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Ann Thorac Surg 2008;85:474-480. doi:10.1016/j.athoracsur.2007.09.047
© 2008 The Society of Thoracic Surgeons
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Right arrow Electrophysiology - arrhythmias

Original Articles: Cardiovascular

The Role of Atrial Remodeling for Ablation of Atrial Fibrillation

Herko Grubitzsch, MD*, Alexandro Menes, MD, Diethelm Modersohn, MD, PhD, Wolfgang Konertz, MD, PhD

Department of Cardiovascular Surgery, Charité–Universitätsmedizin Berlin, Campus Charité Mitte, Berlin, Germany

Accepted for publication September 25, 2007.

* Address correspondence to Dr Grubitzsch, Klinik für Kardiovaskuläre Chirurgie, Charité-Universitätsmedizin Berlin, Campus Charité Mitte, Charité-Platz 1, Berlin, 10117, Germany (Email: herko.grubitzsch{at}charite.de).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Atrial fibrillation (AF) causes electrical, contractile, and structural remodeling of the atria. We investigated remodeling in patients undergoing AF ablation.

Methods: Concomitant ablation of permanent AF, lasting 1 to 240 months, was performed in 73 patients (49.3% men) with a mean age of 66 ± 9.1 years undergoing mitral valve operations. Electrical (AF cycle length from surface electrocardiogram), contractile (force of contraction measured at right atrial muscle bundles), and structural (left atrial [LA] diameter from echocardiography) remodeling was assessed. Predictors for rhythm outcome were determined.

Results: Two patients died perioperatively, and 3 died during follow-up. The deaths were not ablation related. At the last follow-up (mean, 12 ± 6.9 months), 47 patients (71.2%) were in sinus rhythm, 41 (62.1%) without antiarrhythmic drugs. Corresponding to cycle length (126 to 247 ms), force (2 to 18 mN/mm2), and LA diameter (37 to 79 mm), atrial remodeling exhibited a wide interindividual variability but no correlation between different remodeling levels. No relationship was found between remodeling and AF duration or LA hemodynamic load. Univariate analysis demonstrated higher force (7 ± 4.2 vs 4 ± 2.8 mN/mm2, p = 0.078), smaller LA diameter (51 ± 7.1 vs 58 ± 10.2 mm, p < 0.05), and shorter AF duration (34 ± 48.7 vs 73 ± 63.0 months, p < 0.05) associated with successful sinus rhythm restoration, whereas logistic regression analysis revealed AF duration (odds ratio, 1.01; 95% confidence interval, 1.00 to 1.02, p = 0.045) and LA diameter (odds ratio, 1.12; 95% confidence interval, 1.02 to 1.23, p = 0.016) as predictors.

Conclusions: Atrial remodeling exhibited a high interindividual variability but no relationship within different remodeling levels, with AF duration or with LA hemodynamic load. However, AF duration and structural remodeling, but not electrical or contractile remodeling, predicted rhythm outcome.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Atrial fibrillation (AF), the most frequent sustained atrial arrhythmia, is associated with an increased risk of stroke and premature death [1, 2]. A significant number of patients requiring cardiac operations, especially mitral valve operations, present with AF [3, 4]. The surgical approach to the treatment of AF was initially introduced as Maze procedure [5]. During the past decade, a less complex operation for concomitant AF treatment using different technologies for tissue ablation and focusing the lesion pattern on the left atrium was developed [6, 7]. Thus, sinus rhythm can be restored in approximately 80% of patients undergoing mitral valve operations and AF ablation [4, 8].

With time, AF induces several changes in atrial myocardium at electrophysiologic, contractile, and structural levels summarized as atrial remodeling and suggested to cause the progression of the arrhythmia [9]. In addition to shortened atrial refractoriness and reduced conduction velocity, a rise in the atrial fibrillatory rate, which can be determined from a surface electrocardiogram (ECG), is characteristic of electrical remodeling [9, 10]. Loss of contractility is the central finding of contractile remodeling [9]. On a cellular level, AF-induced structural changes include increased cell size, accumulation of glycogen, loss of sarcomeres, altered connexin expression, and fragmentation of sarcoplasmic reticulum, among others, whereas macroscopically, structural remodeling is characterized by left atrial dilatation [9].

