Body-Surface Distribution of Changes in Activation-Recovery Intervals Before and After Catheter Ablation in Patients With Wolff-Parkinson-White Syndrome
Clinical Evidence for Ventricular ‘Electrical Remodeling’ With Prolongation of Action-Potential Duration Over a Preexcited Area
Background T-wave abnormalities after catheter ablation in patients with manifest Wolff-Parkinson-White (WPW) syndrome have been attributed to a continuation of repolarization abnormalities induced by preexcitation (cardiac memory).
Methods and Results To clarify changes in repolarization properties, we analyzed the activation-recovery interval (ARI) obtained from body-surface maps and the relationship between the activation time (AT) and ARI in 30 patients with WPW syndrome (group A, 18 patients with manifest left-sided accessory pathway; group B, 7 patients with manifest right-sided accessory pathway; and group C, 5 patients with concealed left-sided accessory pathway) before, 1 day after, and 1 week after ablation. The ARI significantly decreased 1 week after ablation compared with before and 1 day after ablation over the preexcited area in groups A and B. Correlation coefficients between the AT and ARI showed a significantly (P<.01) stronger inverse relationship before (r=−.58) and 1 week after (r=−.64) ablation than 1 day after ablation (r=−.46) in groups A and B. In group C, the ARI and correlation coefficients between the AT and ARI showed no significant changes.
Conclusions These findings suggest a prolongation of the action-potential duration over the preexcited area before and just after ablation as ventricular “electrical remodeling,” a decrease in the inverse relationship between the AT and action-potential duration 1 day after ablation, and a gradual recovery of the action-potential duration over the preexcited area and inverse relationship 1 week after ablation.
Radiofrequency CA is a principal form of therapy for supraventricular tachyarrhythmias in patients with WPW syndrome.1 Marked T-wave abnormalities on 12-lead ECGs are often present in patients with manifest WPW syndrome after CA, after which these abnormalities gradually disappear.2 3 Kalbfleisch et al2 proposed that these postablation repolarization abnormalities were due to cardiac memory, as introduced by Rosenbaum et al.4 We5 6 have shown by QRST isointegral maps that there are abnormalities in repolarization properties before and 1 day after CA with a small difference over the preexcited area and that the abnormalities gradually disappeared days or weeks after CA in patients with manifest WPW syndrome. However, it is not clear how the parameters of repolarization change before and after CA or in which of these parameters changes occur. Toyoshima and Burgess7 showed that changes of the activation sequence can modulate the local APD by electrotonic interaction. Costard-Jäckle et al8 demonstrated an inverse relation between the AT and the APD in isolated rabbit hearts. This inverse relation diminished after alteration of the ventricular activation sequence and gradually recovered in association with prolongation of the activation sequence. Furthermore, the cardiac-surface ARI has been demonstrated to correlate closely to the local APD.9 The feasibility of measuring the ARI on body-surface ECGs to estimate the cardiac-surface APD has also been reported.10 11 12 13 Furthermore, it has been reported that body-surface ARIs appeared to be correlated with epicardial measures of repolarization in a torso-shaped electric tank model.10 11 Yamaki et al12 13 , on examining the body-surface distribution of the ARI in normal subjects and patients with old myocardial infarction, showed that the distribution of abnormally long ARIs could reflect the severity of arrhythmia and ischemia. However, no studies have analyzed the ARI obtained from body-surface maps in patients with WPW syndrome before and after CA. In the present study, we examined the body-surface distribution of the ARI and the relationship between the AT and the ARI to identify changes in repolarization properties in patients with WPW syndrome before and after CA.
We studied 30 patients (18 men and 12 women; mean age, 48±14 years; range, 24 to 69 years) with WPW syndrome who underwent CA and body-surface mapping before, 1 day after, and 1 week after CA at the Nagoya Daini Red Cross Hospital between March 1992 and July 1995. The inclusion criteria for patients with manifest WPW syndrome were (1) presence of a continuous delta wave in >1 lead on 12-lead ECGs, (2) confirmation of antegrade accessory pathway conduction by an electrophysiological study before CA, and (3) absence of accessory pathway conduction and the delta waves after CA. The inclusion criteria for patients with concealed WPW were (1) confirmation of accessory pathway with only retrograde conduction by an electrophysiological study before CA and (2) absence of retrograde accessory pathway conduction in an additional repeat electrophysiological study 1 week after successful CA. Patients were excluded if they had electrolyte imbalances, severe hypertension, another clinically overt heart disease, or bradycardia (<50 bpm) or tachycardia (>100 bpm) at the time of body-surface mapping. Antiarrhythmic drugs were discontinued for ≥5 elimination half-lives before CA. Patients were divided into three groups according to their basal 12-lead ECGs or electrophysiological studies: group A included 18 patients with manifest left-sided accessory pathway; group B included 7 patients with manifest right-sided accessory pathway; and group C included 5 patients with concealed left-sided accessory pathway. Informed consent was obtained from all subjects before they entered the study.
