Europace Advance Access originally published online on May 30, 2007
Europace 2007 9(7):471-474; doi:10.1093/europace/eum089
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ATRIAL ANEURYSM
Dispersion of P wave duration and P wave vector in patients with atrial septal aneurysm
Swietokrzyskie Centrum Kardiologii WSzZ, ul.Grunwaldzka 45, 25-736 Kielce, Poland
Manuscript submitted 13 November 2006. Accepted after revision 10 April 2007.
* Corresponding author: ul.Grenadierów 44, 25-212 Kielce, Poland. Tel: +48 41 3621717; fax: +48 41 3671456. E-mail address: mjanion{at}interia.pl
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Abstract |
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Aims Atrial septal aneurysm (ASA) may be involved in the genesis of atrial arrhythmias as a consequence of disturbances in the propagation of depolarization, which may be easily assessed by P wave dispersion measurement. The aim of this study is to assess the dispersion of P wave duration and P wave vector in patients with ASA and to determine the effect of associated interatrial shunt on the magnitude of P wave dispersion.
Methods and results The study population consisted of 23 healthy volunteers and 88 patients with ASA base more than 15 mm and protrusion more than 7.5 mm. The size of aneurysms and atria was determined by echocardiography and P wave dispersion was measured on the surface ECG. In ASA patients, dispersion of P wave duration was significantly increased when compared with healthy controls (7.8 ± 12.1 vs. 3.7 ± 3.5 ms; P < 0.01). Dispersion of P wave vector was also significantly increased (8.5 ± 10.1° vs. 4.6 ± 3.6°; P < 0.005). In healthy volunteers, the mean values of both parameters were below the cutoff points.
Conclusion In patients with ASA, there was a significant dispersion of P wave duration and P wave vector. Variation in P wave duration was significantly correlated with the dispersion of P wave vector and age of these patients. Dispersion of P wave vector was significantly decreased in ASA patients with interatrial shunt. P wave dispersion in ASA patients may predispose to the development of atrial arrhythmias.
Key Words: Atrial septal aneurysm, P wave dispersion, P wave duration, P wave vector, Interatrial shunt
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Introduction |
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The first autopsy of a case of atrial septal aneurysm (ASA) was reported over 80 years ago in 1934.1
The introduction of diagnostic ultrasound resulted in a marked increase in the number of patients identified with ASA with the detection rate of 0.2–4.0% by transthoracic echocardiography (TTE) and of 2.0-8.0% by omniplane transesophageal echocardiography (O-TEE).2–5 Atrial septal aneurysm is a risk factor for arterial embolism, as frequently co-existing patent foramen ovale (PFO) or atrial septal defect (ASD) provides an interatrial shunt leading to paradoxical embolism.2–6 The presence of an additional structure in the interatrial septum may be involved in the genesis of atrial arrhythmias as a consequence of disturbances in the propagation of depolarization, which may be easily assessed by P wave dispersion measurement. To the best of our knowledge, there is no analysis of these parameters in patients with ASA. The aim of this study is to evaluate differences in dispersion of P wave duration and P wave vector in patients with ASA and to determine the effect of an associated interatrial shunt on the magnitude of P wave dispersion.
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Methods |
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Patients
The study population consisted of 88 patients—35 (39.8%) men and 53 (60.2%) women—and 23 healthy volunteers who served as the control group. Subjects were selected from 21 588 TTE examinations performed in an echocardiographic laboratory, which serves as a reference centre in the district of over 1 300 000 inhabitants. The mean age of all study patients was 54.3 ± 14.4 and the mean age of the control subjects was 47.5 ± 11.8 years (P < 0.05). Entry criteria included the presence of ASA by echocardiography and sinus rhythm on the surface ECG. Diagnostic examinations were performed in patients with normal serum ion levels and no other metabolic disorders.
Study protocol
Atrial septal aneurysm was detected by transthoracic (TTE) or transesophageal echocardiography (O-TEE) in the longitudinal and transverse projections, providing clear visualization of the interatrial septum. Patients who had an aneurysm with the base > 15 mm and protrusion > 7.5 mm (half of the minimal base dimension) entered the study.7–10 All patients underwent O-TEE to verify the size of the aneurysm.