With reports on depressed atrial contractility in AF patients undergoing cardiac operations [11] or on the predictive role of atrial fibrillatory rate for sinus rhythm conversion after medical AF treatment [12, 13], assessment of atrial remodeling came into focus in clinical medicine. It was postulated that individual quantification of the remodeling process might be useful for predicting treatment efficacy [10]. This study investigated atrial remodeling in patients undergoing mitral valve operations and concomitant AF ablation.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patients and Surgical Procedures
Between January 2003 and February 2006, 73 consecutive patients (49.3% male) with a mean age of 66 ± 9.1 years scheduled for mitral valve operations underwent concomitant AF ablation. All patients had permanent/continuous AF according to established definitions [14, 15], and 11 (15.1%) had a history of thromboembolic events. After obtaining approval of the local Ethics Committee and individual informed consent for the study, preoperative, perioperative, and follow-up data were prospectively entered into an institutional database. Data were retrospectively analyzed.

The detailed procedures of the study cohort are listed in Table 1. Isolated mitral valve surgery was performed in 58.9% (43 of 73) of the patients. For patients who had valve replacement, biologic prostheses were implanted in 84.3% (43 of 51). Standard normothermic cardiopulmonary bypass and warm antegrade blood cardioplegia were used for all procedures.


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  		Table 1 Surgical Procedures
 
The ablation concept used has been described in detail previously [8]. All patients underwent endocardial ablation of the left atrium. Microwave (Flex 4, Guidant Corp, Santa Clara, CA) energy was applied in 42 patients (57.5%) and radiofrequency (Cardioblate, Medtronic Inc, Minneapolis, MN) energy was used in 31 (42.5%), depending on device availability or surgeon’s discretion. The lesion pattern consisted of (1) a box lesion isolating all pulmonary vein ostia, (2) a line into the left atrial appendage, and (3) a line to the mitral valve annulus (P3). The left atrial appendage was oversewn only if there were thrombi inside (n = 2). The probe for transesophageal echocardiography was removed during ablation to avoid esophageal injury.

Perioperative Course and Follow-Up
All patients were anticoagulated with heparin, followed by phenprocoumon, with a target international normalized ratio (INR) of 2.0 to 3.0. After 3 months and stable sinus or atrial-driven pacemaker rhythm in Holter ECG and mechanical atrial function in echocardiogram, anticoagulation treatment was discontinued. Patients with mechanical valve substitutes remained on permanent phenprocoumon therapy (target INR, 3.0 to 4.0). Direct current (DC) shock cardioversion of early recurrent AF was performed if a patient was symptomatic or hemodynamically compromised. Perioperatively, either patient’s preoperative medication (β-blocker) was continued or antiarrhythmic treatment with class III antiarrhythmic drugs (sotalol or amiodarone) was initiated. The decision was left to the discretion of the surgeon. After discharge, the patient’s family physician or cardiologist managed the anticoagulation and antiarrhythmic therapy.

Prospective follow-up was after 3, 6, and 12 months, and annually thereafter. Patients were interviewed and underwent clinical, electrocardiographic, and echocardiographic examination. At the 3- and 12-month follow-up, heart rhythm was monitored by 24-hour Holter ECG. In only 3 patients (4.2%), who were not able to visit the clinic, interviewing was done by telephone, and echocardiographic data were obtained from the referring cardiologist. Any regular atrial-driven rhythm, including atrioventricular (n = 1) and atrial-triggered ventricular (n = 1) pacing, was regarded as sinus rhythm.

Echocardiography
Preoperatively, before discharge and at follow-up, all patients underwent transthoracic echocardiographic examination using the HP Sonos 5500 (Hewlett Packard, Andover, MA). Left atrial and left ventricular (LV) diameter were measured using standard techniques. Left ventricular ejection fraction (LVEF) was assessed by the Simpson method. The presence of mechanical left atrial function was checked using the pulsed-wave signal of diastolic transmitral flow. Maximal flow velocities of E and A waves were measured and the E/A ratio was calculated. Quantification of atrial contractility by transesophageal echocardiography was beyond the scope of this study.

