Prolonged P wave duration in adults with secundum atrial septal defect: a marker of delayed conduction rather than increased atrial size?
Department of Cardiology, Lund University Hospital, SE-221 85 LUND, Sweden
* Corresponding author. Fax: +46 46 15 78 57.E-mail address: ulf.thilen{at}skane.se
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Abstract |
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Aims: Although atrial fibrillation is a frequent complication of an atrial septal defect (ASD) of the secundum type, the underlying mechanisms are poorly understood. Atrial conduction disturbances, manifested as a prolonged P-wave duration, have been suggested as a substrate for arrhythmia. Prolongation of the P-wave in unrepaired ASD has been demonstrated by means of the conventional ECG, but not by more sophisticated methods. The aim of the study was to analyse P-wave duration and morphology by high-resolution P-wave signal-averaged ECG (PSA-ECG) and to investigate potential atrial mechano-electrical interactions in adults with an unrepaired ASD.
Methods and results: P-wave signal-averaged-ECG was obtained in 35 adult patients (age 53 ± 15 years) with ASD and compared with an equal number of sex- and age-matched healthy controls. Right and left atrial sizes were assessed by echocardiography in the ASD group. P wave duration was significantly longer in the ASD group than in control subjects (148 ± 16 vs. 128 ± 15 ms, P < 0.0001). P-wave morphology did not differ significantly between patients and controls. There was no clear relation between P-wave duration and atrial size.
Conclusion: Atrial septal defect in the adult is characterized by a prolonged P-wave duration, indicating delayed atrial conduction, which is not related to the enlargement of the atria but rather to conduction delay. The nature and potential reversibility of this warrant further investigation.
Key Words: Atrial septal defect, Signal-averaged ECG, P-wave duration, Atrial fibrillation, Electrical remodelling
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Introduction |
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Atrial fibrillation is a part of the natural history of the secundum atrial septal defect (ASD) with prevalence at least 10-fold that in the normal population. The prevalence increases in middle-aged and old ASD patients with around half of them having experienced atrial fibrillation.1
–3 Even when the defect is surgically closed, the risk of atrial fibrillation remains high during long-term follow-up and it is still debatable if, or to what extent, early closure of the defect reduces the risk of later atrial arrhythmia.1,4–7
The reasons and the mechanisms for the increased prevalence of atrial fibrillation in ASD are by and large still unclear. Disturbances of atrial conduction have been suggested to favour the development of atrial fibrillation, and reports, in different cardiac conditions, have shown that the risk of atrial fibrillation is associated with the prolongation of the P-wave, which is a marker of altered atrial conduction.8–11 On the basis of the manual analyses of conventional ECG, prolonged P-wave duration has been reported in adults with unrepaired ASD.12,13 However, high-resolution signal-averaged ECG, which offers a more accurate and detailed information about atrial excitation, has not yet been described in this setting. Although orthogonal leads routinely used for signal-averaged P-wave analysis seldom are recorded in clinical routine, they can be derived from a conventional 12-lead ECG.14,15
The aim of the present study is to determine and compare the P-wave duration and morphology in healthy adult subjects with an ASD by high-resolution orthogonal P-wave signal-averaged ECG (PSA-ECG). Furthermore, we investigated whether there was any atrial mechano-electrical interaction by means of echocardiographic assessment of right and left atrial sizes.
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Materials and methods |
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The study group consisted of 35 adult patients with an isolated haemodynamically significant (right heart dilatation) ASD of the secundum type scheduled for closure. The control group contained 35 sex- and age-matched healthy individuals without any history of heart disease. All subjects had sinus rhythm at the time of investigation. In the ASD group, six patients had a history of paroxysmal atrial fibrillation. Two of them were treated with sotalol or a beta-blocker, combined with amiodarone in one case. One patient had digoxin and another was treated with a low dose of flecainide. Demographic data of patients and controls are given in Table 1.
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High-resolution PSA-ECG was obtained from the orthogonal XYZ-leads of the vector cardiogram, derived from a conventional 12-lead ECG using an inverse Dower transformation.14
,15 One patient had to be excluded because of low signal quality of the 12-lead ECG, making a reliable transformation to a vector cardiogram impossible. Total P-wave duration and the time from P-wave onset and the magnitude of the atrial electrical activation in the orthogonal leads X, Y, and Z (Xmax, Ymax, Zzero, Zmin, and Zmax) (Figure 1) were determined. P-wave onset and end were manually defined as the earliest and the latest activation in any of the three orthogonal leads when displayed simultaneously. Locations and amplitudes of maximum and minimum values were obtained automatically by the analysis software using the manually acquired onset of the P-wave as the starting point.
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P-wave morphology, based on the pattern in the three spatial planes, was categorized into one of four different types:
- Type 1: positive deflection in leads X and Y and a completely negative deflection in lead Z;
- Type 2: positive deflection in leads X and Y and a biphasic lead Z, starting with a negative and ending with a positive deflection;
- Type 3: positive lead X, biphasic (positive–negative) lead Y, and biphasic (negative–positive) lead Z;
- Type 4, atypical: those who did not fit into types 1–3.
