendocardial resection with additional cryoablation of the annular isthmus results in improved control of ventricular tachycardia in patients with ventricular tachycardia associated with inferior wall myocardial infarction. Mitral valve replacement is not required unless intrinsic mitral valve disease is present. These data also suggest that the annular isthmus is a critical component of the reentrant circuit in these tachycardias.

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia.

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI. Total electrical activity recorded during sinus rhythm was 164 +/- 46 ms in inferior and 144 +/- 28 ms in anterior AMI (p = 0.05). Nine of the 10 patients with inferior AMI had complete activation of the anterior wall within the initial one-half of the QRS complex, compared with only 15 of the 27 patients with anterior AMI (p = 0.05). All 10 patients with inferior AMI had activation of the ventricular septum within the initial half of the QRS complex compared with only 13 of 27 with anterior AMI (p less than 0.005). None of the patients with inferior AMI had activation of the inferoposterior base within the initial one-half of the QRS complex, compared with 21 of 27 patients with anterior AMI (p less than 0.001). Complete activation of the anterior wall occurred at 33 +/- 15 ms in inferior and 58 +/- 30 ms in anterior AMI (p less than 0.005). Complete activation of the septum occurred at 38 +/- 12 ms in inferior and 63 +/- 28 ms in anterior AMI (p less than 0.005). Complete activation of the inferoposterior base occurred at 100 +/- 38 ms in inferior and 50 +/- 21 ms in anterior AMI (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease.

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Intermittent failure of local conduction during ventricular tachycardia.

Forty-three patients with sustained ventricular tachycardia (VT) caused by prior myocardial infarction underwent intraoperative endocardial activation mapping during a total of 122 episodes of VT. Electrograms obtained during mapping were analyzed to determine the prevalence of local conduction failure during VT (defined as a portion of the local electrogram that did not repeat with every tachycardia cycle). Local conduction failure during VT was observed in 37 (86%) patients and 73 (65%) tachycardias. VT in which local conduction failure was observed were faster than VTs without local conduction failure (cycle length 315 vs 345 msec; p less than .05). Local conduction failure occurred most frequently at or near sites having the earliest recorded electrical activity during VT ("site of origin"). Twenty-three patients also had sinus rhythm endocardial mapping at the time of surgery. Areas with abnormal or fractionated electrograms in sinus rhythm were more likely to demonstrate local conduction failure in VT than areas with normal electrograms in sinus rhythm (16% vs 8%; p less than .01). Although the mechanism responsible for local conduction failure in VT is unclear, it is a common occurrence and is significant in that it can occasionally mimic "early" sites of endocardial activation, unless enough VT cycles are observed at a given site.

Relation of late potentials to site of origin of ventricular tachycardia associated with coronary heart disease.

Signal-averaged electrocardiograms and endocardial catheter mapping were performed in 41 patients with coronary artery disease and sustained ventricular tachycardia (VT) to determine the relation between signal-averaged late potentials (SA-LPs) and catheter-mapped late activity (CM-LA) to the site of origin of VT. The 41 patients had 79 morphologically distinct VTs. Either CM-LA or SA-LP was present during sinus rhythm in 37 of 41 patients (90%). Twenty-two out of 30 patients (73%) had CM-LA corresponding to SA-LP during normal sinus rhythm. Patients with SA-LP had a significantly greater number of sites of CM-LA, which were later and longer in duration than patients without SA-LP present during sinus rhythm. In a select group of patients, those with both SA-LP and CM-LA, the site of origin of VT was located at or adjacent to a site of CM-LA during sinus rhythm in 38 of 44 (86%); however, 36 of 78 sites (46%) of CM-LA were clearly distant from the site of origin of VT. In conclusion, CM-LA corresponding to SA-LP in patients with VT is sensitive but not specific for the site of origin of VT.

Catheter mapping during sinus rhythm: relation of local electrogram duration to ventricular tachycardia cycle length.

Catheter mapping was performed during sinus rhythm in 52 patients with 102 morphologically distinct ventricular tachycardias (VT). Twenty patients had a single VT morphologic pattern. The cycle length of VT was correlated with the duration of all electrograms and various electrogram subgroups, including abnormal, fractionated, late, and longest electrograms, as well as the electrogram recorded at the site of origin of VT and at sites other than the site of origin using linear regression analysis. No correlation was found between local electrogram duration of any of these groups and VT cycle length. There was no relation regardless of whether the patient had a single or multiple morphologic patterns. Thus, the local electrogram duration measured with catheter mapping during sinus rhythm does not correlate with VT cycle length. This finding provides additional support that catheter mapping during sinus rhythm does not give sufficient information to guide localized endocardial resection for VT surgery.

Use of programmed electrical stimulation to predict sudden death after myocardial infarction.

The use of programmed ventricular stimulation to identify patients at risk for sudden cardiac death following myocardial infarction has not yet been firmly established. The repetitive ventricular response following extrastimuli does not appear to be useful in identifying patients at risk and should not be used to guide antiarrhythmic therapy. Similarly, the response to single and/or double ventricular extrastimuli delivered at twice diastolic threshold from a single right ventricular site during normal sinus rhythm and ventricular pacing also does not appear to be helpful in identifying patients at risk for life-threatening ventricular arrhythmias. A more vigorous stimulation protocol that involves more than one right ventricular site and increased current strength may be necessary to elicit a predictive electrophysiologic response. The need for a more vigorous stimulation is suggested by two preliminary studies. Confirmation of initial reports is necessary. The predictive value of the response to programmed ventricular stimulation must be compared with other noninvasive and invasive measurements of left ventricular dysfunction and the degree of spontaneous ventricular ectopy to determine its superiority or to ascertain multiple variables that can be used together to identify those patients most likely to die suddenly after myocardial infarction. Stimulation protocols used during programmed stimulation must have sufficient sensitivity without sacrificing specificity. A concerted effort using uniform stimulation protocols in large numbers of patients is essential to resolve this important clinical problem.

Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)