Assessment of Atrial Remodeling
Atrial fibrillatory activity allows individual quantification of electrical remodeling and can be reliably obtained from surface potentials [10]. Before operation, mean fibrillatory rate and corresponding atrial fibrillatory cycle length (AFCL) were determined using a high-gain, high-resolution surface ECG (CardioLink, Getemed, Teltow, Germany). After QRST cancellation, the resulting atrial ECG was down-sampled to 50 Hz, and spectral analysis was performed by fast-Fourier transform. The resulting power spectrum was analyzed in the 3- to 12-Hz (180 to 720 fibrillations/min [fpm]) range. The peak frequency component was converted to the dominant AFCL (AFCL [ms] = 60,000 [ms]/fibrillatory rate [fpm]).

After obtaining additional informed consent, specimens of right atrial appendages were excised before starting cardiopulmonary bypass for assessment of atrial contractile remodeling. Right atrial force of contraction certainly reflects the specific contractile remodeling due to AF, whereas left atrial contractility is also influenced by hemodynamic load (mitral valve disease).

The specimens were placed into cold cardioplegic solution (pH 7.4) containing 2,3-butane-dione-monoxime and delivered to the laboratory immediately. After equilibrating at room temperature, thin myocardial muscle bundles (length, 4 to 10 mm) in parallel with the muscle fiber direction were prepared under microscopic control. The average diameter and corresponding cross sectional area were 0.45 ± 0.03 mm and 2.3 ± 0.15 mm2, respectively. The muscle strips were placed in an organ bath filled and perfused (1 to 2 mL/min) with prewarmed (37°C) modified Tyrode solution (pH 7.4, continuously gassed with 95% oxygen and 5% carbon dioxide), fixed to the chamber with a hanger and attached to a precalibrated force transducer with a silk loop and a stainless steel hook.

After an equilibration period of 20 minutes, the muscles were stretched to nearly 1.0 mN. External field stimulation was performed with rectangular pulses (5 ms, 5% to 10% above threshold) at 1 Hz. Resting tension was increased stepwise by 0.1 mN until the muscle length providing maximal active force generation was reached (Lmax 5.1 ± 0.2 mm). Force of contraction (force) was determined before and after an equilibration period of 30 minutes. Two muscle preparations that showed a force of less than 1.0 mN or a force decline exceeding 5% during this period were excluded from the study.

The left atrial diameter was used as measure for structural remodeling. It was determined by echocardiography using M-mode measurement in the parasternal long axis.

Statistical Analysis
Unless otherwise indicated, data are presented as mean ± standard deviation or absolute and relative frequencies. For comparison between groups, the nonparametric Mann-Whitney test was used for continuous variables and the {chi}2 test for categoric variables. For comparison of follow-up and preoperative data within groups, the nonparametric Wilcoxon rank sum test was applied. Covariation between different remodeling parameters was analyzed by the Pearson product-moment correlation coefficient (r) and the coefficient of determination (r 2). Binary logistic regression analysis was used for identifying factors predicting sinus rhythm conversion. Factors found significant (p < 0.1) on univariate testing were entered in the multivariate analysis to identify independent risk factors. The odds ratios (OR), 95% confidence intervals (CI), and p values were calculated for each risk factor. During follow-up, freedom from recurrent AF was calculated according to the Kaplan-Meier method, and differences were analyzed by log-rank test. All tests of significance were two-tailed, and a value of p < 0.05 was considered significant. Statistical analysis was performed using SPSS 13.0 software (SPSS Inc, Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Baseline Data of the Study Cohort
AF duration was 47 ± 60.9 months (range, 1 to 240 months). At baseline, patients were in New York Heart Association (NYHA) functional class 3.0 ± 0.70 (range, I to IV), but presented mostly with normal LV function according to LVEF (0.51 ± 0.11; range, 0.20 to 0.79) and left ventricular end-diastolic diameter (LVEDD; 55 ± 8.2 mm; range, 36 to 71 mm). Etiology of mitral valve disease was degenerative in 36 patients (49.3%), rheumatic in 23 (31.5%), and functional in 14 (19.2%). Valvular dysfunction was regurgitation in 50 patients (68.5%), mixed lesion in 18 (24.7%), and stenosis in 5 (6.8%). The left atrial hemodynamic load, as referred to left ventricular end-diastolic pressure (LVEDP) or pulmonary capillary wedge pressure (PCWP), was 15 ± 6.8 mm Hg (range, 3 to 38 mm Hg). Coronary artery disease was present in 29 patients (39.7%), pulmonary hypertension in 52 (71.2%), and 11 (15.1%) had a history of thromboembolic events. When evaluated by the logistic European System for Cardiac Operative Risk Evaluation (EuroSCORE), expected perioperative mortality was 9.6% ± 11.35% (range, 1.5% to 61.7%).