All ASD patients were assessed by transthoracic and transoesophageal echocardiography, the latter giving the diameter of the ASD. If the defect was oval, the given diameter was the average of the long- and short-axis distance. From a transthoracic four-chamber view, the areas of the left and right atria were measured when it was at its largest (pre-emptying). As no patient had pulmonary stenosis, the systolic right ventricular/right atrial Doppler pressure gradient derived from tricuspid regurgitation served as an indicator of the pressure levels in the pulmonary circulation.
The study was approved by the local Ethics Committee of Lund University (approval no. 516/2005).
Statistics
Data are given as mean ± SD. In comparisons, paired and unpaired t-tests were used for continuous variables and a 
2 test for categorical variables. A P-value less than 0.05 was considered statistically significant. Statview® statistical software was used for analysis.
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Results |
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P-wave duration was significantly longer in the ASD group when compared with controls (148 ± 16 vs. 128 ± 15 ms, P < 0.0001, Table 1). In leads X and Y, the time pattern did not differ between ASD patients and controls, whereas in lead Z, the minimal and maximal, but not the zero position, was located significantly later in the ASD group than in the controls (Table 1). Amplitudes, with the exception of Ymax, were significantly larger in patients when compared with controls (Table 1).
Overall, P-wave duration was not related to age or sex. However, in the ASD group, six patients with a history of atrial fibrillation were significantly older and had significantly longer P-wave duration than those without arrhythmia (Table 2).
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In the ASD group, there were no significant correlations between right and left atrial sizes, isolated or combined, and P-wave duration (Figure 2
–4). P-wave duration was weakly related to the diameter of the ASD (P = 0.03, r = 0.37). There was no significant relation between P-wave duration and systolic pulmonary pressure determined as right ventricular/right atrial pressure gradient (P = 0.15, r = 0.25).
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P-wave duration in ASD patients derived from PSA-ECG was significantly longer than that obtained from the manually read 12-lead ECG (148 ± 16 vs. 114 ± 13 ms, P < 0.0001). Using a Bland–Altman analysis, no significant relation was found between the P-wave duration and the difference between the two methods.
No significant relations could be demonstrated between amplitudes or locations of Xmax, Ymax, Zmin, Zzero, or Zmax and the left or right atrial size. The distribution of P-wave morphology, in terms of types 1–4, did not significantly differ between patients and controls (Table 3).
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Discussion |
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The present study shows, for the first time by means of orthogonal PSA analysis, that P-wave duration is prolonged in adult patients with an unrepaired ASD, thereby confirming earlier reports based on manual assessment of a conventional ECG.13
,14 Having in mind the high prevalence of atrial fibrillation in the natural course of an ASD and the established relation between P-wave duration and atrial conduction, this finding suggests that atrial conduction disturbances play an important pathogenetic role. Although the number of patients is small, our finding that those who had experienced atrial fibrillation had an even longer P-wave duration than those without a history of arrhythmia could further stress the link between atrial conduction disturbances and atrial fibrillation in this context. However, this should be interpreted with caution as atrial fibrillation itself promotes electrical remodelling and that anti-arrhythmic medication may influence atrial conduction properties.16 The predictive value for atrial fibrillation of the P-wave duration from an individual point of view was low, as there was no level of P-wave duration that could accurately separate those with and without a history of paroxysmal atrial fibrillation.
The absence of any positive relation between atrial sizes and P-wave duration or temporal P-wave morphology parameters in the ASD group harmonizes with earlier reports on patients with ASD as well as a report on patients with lone atrial fibrillation.12,13,17 It is therefore likely that slowing of conduction rather than increased atrial myocardial mass is the cause of the prolongation of the P-wave. However, it should be recognized that atrial area, used in this study, is just a surrogate for volume and particularly for atrial myocardial mass as atrial wall thickness is not known.
In a small invasive electrophysiological study on adult patients with ASD, it has been demonstrated that conduction delay in the right atrium is rather regional than uniform, located at the crista terminalis.12 This is in agreement with our finding that the signal maxima in ASD patients compared with controls were not delayed in all orthogonal leads. Invasive electrophysiological studies have also found a high incidence of sinus node dysfunction in ASD, even in children, suggesting that electrophysiological disturbances in different parts of the atria are a common phenomena in ASD.12,18 The same authors suggested that the electric remodelling in ASD was caused or promoted by chronic right atrial stretch. Besides that, alterations in the left atrium must be considered as the increased volume load of an ASD also affects the left atrium. However, the possibility of a congenital origin must also be taken into account: abnormal electrophysiological properties or increased vulnerability to atrial stretch is an associated part of the malformation itself. Prolonged P-wave duration and sinus node dysfunction have been reported in children with ASD, demonstrating that these abnormalities occur very early.18,19
Limitations
A limitation of the present study is that echocardiography was not performed in the control group.