Electrophysiological Study and CA
Radiofrequency CA was performed on 30 patients at the Daini Red Cross Hospital. Multiple 6F multipolar electrode catheters were introduced percutaneously into the femoral and subclavian veins for electrophysiological studies. For ablation of the accessory pathway, a 7F steerable, quadripolar electrode catheter with a 4-mm tip electrode (EPT) was inserted through the right femoral vein or artery. Ablation procedures were defined as successful if the antegrade and retrograde accessory AV conductions were completely abolished in patients with manifest WPW syndrome or if the retrograde accessory AV conductions were no longer present in patients with concealed WPW syndrome. The location of accessory pathways was determined from the position of the catheter at a successfully ablated site in right- and left-anterior-oblique fluoroscopic views. The creatine kinase–MB fraction was measured every 4 hours for 24 hours after the procedure.
Body-surface ECGs were recorded to construct body-surface maps by use of a VCM-3000 (Chunichi Denshi Company). Because the details of data acquisition and processing have been described elsewhere,14 we discuss them only briefly. Unipolar ECGs were recorded simultaneously from 87 lead points on the chest surface (59 and 28 lead points on the anterior and posterior chest, respectively) with reference to Wilson’s central terminal. Standard 12-lead ECGs and the Frank X, Y, and Z ECGs were also recorded simultaneously. These ECG data were scanned by multiplexers and digitized by analog-to-digital convertors at a rate of 1000 samples per second. After a two-point baseline adjustment using the flat portion of the TP segment, these data were stored on floppy disks. Data sampling was performed at the expiratory level with the subject in the supine position before, 1 day after, and 1 week after CA.
The mapping data were transferred to a personal computer (PC-9821 AP, NEC) with an analysis program developed at our institution. A root-mean-square voltage-versus-time curve based on the 87 leads was plotted to help identify the beginning of QRS and the end of T deflection, which were manually selected from this curve. The AT was defined as the duration between the QRS onset and the minimum dV/dt of the QRS wave. The ARI was defined as the interval between the minimum dV/dt of the QRS wave and the maximum dV/dt of the T wave.9 The maximum and minimum dV/dt points determined by the computer were checked visually and edited manually according to a previous report9 in a blinded fashion by two cardiologists.
The QRST value was calculated by integrating each lead over the appropriate interval as previously described.5 14 To construct QRST I-departure maps, the mean and SD values of the normal QRST at each lead point were calculated from data collected from control subjects. The control subjects were 607 normal individuals (376 men and 231 women; mean age, 42 years; age range, 17 to 81 years) who were registered by the Japanese Circulation Society Task Force Committee on Body Surface Mapping.15 The departure index at each lead was calculated with the VCM-3000 as follows: Departure Index=(x−mean)/SD, where x represents the QRST at the corresponding lead for each patient.16 Areas in which the departure index values were <−2 and >2 on the departure map were designated as −2SD areas and +2SD areas, respectively.
Values are expressed as mean±SD. Differences among groups were analyzed by one-way ANOVA, and intragroup comparisons were performed by use of ANOVA for repeated measures followed by Scheffé’s test. A value of P<.05 was considered statistically significant.
There were no significant differences among groups in age, sex, total energy delivered, or heart rate before, 1 day after, and 1 week after CA (Table 1⇓). No abnormal increase in the creatine kinase–MB fraction was observed after CA.