Perioperative Course and Follow-Up
Overall, respective times for aortic cross-clamp, cardiopulmonary bypass, and operation were 78 ± 20.8, 110 ± 29.2, and 198 ± 50.9 minutes. Patients were discharged from the hospital after 12 ± 11.3 days. Perioperative morbidity was characterized by reexploration for bleeding in 1 patient, late pericardial effusion in 2, heart failure in 6 necessitating intraaortic balloon pump support in 3 and temporary left ventricular assist device placement in 1, renal failure in 2, and intracerebral hemorrhage in 1. No thromboembolic events occurred. Two patients (2.7%) died within 30 days of operation of cardiac and multiple organ failure. The ablation procedure itself did not cause any injury or death.

Mean follow-up was after 12 ± 6.9 months. Two patients (2.8%) were lost to follow-up, and 3 (4.2%) died, 1 each of heart failure, sudden cardiac death, and multiple organ failure after major abdominal surgery.

Atrial Remodeling
Atrial remodeling was characterized by a wide interindividual variability on electrical (AFCL, 156 ± 22.1 ms; range, 126 to 247 ms), contractile force (6 ± 3.9 mN/mm2; range, 2 to 18 mN/mm2), and structural level (left atrium diameter, 53 ± 9.0 mm; range, 37 to 79 mm). Table 2 illustrates that there was no relationship between AF duration, left atrial hemodynamic load, or measures of remodeling. Furthermore, using covariation analysis, we were unable to detect any association within remodeling criteria between AFCL and force (r = –0.134, r 2 = 0.018, p = 0.290), between AFCL and left atrial diameter (r = 0.054, r 2 = 0.003, p = 0.668), or between force and left atrial diameter (r = 0.221, r 2 = 0.05, p = 0.174).


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  		Table 2 Atrial Remodeling
 
Rhythm Outcome
Figure 1 shows the sinus rhythm prevalence for the overall cohort immediately after operation and during follow-up. Direct current shock cardioversion was performed in 4 patients before discharge and in 2 during follow-up. After 4 months, 1 patient underwent successful interventional ablation of left atrial flutter that was caused by an incomplete mitral isthmus line. Pacemakers were implanted in 3 patients early and in 2 late after operation. At last follow-up, 47 patients (71.2%) were in sinus rhythm, 41 (62.1%) without antiarrhythmic drugs. Characteristic follow-up data are listed in Table 3. Sinus rhythm was associated with improved outcome in NYHA functional class and palpitations. According to transmitral diastolic flow pattern (pulsed-wave Doppler signal), 80.5% of patients with sinus rhythm exhibited normal atrial contraction with an E/A ratio of 2.5 ± 1.01.


Figure 1
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  		Fig 1. Prevalence of sinus rhythm. The lower graph depicts the sinus rhythm conversion rate immediately after operation, whereas the upper graph shows the sinus rhythm conversion rate during follow-up. Figures in the bars indicate absolute frequencies of patients with sinus rhythm. (POD = postoperative day.)