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Conclusion |
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Atrial electric activity in adult patients with a haemodynamically important ASD is characterized by a prolonged P-wave duration. This seems to be related to regional atrial conduction disturbances rather than to atrial enlargement. Further studies explaining the nature and potential reversibility of the altered atrial conduction in ASD are warranted.
Conflict of interest: none declared.
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References |
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[1] Murphy JG, Gersh BJ, McGoon MD, Mair DD, Porter CJ, Ilstrup DM, et al. Long-term outcome after surgical repair of isolated atrial septal defect. Follow-up at 27 to 32 years. N Engl J Med (1990) 323:1645–50.[Abstract]
[2] Oliver JM, Gallego P, Gonzalez A, Benito F, Mesa JM, Sobrino JA. Predisposing conditions for atrial fibrillation in atrial septal defect with and without operative closure. Am J Cardiol (2002) 89:39–43.[Web of Science][Medline]
[3] Shah D, Azhar M, Oakley CM, Cleland JG, Nihoyannopoulos P. Natural history of secundum atrial septal defect in adults after medical or surgical treatment: a historical prospective study. Br Heart J (1994) 71:224–7. discussion 228.
[4] Konstantinides S, Geibel A, Olschewski M, Gornandt L, Roskamm H, Spillner G, et al. A comparison of surgical and medical therapy for atrial septal defect in adults. N Engl J Med (1995) 333:469–73.
[5] Roos-Hesselink JW, Meijboom FJ, Spitaels SE, van Domburg R, van Rijen EH, Utens EM, et al. Excellent survival and low incidence of arrhythmias, stroke and heart failure long-term after surgical ASD closure at young age. A prospective follow-up study of 21–33 years. Eur Heart J (2003) 24:190–7.
[6] Thilen U, Berlind S, Varnauskas E. Atrial septal defect in adults. Thirty-eight-year follow-up of a surgically and a conservatively managed group. Scand Cardiovasc J (2000) 34:79–83.[CrossRef][Web of Science][Medline]
[7] Thilen UJ. Closure of atrial septal defect: is the debate over? Eur Heart J (2003) 24:1797. author reply 1797–8.
[8] Tuzcu V, Ozkan B, Sullivan N, Karpawich P, Epstein ML. P wave signal-averaged electrocardiogram as a new marker for atrial tachyarrhythmias in postoperative Fontan patients. J Am Coll Cardiol (2000) 36:602–7.
[9] Rosenheck S. Signal-averaged P wave in patients with paroxysmal atrial fibrillation. Pacing Clin Electrophysiol (1997) 20:2577–86.[CrossRef][Medline]
[10] Fukunami M, Yamada T, Ohmori M, Kumagai K, Umemoto K, Sakai A, et al. Detection of patients at risk for paroxysmal atrial fibrillation during sinus rhythm by P wave-triggered signal-averaged electrocardiogram. Circulation (1991) 83:162–9.
[11] Nitta T, Imura H, Bessho R, Hosaka H, Yamauchi S, Tanaka S. Wavelength and conduction inhomogeneity in each atrium in patients with isolated mitral valve disease and atrial fibrillation. J Cardiovasc Electrophysiol (1999) 10:521–8.[Web of Science][Medline]
[12] Morton JB, Sanders P, Vohra JK, Sparks PB, Morgan JG, Spence SJ, et al. Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect. Circulation (2003) 107:1775–82.
[13] Guray U, Guray Y, Yylmaz MB, Mecit B, Sasmaz H, Korknaz S, et al. Evaluation of P wave duration and P wave dispersion in adult patients with secundum atrial septal defect during normal sinus rhythm. Int J Cardiol (2003) 91:75–9.[CrossRef][Web of Science][Medline]
[14] Carlson J, Havmoller R, Herreros A, Platonov P, Johansson R, Olsson B. Can orthogonal lead indicators of propensity to atrial fibrillation be accurately assessed from the 12-lead ECG? Europace (2005) 7:39–48.
[15] Carlson J. Exploration of supraventricular conduction with respect to atrial fibrillation. Methodological aspects on selected techniques. (2005) Lund University. PhD Thesis http://theses.lub.lu.se/postgrad/search.tkl?field_query1=pubid&query1=med_1202&recordformat=display.
[16] Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation (1995) 92:1954–68.
[17] Platonov PG, Carlson J, Ingemansson MP, Roijer A, Hansson A, Chireikin LV, et al. Detection of inter-atrial conduction defects with unfiltered signal-averaged P-wave ECG in patients with lone atrial fibrillation. Europace (2000) 2:32–41.
[18] Bink-Boelkens MT, Bergstra A, Landsman ML. Functional abnormalities of the conduction system in children with an atrial septal defect. Int J Cardiol (1988) 20:263–72.[CrossRef][Web of Science][Medline]
[19] Ho TF, Chia EL, Yip WC, Chan KY. Analysis of P wave and P dispersion in children with secundum atrial septal defect. Ann Noninvasive Electrocardiol (2001) 6:305–9.[CrossRef][Web of Science][Medline]
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