Left atrial size (excluding ASA area) was determined by M-mode in the parasternal long-axis projection; cavity area of both atria was measured planimetrically in the apical four-chamber view (2D). The presence of associated interatrial shunt was recorded without its magnitude assessment.
Dispersion of P wave duration or P wave vector was determined on the 12-lead ECG recorded twice with a 30 s interval. Data on the P wave duration and vector were provided during ECG recording by the analysing programme (Marquette MAC 1200, GE Medical Systems Co., DRG MedTex sp. z o.o, 02-661 Warszawa, ul. Wita Stwosza 24; www.drgmedtek.pl). Automatic measurements of P wave parameters were reported previously.11 Mean P wave duration in the first and the second recordings (tP1 and tP2, respectively) in milliseconds (ms) and mean P wave vector axis (VP1 and VP2, respectively) in degrees were measured. Dispersion of both parameters was defined as the absolute difference between the mean values, if the difference in P wave duration (tP1–tP2) exceeded 5 ms or the difference in P wave vector (VP1–VP2) exceeded 5°.
Patients with ASA subsequently underwent 24 h ECG monitoring for the detection of atrial fibrillation and/or flutter that may accompany ASA.
Statistical analysis
Data were expressed as mean ± standard deviation. Student's t-test was performed to estimate the statistical significance of the results. A P-value less than 0.05 was considered statistically significant.
Ethics
The study complies with the Declaration of Helsinki. The research protocol was approved by the local Ethics Committee. The informed consents of the subjects were obtained.
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Results |
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Table 1 summarizes the results. Dispersion of P wave duration was significantly increased in patients with ASA when compared with healthy controls (7.8 ± 12.1 vs. 3.7 ± 3.5; P < 0.01). Dispersion of P wave vector was also significantly increased in patients with ASA when compared with healthy controls (8.5 ± 10.1° vs. 4.6 ± 3.6°; P < 0.005). There was no dispersion of P wave duration and P wave vector in the control group.
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In the study group, there was a significant correlation between the dispersion of P wave duration and that of the P wave vector: (tP1–tP2) = 0.167(VP1–VP2) + 4.704; P < 0.003 (Figure 1) and a positive relationship with patient age (tP1–tP2) = 0.098x + 0.448; P < 0.005 (Figure 2). Cavity area of both atria was also significantly larger in patients with ASA than in healthy controls; however, there was no significant relationship between vector dispersion and left and right atrial size and cavity area.
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Of 88 patients with ASA, echocardiography detected interatrial shunting in 47 (53.4%) patients. Of the 47 patients, 28 (57%) subjects had PFO and 21 (43%) ASD. There was no correlation between aneurysm parameters or atrial size and the frequency of PFO or ASD. Dispersion values in patients with and without interatrial shunt are given in Table 2. Dispersion of P wave vector (VP1–VP2) in patients without interatrial shunt is significantly higher than that in patients with the shunt.
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Twenty-four hour ECG monitoring detected paroxysms of atrial fibrillation and/or flutter in 15 (17.0%) patients with ASA. There was a significant relationship between the presence of atrial arrhythmias and the dispersion of P wave duration (P < 0.005).
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Discussion |
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Electrocardiographic recording of sinus P wave provides information on its duration, amplitude, dispersion, and direction of electrical vector. Depending on atrial area, dispersion of P wave duration varies from 0 to 80 ms, whereas dispersion of P wave vector varies from –50 to + 60°.12
Patients with ASA may be subject to additional risk related to variation in these parameters, because of disturbances in the propagation of depolarization due to the presence of pathological structure.
P wave dispersion has been extensively studied in various disease states.13–26 Left ventricular inflow obstruction due to structural or functional changes in the left ventricle may cause P wave dispersion.16,20,22,23 Pathophysiological abnormalities in the atria, such as post-ablation injury, give rise to differences in P wave duration.17 Dispersion has also been found in patients with psychotic disorders such as anxiety19 and prior to haemodialysis.21 However, all those patients did not have ASA. The purpose of this study was to estimate dispersion of P wave vector in patients with ASA. Dispersion of P wave duration and P wave vector was significantly increased in the study patients when compared with healthy controls, confirming the suggestion that ASA may be a source of such variation. Furthermore, the presence and magnitude of P wave dispersion were independent of aneurysm and atrial size.