 

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  		Table 3 Follow-Up Data
 
Predictors for Rhythm Outcome
The association of sinus rhythm conversion and measures of atrial remodeling is shown in Figure 2. Whereas the preoperative left atrial diameter was significantly smaller and atrial contractility somewhat greater in patients regaining sinus rhythm, AFCL demonstrated no difference in rhythm outcome. Analysis of the relationship between clinical characteristics and successful AF treatment (Table 4) shows that patients who were in sinus rhythm at last follow-up exhibited significantly shorter preoperative AF duration and presented more frequently with coronary artery disease. In patients without sinus rhythm, there was a nonsignificant trend towards the use of microwave technology for ablation. Logistic regression analysis of factors found significant in univariate testing (AF duration, force, left atrial diameter, presence of coronary artery disease, and ablation technology) revealed only AF duration (OR. 1.01; 95% CI, 1.00 to 1.02; p = 0.045) and left atrial diameter (OR, 1.12; 95% CI, 1.02 to 1.23; p = 0.016) as independent risk factors for AF persistence. Kaplan-Meier estimates (Fig 3) illustrate that freedom from recurrent AF significantly depended on preoperative AF duration and structural remodeling of the left atrium.


Figure 2
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  		Fig 2. Rhythm outcome and atrial remodeling. The graphs show the relationship of (A) electrical, (B) contractile, and (C) structural remodeling and rhythm outcome at the latest follow-up. The range bars show the standard deviation. (AFCL = atrial fibrillatory cycle length; FOC = force of contraction; LA = left atrial; SR = sinus rhythm.)

 

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  		Table 4 Rhythm Outcome and Clinical Characteristics
 

Figure 3
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  		Fig 3. Kaplan-Meier estimates. Freedom from atrial fibrillation (AF) according to (A) preoperative AF of 24 months or less (solid line) and exceeding 24 months duration (dashed line), and (B) left atrial (LA) size of 55 mm or less (solid line) and diameter exceeding 55 mm (dashed line).

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
AF frequently accompanies structural heart disease and occurs in approximately 5% of patients with mitral valve disease per year [3]. Its progressive nature results from electrical, contractile, and structural remodeling of the atria induced by the underlying heart disease and the arrhythmia itself [9]. Individual quantification of the remodeling process was postulated to be useful for predicting treatment efficacy [10]. In this study we investigated atrial remodeling in AF and mitral valve disease and its influence on results of AF ablation.

In addition to preoperative AF duration, we found structural remodeling (left atrial dilatation) predictive for rhythm outcome after AF ablation. In contrast, electrical and contractile remodeling exhibited no influence according to the multifactorial model. For remodeling in general, we were not able to detect any association with AF duration or left atrial hemodynamic load, and we found no relationship among the measures of electrical, contractile, or structural remodeling.

Undoubtedly, compared with sinus rhythm, AF is associated with remarkable alterations on the electrical, contractile, and structural level [9, 11, 16, 17]. During the transition from sinus rhythm to paroxysmal AF and further on to persistent AF, a shortening of the atrial effective refractory period, a reduced conduction velocity, and a rise in atrial fibrillatory rate were shown to be characteristic of electrical remodeling [16, 17]. In persistent AF, a lower frequency was observed with shorter compared with longer AF duration, and the mean AFCL decreased significantly over time [12, 18]. Very recently we found a nonsignificant trend towards shorter AFCL, with longer AF duration in a subset of 52 patients with persistent AF [unpublished data].

A reason why this and other reports [17] have failed to demonstrate a relationship between AF duration and fibrillation frequency could be that AFCL in longer-lasting AF (>3 months) is often near the physiologic frequency limit, rendering detection of significant differences difficult. Some studies showed that atrial fibrillatory frequency predicted sinus rhythm conversion after treatment with antiarrhythmic drugs [12, 13]. It can be concluded from these reports that the "AF conversion threshold" ranges between 250 and 300 ms of AFCL with drug-induced frequency reduction. The cycle length in our patients who either regained sinus rhythm (155 ± 23.2 ms) or did not (150 ± 16.0 ms) was far from this threshold and did not exceed 247 ms at baseline, which may explain why we were not able to demonstrate an influence on sinus rhythm conversion.

Compared with sinus rhythm (data not shown), atrial contractility was significantly depressed in patients with persistent AF; this is probably due to quantitative or functional changes, or both, of the L-type Ca2+ channel [11]. Echocardiographic studies after cardioversion have shown that atrial contractile dysfunction recovered completely within 24 hours of sinus rhythm when AF lasted 2 weeks, whereas recovery took more than 1 month when AF lasted more than 6 weeks [19]. We, however, were unable to demonstrate a relationship between force and AF duration; furthermore, contractility was not associated with other remodeling parameters or hemodynamic stress. As for AFCL, detection of significant differences or relationships might have failed because contractile dysfunction was advanced and near its nadir. Regarding the lack of any association between contractility and left atrial load, it should be taken into account that force was measured on right atrial tissue. The weak trend in univariate analysis toward better atrial contractility in patients who regained sinus rhythm (Fig 2) could reinforce the idea that AF could be easier to terminate in patients with an earlier stage of contractile remodeling.