ARI Map in a Patient With Manifest WPW Syndrome and Right-Sided Accessory Pathway
Fig 1⇓ shows the 12-lead ECGs and the ARI map before CA of a representative patient from group B in whom ablation of the right posterior accessory pathway proved successful. In 12-lead ECGs (Fig 1A⇓), there were negative delta waves in leads III, aVF, and V1. In the ARI map (Fig 1B⇓), the longest duration was located over the right clavicular area and the shortest was over the midanterior chest. In the I-departure map (not shown), the −2SD area was distributed over the right lower chest and the +2SD area was located over the upper chest. Fig 2⇓ shows the 12-lead ECGs and the ARI map 1 day after CA of the same patient as in Fig 1⇓. In 12-lead ECGs (Fig 2A⇓), the delta waves had disappeared, and there were normally directed QRS deflections with negative T waves in leads III and aVF. Although the configuration of 12-lead ECGs after CA differed from that before CA, the ARI map (Fig 2B⇓) and the I-departure map were similar to those before CA. Fig 3⇓ shows the 12-lead ECGs and the ARI map 1 week after CA of the same patient as in Fig 1⇓. In the 12-lead ECGs (Fig 3A⇓), negative T waves in leads III and aVF had disappeared. In the ARI map (Fig 3B⇓), the ARI decreased over the right lower chest 1 week after CA compared with before and 1 day after CA. In the I-departure map, the −2SD and +2SD areas had disappeared.
ARI Map in a Patient With Manifest WPW Syndrome and Left-Sided Accessory Pathway
Fig 4⇓ shows the ARI maps before, 1 day after, and 1 week after CA of a representative patient from group A in whom ablation of the left posterior accessory pathway proved successful. In the ARI map before CA (Fig 4A⇓), the longest duration was located over the right upper chest and the shortest duration over the midanterior chest. The ARI map 1 day after CA (Fig 4B⇓) was similar to those before CA. The ARI decreased over the lower back 1 week after CA compared with before and 1 day after CA (Fig 4C⇓). In the I-departure map before and 1 day after CA, the −2SD area was over the back and the +2SD area over the right anterior upper chest. The −2SD and +2SD areas had disappeared 1 week after CA.
ARI Map in a Patient With Concealed WPW Syndrome
Fig 5⇓ shows the ARI maps of a representative patient from group C in whom ablation of the concealed left posterior accessory pathway proved successful. There were few changes in the ARI maps before, 1 day after, and 1 week after CA. There was no −2SD or +2SD area before, 1 day after, or 1 week after CA in the I-departure map.
Changes in ARI on Body-Surface Maps
Fig 6⇓ shows the body-surface distribution of leads in which the ARI showed significant changes before, 1 day after, and 1 week after CA. There were no significant changes in the ARI between before and 1 day after CA in any group. In group A, the ARI significantly decreased over the back and increased over the right anterior upper chest 1 week after CA compared with before CA. QRST values significantly increased over the back and decreased over the right anterior chest 1 week after CA compared with before and 1 day after CA. In group B, the ARI significantly decreased over the lower chest and increased over the upper chest 1 week after CA compared with before CA. QRST values significantly increased over the lower chest and decreased over the upper chest 1 week after CA compared with before and 1 day after CA. In both groups A and B, the distribution of significant decreases and increases in the ARI corresponded to the distribution of significant increases and decreases in QRST values. In group C, there were no significant differences in the ARI and QRST values before, 1 day after, and 1 week after CA.
Table 2⇓ shows the ARI data in one lead point in which the ARI showed the largest decrease 1 week after CA compared with before and 1 day after CA in groups A and B, with the ARI over the left anterior chest used for a reference in both groups. The ARI significantly decreased 1 week after CA compared with before and 1 day after CA over the preexcited area (the back and right lower chest in groups A and B, respectively). However, there were no significant differences in the ARI over the left anterior chest, where we found no significant changes in QRST values. In group C, there were no significant differences in the ARI before, 1 day after, and 1 week after CA in any lead point.
Changes in Relationship Between AT and ARI
The correlation coefficient between the AT and the ARI (Fig 7⇓) showed a significantly stronger inverse correlation (P<.01) before and 1 week after CA than 1 day after CA in groups A and B (r=−.58, −.46, and −.64 for before, 1 day after, and 1 week after CA, respectively) (Fig 7A⇓). In group C, there was no significant difference in the correlation coefficient before, 1 day after, and 1 week after CA (Fig 7B⇓).