In patients with ASD, dispersion was diagnosed prior to surgical operation and decreased after defect closure.12–14,24 In the present study, P wave dispersion in patients with ASA and associated interatrial shunt was smaller than that in subjects without shunting, and the wall of the aneurysm was markedly deformed because of pressure gradient between the atria. Evidence shows that closure of the defect is not sufficient to eliminate dispersion; it is also necessary to add rigidity to atrial septal structures to eliminate septal pulsation.13
Several investigators demonstrated the relationship between dispersion and paroxysmal atrial fibrillation.14,16,17,21,22,25,26 Dispersion was also found to predict recurrent atrial fibrillation or flutter in patients after cardioversion.16,17 In the present study, 17% of patients with ASA had atrial fibrillation/flutter on the ECG monitoring, which is consistent with the results of studies in patients with paroxysmal atrial fibrillation.15,16,18,22,25,26
There is controversy regarding the impact of atrial cavity size on the magnitude of P wave dispersion. In one study, there was a correlation between atrial cavity size and the magnitude of P wave dispersion, but other investigators did not demonstrate such relationship.14,17 The present study corroborates the latter finding.
Study limitation
The subjects in the control group were significantly younger than those in the study group. Although this was unintentional, only those agreed to serve as controls.
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Conclusions |
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In patients with ASA, there was a significant dispersion of P wave duration and P wave vector. The differences were independent of the size of the aneurysm. Variation in P wave duration was significantly correlated with dispersion of P wave vector and age of these patients. In patients with ASA and interatrial shunt, dispersion of P wave vector was significantly decreased when compared with patients without the shunt. P wave dispersion in ASA patients may predispose to the development of atrial arrhythmias such as atrial fibrillation or flutter.
Conflict of interest: none declared.
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References |
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[1] Lang FJ, Posselt A. Aneurrysmatische Vorwolburg der Fossa ovalis in den linken Vorhof. Wien Med Wochenschr (1934) 84:392–6.
[2] Hanley PC, Tajik AJ, Hynes JK, Edwards WD, Reeder GS, Hagler DJ, et al. Diagnosis and classification of atrial septal aneurysms by two-dimensional echocardiography: report of 80 consecutive cases. J Am Coll Cardiol (1985) 6:1370–83.[Abstract]
[3] Marazanhof M, Roudaut R, Cohen A, Tribouilloy C, Malergues MC, Halphen C, et al. Atrial septal aneurysm. Morphological characteristics in large population: pathological associations. A French multicenter study on 259 investigated by transesophageal echocardiography. Int J Cardiol (1995) 52:59–65.[CrossRef][Web of Science][Medline]
[4] Agmon Y, Khandheria BK, Meissner I, Gentile F, Whisnant JP, Sicks JD, et al. Frequency of atrial septal aneurysms in patients with cerebral ischaemic events. Circulation (1999) 99:1942–44.
[5] Ossemann M, Laloux P, Marchandise B, Jamart J. Association between stroke and atrial septal aneurysm assessed by transesophageal echocardiography in a cardiologic population. Acta Neurol Belg (1995) 95:170–7.[Web of Science][Medline]
[6] Coskun S, Sekuri C, Bayturan O. Diagnosis of asymptomatic atrial septal aneurysms using two dimensional color Doppler and contrast transthoracic echocardiography. Chin Med J (2003) 116:699–702.[Web of Science][Medline]
[7] Mugge A, Daniel GD, Angermann C, Spes C, Khandheria B, Kronzon I, et al. Atrial septal aneurysm in adult patients. Circulation (1995) 91:2785–92.
[8] Hanley PC, Tajik AJ, Hynes JK, Edwards WD, Reeder GS, Hagler DJ, et al. Diagnosis and classification of atrial septal aneurysms by two-dimensional echocardiography: report of 80 consecutive cases. J Am Coll Cardiol (1985) 6:1370–83.[Abstract]
[9] Pearson AC, Nagelhout D, Castello R, Gomez CR, Labowitz AJ. Atrial septal aneurysm and stroke: a transesophageal echocardiography study. J Am Coll Cardiol (1991) 18:1223–9.[Abstract]
[10] Silver MD, Dorsey JS. Aneurysms of the septum primum in adults. Arch Pathol Lab Med (1978) 102:62–5.[Web of Science][Medline]
[11] Madias JE. P-wave duration and dispersion in patients with peripheral edema and its amelioration. Indian Pacing Electrophysiol J (2007) 7:7–18.[Medline]
[12] Fisch C. Electrocardiography. In: Heart Disease. A Textbook of Cardiovascular Medicine—Braunwald E, ed. (1997) 5th ed. Philadelphia: WB Saunders. p111.