AF-dependent loss of contractility causes atrial dilatation, the most prominent sign of structural remodeling [20] and vice versa, enlargement and the associated fibrosis of the atria perpetuate the susceptibility to AF [9]. This vicious circle is exacerbated by mitral valve disease, which by left atrial pressure increase stimulates left atrial dilatation, explaining its association with AF [3].

Structural remodeling usually develops after months, whereas electrical and contractile remodeling occurs immediately after AF initiation [9]. Similarly, electrical remodeling after reestablishing sinus rhythm reverses rapidly and completely, whereas renormalization of structural remodeling takes time and is possibly incomplete [21]. Therefore, it was hypothesized that structural changes are an important factor for the development of permanent AF [9]. Recent reports [8, 13, 22–24] and our findings (Fig 3B) strongly suggest that they are an important predictor for AF termination as well.

Although well-defined animal experiments of short-term AF were able to demonstrate a close relation between different levels of remodeling [25], clinical studies have failed to do so [12]. As in our patients, a high interindividual variability in remodeling measures and AF duration, as well as the presence of additional patient- and disease-related factors, apparently hamper the detection of any supposed relationship.

Our results of 71% sinus rhythm (62% without antiarrhythmic drugs) are in line with other reports of 60% to 80% sinus rhythm [4], although we used a strict left atrial approach in contrast to the classical biatrial approach. Because it was shown that AF will not recur if macro-reentry can be prevented by lesions critically placed in the left atrium [6, 15], a less complex procedure might be beneficial, particularly for concomitant AF treatment.

Freedom from recurrent AF during follow-up was greater in patients with AF lasting less than 2 years and a left atrial diameter smaller than 55 mm (Fig 3). Patients who were in sinus rhythm at follow-up had significantly fewer palpitations. They were also in a better NYHA functional class, although left ventricular function was comparable in patients with and without sinus rhythm (Table 3). These data suggest that reestablishing sinus rhythm in fact attenuates AF sequelae.

The study has some limitations. Because left atrial size was renormalized irrespective of rhythm outcome, interpretation of our results must not ignore primary cardiac surgery. This might account for restoration and maintenance of sinus rhythm just as for any other detected symptomatic improvement, but we are unable to assess its relative contribution vs the ablation procedure itself. However, patients with or without sinus rhythm had undergone similar mitral valve procedures (Table 4). Fibrillation frequency, force, and left atrial diameter are not the only variables that change due to AF; however, they are characteristics that can be easily assessed and are able to predict the response to AF treatment [10, 11]. In fact, we simultaneously investigated electrical, contractile, and structural remodeling in patients undergoing AF ablation. To add weight to our findings, we did not include patients with paroxysmal/intermittent AF. Nonetheless, heterogeneity within our cohort resulting from the variability of patient- or disease-related factors such as age or AF duration has to be considered.

Owing to its design, the study has the general limitations inherent in noncontrolled observational studies. Procedure-related bias is considered negligible because all surgeons used an identical lesion pattern. Moreover, it was demonstrated that results do not depend on surgeon’s experience or energy source used for tissue ablation [7, 26].

In conclusion, sinus rhythm could be restored in 71% of patients (62% without antiarrhythmic drugs) undergoing mitral valve surgery and concomitant AF ablation. Atrial remodeling exhibited a high interindividual variability. No relationship existed between remodeling, AF duration, or left atrial hemodynamic load, or between measures of electrical, contractile, or structural remodeling. However, rhythm outcome after AF ablation was independently predicted by AF duration and structural remodeling (left atrium size) but not by electrical or contractile remodeling.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
Alexandro Menes was supported by a grant from the Deutscher Akademischer Austauschdienst (DAAD). We thank Doreen Boettner for excellent coordination of patients’ follow up.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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