Recent studies have shown that T-wave abnormalities on 12-lead ECGs often appear in patients with manifest WPW syndrome after CA.2 3 Because of the presence of secondary ST-T changes due to preexcitation in patients with manifest WPW syndrome, it is difficult to determine from the 12-lead ECGs whether these abnormalities in repolarization properties are present before CA. Since Wilson et al17 first proposed the concept of the ventricular gradient, a number of studies18 19 20 21 22 23 24 25 have shown that QRST time-integral values are dependent on repolarization properties and largely independent of the activation sequence. We previously analyzed body-surface QRST isointegral maps in patients with WPW syndrome before, 1 day after, and 1 week after CA.5 6 We showed a similarity of QRST isointegral maps with abnormally low QRST values over the preexcited area before compared with immediately after CA. Radiofrequency CA did not significantly influence repolarization properties over areas without preexisting abnormalities. However, it gradually reduced preexisting repolarization abnormalities, which were closely related to the location of the antegrade AV accessory connection.6 These repolarization abnormalities found after CA have been attributed to both the presence of an abnormal activation sequence before CA and to cardiac memory.2 3 In the present study, the ARI over the preexcited area (the lower chest in patients with right-sided accessory pathway and the left back in patients with left-sided accessory pathway) was significantly longer before and 1 day after CA compared with 1 week after CA. Body-surface distribution of significant changes in the ARI corresponded with the previously reported distribution of significant differences in QRST values after CA.6 We also found a significantly stronger inverse relationship between the AT and the ARI before and 1 week after CA compared with 1 day after CA. The APD over the preexcited area might be prolonged before and just after CA and then decrease 1 week after CA. These findings suggest that T-wave changes after CA result in part from cardiac memory of a prolonged APD over the preexcited area. The inverse relationship between AT and APD might have decreased 1 day after CA and then gradually recovered 1 week after CA. These APD prolongations over the preexcited area might be called “electrical remodeling”26 in the ventricular myocardium induced by and adapted to preexcitation.
ARI Obtained From Body-Surface Maps
Although the ARI has been reported to be a good estimate of the APD and refractory periods in animal epicardial and intramural experiments,9 27 28 29 30 a human epicardial study,31 and a computer simulation model,32 there have been few studies on the feasibility of determining the ARI from the body surface.10 11 12 13 Haws and Lux9 demonstrated that the ARI measured over the epicardium is a good estimate of the local APD even during ectopic pacing in dogs. El-Sherif et al29 reported that ARIs were significantly (r=.99) related to effective refractory periods measured at canine epicardial, endocardial, and intramural sites. Ikeno et al28 showed that the cardiac-surface ARIs over distant sites were insensitive to local temperature alteration or ischemia in animal experiments, despite remarkable changes in ECG waveform. Steinhaus32 used computer simulation to demonstrate that the minimum dV/dt of QRS deflection and maximum dV/dt of the T wave are good estimates of activation and recovery time in unipolar electrograms.
Shimizu et al33 measured the recovery time (the interval between the QRS onset and the maximum dV/dt of the T wave, ie, the sum of the AT and the ARI) on the body surface in patients with congenital long-QT syndrome. They found that the recovery-time dispersions were significantly longer in patients with long-QT syndrome than in the control group and that the recovery time calculated by the maximum dV/dt from body-surface ECGs might provide clinically useful information on the disparity in recovery that could not be obtained from QT-interval analysis. Burgess et al10 compared the ARI calculated over the torso with refractory periods measured on the epicardium. They found that the ARI over the torso accurately represents epicardial refractory periods within several centimeters from the epicardial surface. Lux et al11 also reported that body-surface ARIs appeared to be correlated with epicardial measures of repolarization in a torso-shaped electric tank model. Yamaki et al13 examined the body-surface distribution of ARIs in normal subjects and patients with old myocardial infarction. They attributed a greater ARI over the right upper chest to a longer APD on the endocardium and a smaller ARI over the left anterior chest to a shorter APD on the apical epicardium, a finding consistent with ARI distribution in the present study. They also suggested that the distribution of the ARI could reflect the severity of arrhythmia and coronary stenosis in patients with myocardial infarction. These findings support the feasibility of the body-surface ARI as a noninvasive estimation of the APD. Because it is impossible to repeatedly measure the APD or ARI from epicardial electrograms in closed-chest patients, the body-surface ARI may be clinically useful for a noninvasive estimation of repolarization properties in the human heart.