[13] Guray U, Guray Y, Mercit B, Yilmaz MB, Sasmaz H, Korkmaz S. Maximum P wave duration and P wave dispersion in adult patients with secundum atrial septal defect: the impact of surgical repair. Ann Noninvasive Electrocardiol (2004) 9:136–41.[CrossRef][Web of Science][Medline]
[14] Guray U, Guray Y, Yilmaz MB, Mercit B, Sasmaz H, Korkmaz S. 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]
[15] Dogan A, Kahraman H, Ozturk M, Avsar A. P wave dispersion and left atrial appendage function for predicting recurrence after conversion of atrial fibrillation and relation of P wave dispersion to appendage function. Echocardiography (2004) 21:523–30.[CrossRef][Web of Science][Medline]
[16] Yilmaz R, Demirbag R, Durmus I, Kasap H, Baykan M, Kucukosmanoglu M, et al. Association of stage of left ventricular diastolic dysfunction with P wave dispersion and occurrence of atrial fibrillation after first acute anterior myocardial infarction. Ann Noninvasive Electrocardiol (2004) 9:330–8.[CrossRef][Web of Science][Medline]
[17] Soylu M, Demir AD, Ozdemir O, Soylu O, Korkmaz S. Increased P wave dispersion after the audiofrequency catheter ablation in overt pre-excitation patients: the role of atrial vulnerability. Int J Cardiol (2004) 95:167–70.[CrossRef][Web of Science][Medline]
[18] Hallioglu O, Aytemir K, Celiker A. The significance of P wave duration and P wave dispersion for risk assessment of atrial tachyarrhythmias in patients with corrected tetralogy of Fallot. Ann Noninvasive Electrocardiol (2004) 9:339–44.[CrossRef][Web of Science][Medline]
[19] Uyarel H, Kasikkcioglu H, Dayi SU, Tartan Z, Karabulut A, Uzunlar B, et al. Anxiety and P wave dispersion in a healthy young population. Cardiology (2005) 104:162–8.[CrossRef][Web of Science][Medline]
[20] Celik T, Iyisoy A, Kurasaklioglu H, Kilic S, Kose S, Amasyali B, et al. Effects of primary percutaneous coronary intervention on P wave dispersion. Ann Noninvasive Electrocardiol (2005) 10:342–7.[CrossRef][Web of Science][Medline]
[21] Tezcan UK, Amasyali B, Can I, Aytemir K, Kose S, Yavuz I, et al. Increased P wave dispersion and maximum P wave duration after hemodialysis. Ann Noninvasive Electrocardiol (2004) 9:34–8.[CrossRef][Web of Science][Medline]
[22] Rosiak M, Bolinska H, Ruta J. P wave dispersion and P wave duration on SAECG in predicting atrial fibrillation in patients with acute myocardial infarction. Ann Noninvasive Electrocardiol (2002) 7:363–8.[CrossRef][Web of Science][Medline]
[23] Gunduz H, Biank E, Arinc H, Akdemir R, Ozhan H, Tamer A, et al. The relationship between P-wave dispersion and diastolic dysfunction. Tex Heart Inst J (2005) 32:163–7.[Web of Science][Medline]
[24] Ho TF, China 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]
[25] Aytemir K, Ozer N, Atalar E, Sade E, Aksoyek S, Ovunc K, et al. P wave dispersion on 12-lead electrocardiography in patients with paroxysmal atrial fibrillation. Pacing Clin Electrophysiol (2000) 23:1109–12.[CrossRef][Medline]
[26] Altunkeser BB, Ozdemir K, Gok H, Temizhan A, Tokac M, Karabag T. Can P wave parameters obtained from 12-lead surface electrocardiogram be a predictor for atrial fibrillation in patients who have structural heart disease? Angiology (2003) 54:475–9.[Web of Science][Medline]
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