Relationship Between Repolarization Abnormalities and Accessory Pathway Location
Recently, it has been reported that an altered activation sequence can modulate local repolarization properties due to electrotonic interactions.7 We5 6 previously reported that abnormally low QRST values were present over the left back before and 1 day after CA in patients with manifest WPW syndrome due to left-sided accessory pathway. These abnormal QRST values decreased gradually during the week after CA. In the present study, the ARI significantly decreased over the back 1 week after CA compared with before and 1 day after CA in patients with manifest WPW syndrome due to left-sided accessory pathway. In patients with manifest WPW syndrome due to right-sided accessory pathway, the ARI significantly decreased over the lower chest 1 week after CA compared with before and 1 day after CA where abnormally low QRST values were located before and 1 day after CA.5 6 Thus, the body-surface distribution of significant shortening of the ARI 1 week after CA corresponds with the distribution of abnormally low QRST values before CA. These findings suggest that the APD near the site of the accessory pathway connection during preexcitation is prolonged in part by a downstream effect of electrotonic interaction and gradually decreases with normalization of the activation sequence after CA. The concordance of QRS and T waves in a normal ECG is explained by the fact that the APD is shorter in the epicardium than in the endocardium, resulting in discordant sequences of activation and repolarization between the epicardium and endocardium. ECGs recorded immediately after CA show negative T waves in inferior leads and peaked T waves in V1 and/or V2 leads, respectively, in patients with manifest WPW syndrome due to right- and left-sided accessory pathways. The prolonged APD in the epicardium over the preexcited area may explain these T-wave abnormalities.
In the present study, the ARI significantly increased 1 week after CA compared with before and 1 day after CA over the upper chest and the right upper anterior chest in patients with manifest WPW syndrome due to right- and left-sided accessory pathways, respectively. The reasons for these changes were unclear from this study. However, the changes might be attributable to the disappearance of the cardiac memory with a shortened APD over the areas, resulting in part from the upstream effect of electrotonic interaction during preexcitation. Although previous reports proposed an electrotonic interaction as one of the possible mechanisms for APD changes due to an altered activation sequence, this mechanism alone cannot be responsible for APD changes and their slow modulation. Other mechanisms such as changes in cellular electrical communication with the decrease in intercellular gap junction resistance, the modification of potassium channels, and the appearance of altered gene products for the channels have been postulated.8 34
Inverse Relationship Between AT and ARI
Costard-Jäckle et al8 examined the effect of pacing on the distribution of APDs in nine isolated, Langendorff-perfused rabbit hearts. They found that the APD was inversely related to the AT and that this inverse relationship disappeared when a different activation sequence was initiated with ectopic pacing. However, the inverse relationship was reestablished when ectopic pacing was continued. They attributed these findings to cardiac memory, speculating that the sequence of ventricular activation modulates the sequence of ventricular repolarization by an as-yet-unidentified process with very slow onset and offset characteristics. In the present study, the inverse relationship between the AT and the ARI was stronger before and 1 week after CA than 1 day after CA. The weaker inverse relationship between the AT and the ARI immediately after CA and the gradual postablation increase in the inverse relationship in patients with manifest WPW syndrome were in accordance with the animal experiments.8 The inverse relationship between the AT and the APD has been considered important for the genesis of concordant T waves.35 The present study is the first to show that the inverse relationship between the AT and the ARI on body-surface ECGs changes before and after an alteration of ventricular activation. Furthermore, Chiang et al36 reported that the number of ventricular premature contractions increased 1 day after radiofrequency CA of supraventricular tachycardia. The transient increases in ventricular arrhythmias36 might be induced in part by the weaker inverse relationship between the AT and the ARI immediately after CA, as well as by an altered sympathetic tone after CA.37
Mechanism of Repolarization Abnormalities in Patients With Manifest WPW Syndrome
Rosenbaum et al4 reported that long-lasting alterations in the activation sequence induced long-lasting modulations of the T wave that became apparent only when the normal activation sequence was reestablished. They suggested that modulated T-wave changes show accumulation and memory. T-wave inversions in ECGs have been observed during normal AV conduction after a period of right ventricular pacing in open-chest anesthetized dogs.38 These T-wave inversions disappeared after administration of 4-aminopyridine, a drug that blocks the Ito, but not after administration of lidocaine, a sodium channel blocker. Geller and Rosen39 demonstrated that alterations in the activation sequence induced changes in T waves and action potential that differed between the epicardium and the endocardium of the canine ventricle and that 4-aminopyridine abolished these changes. They suggested that the voltage gradient established by differences between the epicardium and the endocardium in the expression of Ito may contribute to T-wave changes in cardiac memory. Potassium channels consist of subunits with four domains. However, these domains are not linked to each other by peptide bonds.34 40 41 More varied combinations of different domains resulting in changes in channel property may occur in potassium channels than in other channels with tight peptide-bonded domains, such as sodium and calcium channels. Katz34 suggested the modification of potassium channels as a basis for long-lasting repolarization abnormalities and the appearance of altered gene product as an important mechanism for changes in cardiac repolarization. Wijffels et al26 demonstrated that atrial fibrillation begets atrial fibrillation by marked shortening of atrial effective refractory periods reversible within 1 week of sinus rhythm. They called this phenomenon “electrical remodeling” and pointed out changes in gene expression and protein synthesis of ionic channels such as potassium channels as one of the most intriguing possibilities of the underlying mechanisms. We think that the possible prolongation of APD over the preexcited area may be one form of ventricular electrical remodeling triggered by and adapted to preexcitation when we use electrical remodeling as a long-lasting modification of repolarization properties of the myocardium induced by changes in cycle length and/or activation sequence. We did not find direct evidence of the mechanisms of repolarization abnormalities in the present study. However, our data suggest that an altered activation sequence and cardiac memory are responsible for postablation repolarization abnormalities by long-lasting prolongation of the APD over the preexcited area in patients with manifest WPW syndrome.
There are some limitations to this study. First, although electrotonic interaction and the modification of potassium channels have been reported as possible mechanisms of repolarization changes resulting from altered activation, the mechanisms of repolarization changes as well as those of cardiac memory were not fully investigated. These mechanisms remain to be clarified in subsequent studies. Second, although the AT and the ARI showed a significant inverse relationship with leads over the chest, it has been reported in experiments with canine hearts that some body-surface leads located far from the epicardium might not precisely reflect the repolarization measurements. Measurements from body-surface leads near the cardiac surface, on the other hand, have been proposed as reasonably reliable.10 11 We think that a significant change in ARI over the same body-surface lead, even if ARI itself is less accurate in leads distant from the epicardium than in those near the epicardium, may reflect the changes in APD over the epicardium, especially during the same activation sequence. It would be necessary to compare the cardiac- and body-surface ARIs and clarify inadequate body-surface areas for recovery measurements in human subjects. Third, additional studies are needed to provide direct evidence of changes in action potential, such as serial changes in monophasic action potential. However, it is clinically difficult to repeatedly measure the APD over the epicardium after CA.
In the present study, we found that ARIs over the preexcited area significantly decreased 1 week after CA compared with before and 1 day after CA and that the inverse relationship between the AT and the ARI decreased 1 day after CA and was reestablished 1 week after CA. Body-surface distribution of significant changes in the ARI corresponded with the distribution of significant differences in QRST values after CA. No such changes were found in patients with concealed WPW syndrome. These findings suggest that the increased APD over the preexcited area before CA may be one form of ventricular electrical remodeling induced by and adapted to preexcitation and that T-wave changes after CA result in part from cardiac memory of a prolonged APD over the preexcited area. ARIs obtained from body-surface maps may provide useful information on the spatial characteristics of repolarization.
Selected Abbreviations and Acronyms
|−2SD area||=||an area on the departure map in which the departure index value was <−2|
|+2SD area||=||an area on the departure map in which the departure index value was >2|
|Ito||=||transient outward potassium current|
This study was supported in part by a grant-in-aid for general scientific research (07670773) from the Ministry of Education, Science, Sports and Culture of Japan and by a research grant for cardiovascular disease from the Ministry of Health and Welfare of Japan. We are grateful to Nobuyuki Kitagawa, a computer engineer of Fukuda Denshi Co Ltd, for his assistance in processing the data on computer. We appreciate the assistance of Mamoru Ito, Hiroko Ito, Hanako Kawai, Kondo Noriaki, and the staff of the Division of Cardiology of the Daini Red Cross Hospital in performing the study.
Presented in part at the 45th Annual Scientific Session, American College of Cardiology, Orlando, Fla, March 27, 1996.
- Received December 18, 1996.
- Revision received March 10, 1997.
- Accepted March 30, 1997.
- Copyright © 1997 by American Heart Association
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