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European Journal of Heart Failure 2004 6(5):567-569; doi:10.1016/j.ejheart.2003.12.020
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© 2004 European Society of Cardiology

P-wave duration and P-wave dispersion in patients with dilated cardiomyopathy

Kubilay Senena, Hasan Turhana,*, Ali Riza Erbaya, Nurcan Basara, Ayse Saatci Yasara, Onur Sahina and Ertan Yetkinb

a Turkiye Yuksek Ihtisas Hospital, Department of Cardiology Ankara, Turkey
b Inonu University, Medical Faculty, Department of Cardiology Malatya, Turkey

* Corresponding author. Tel.: +90-312-2867658. E-mail address: drhturhan{at}yahoo.com


   Abstract
Top
 Abstract
1. Introduction
 2. Material and method
 3. Results
 4. Discussion
 References
 
Background: P-wave dispersion (PWD) has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses. In the present study, we aimed to investigate PWD in patients with dilated cardiomyopathy.

Method: The study population consisted of 72 patients with dilated cardiomyopathy and 72 healthy control subjects. Left atrial diameter, left ventricular end-diastolic and end-systolic diameters and left ventricular ejection fraction of all patients and control subjects were measured by means of transthoracic echocardiography. Maximum P-wave duration (Pmaximum) and minimum P-wave duration (Pminimum) were measured from the 12-lead surface electrocardiogram. PWD was calculated as the difference between Pmaximum and Pminimum.

Results: Pmaximum and PWD of patients with dilated cardiomyopathy were significantly higher than those of control subjects (Pmaximum: 126±12 ms vs. 116±10 ms, PWD: 47±6 ms vs. 38±7 ms, respectively, P<0.001 for all). However, there was no statistically significant difference between patient group and control group regarding Pminimum (79±7 ms vs. 78±6 ms, respectively, P=0.27). Left atrial diameter was significantly higher in patients with dilated cardiomyopathy compared to control subjects (4.51±0.62 cm vs. 3.60±0.43 cm, respectively, P<0.001). Left ventricular ejection fraction was found to be significantly lower in patients with dilated cardiomyopathy compared to control subjects (33±5% vs. 63±7%, respectively, P<0.001).

Conclusion: PWD was found to be significantly higher in patients with dilated cardiomyopathy than in healthy control subjects.

Key Words: Dilated cardiomyopathy • P-wave dispersion • Atrial fibrillation

Received July 11, 2003; Revised December 1, 2003; Accepted December 10, 2003


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and method
 3. Results
 4. Discussion
 References
 
P-wave dispersion (PWD) is a new and simple electrocardiographic marker that has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses [1,2]. It has been defined as the difference between shortest and longest P-wave durations [1]. Previously, PWD has been studied in some cardiac conditions such as hypertension, paroxysmal atrial fibrillation, mitral stenosis, aortic stenosis, during spontaneous angina pectoris and during coronary angioplasty [3–8]. Prolonged P wave duration and increased PWD have been reported to carry an increased risk for atrial fibrillation [1,3]. Dilated cardiomyopathy imposed the greatest risk for the development of atrial fibrillation with a four-to-six fold increased risk [9]. Accordingly, in the present study we aimed to investigate this new electrocardiographic marker, PWD, in patients with dilated cardiomyopathy and compare with healthy control subjects.


   2. Material and method
Top
 Abstract
 1. Introduction
 2. Material and method
3. Results
 4. Discussion
 References
 
The study population consisted of two groups: Group I consisted of 72 patients with dilated cardiomyopathy (55 men, 17 women; aged 63±8 years) and group II consisted of 72 healthy control subjects (55 men, 17 women; aged 62±9 years) without any clinically apparent cardiovascular disease. All patients and control subjects were selected from patients who were undergoing coronary angiography in our hospital with the suspicion of coronary artery disease and detected as having angiographically normal coronary arteries. Patients who had coronary artery disease, diabetes mellitus, uncontrolled hypertension, valvular heart disease, hyperthyroidism, chronic obstructive pulmonary disease, ventricular preexcitation, atrioventricular conduction abnormalities, or abnormal serum electrolytes were excluded from the study. All patients and control subjects underwent routine transthoracic echocardiographic examination (Hitachi EUB 6000, Tokyo, Japan). During transthoracic echocardiographic examination left atrial diameter, left ventricular end-diastolic and end-systolic diameters and left ventricular ejection fraction were measured in M-mode according to the recommendations of the American Society of Echocardiography [10]. Twelve-lead electrocardiogram was recorded for each patient and control subject at a rate of 50 mm/s. At the time of electrocardiographic recording, all subjects were in sinus rhythm and none were taking any type of antiarrhythmic agent. The measurement of the P-wave duration was performed manually by two of the investigators without knowledge of the clinical status of the patients and control subjects. To improve accuracy, measurements were performed with calipers and magnifying lens. The onset of the P-wave was defined as the junction between the isoelectric line and the beginning of the P-wave deflection and the offset of the P-wave as the junction between the end of the P-wave deflection and the isoelectric line [4,11]. Maximum and minimum P-wave durations were measured from the 12-lead surface electrocardiogram. Patients with measurable P-waves in nine or fewer electrocardiographic leads were excluded from the study. PWD was calculated as the difference between maximum P-wave duration (Pmax) and minimum P-wave duration (Pmin), (PWD=Pmax–Pmin) [1,11].

All numeric variables were expressed as mean±S.D. and categorical variables were expressed as a percentage. Statistical analysis was performed using unpaired t test, Mann–Whitney U test and Chi-square test where appopriate, and Pearson correlation test was used to determine the correlation between electrocardiographic and echocardiographic variables. A P value <0.05 was considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and method
 3. Results
4. Discussion
 References
 
There was no statistically significant difference between the two groups with respect to age and gender (P>0.05, Table 1). Maximum P-wave duration and PWD of patients with dilated cardiomyopathy were found to be significantly higher than those of control subjects (Table 1). However, there was no statistically significant difference between patient group and control group regarding minimum P-wave duration (Table 1). Left atrial diameter was significantly higher in patients with dilated cardiomyopathy compared to control subjects (Table 1). Left ventricular ejection fraction was found to be significantly lower in patients with dilated cardiomyopathy compared to control subjects (Table 1). Besides, maximum P-wave duration and PWD were found to be positively correlated with left atrial diameter (r=0.556, P<0.001 and r=0.488, P<0.001, respectively) and negatively correlated with left ventricular ejection fraction (r=–0.558, P<0.001 and r=–0.573, P<0.001, respectively). A highly significant positive correlation was detected between maximum P-wave duration and PWD (r=0.952, P<0.001). However, no correlation was detected between minimum P-wave duration and PWD (r=0.058, P=0.6).


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  		Table 1 Comparison of clinical, echocardiographic and electrocardiographic features of patients with dilated cardiomyopathy and control subjects

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Material and method
 3. Results
 4. Discussion
References
 
PWD defined as the difference between maximum and minimum P-wave durations. It has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses through the atrial wall. In the present study, maximum P-wave duration and PWD were detected to be significantly higher in patients with dilated cardiomyopathy compared to control subjects. In addition, left atrial diameter was found to be significantly higher and left ventricular ejection fraction was detected to be significantly lower in patients with dilated cardiomyopathy. Furthermore, we found a positive correlation between PWD and left atrial diameter and a negative correlation between PWD and left ventricular ejection fraction. It has been previously reported that changes in left atrial dimension and pressure may influence P-wave duration [12]. P-wave abnormalities have been reported to be related with left atrial enlargement [13,14], left atrial hypertension [15], altered conduction [16], or a combination of multiple factors [17,18]. On the contrary, we have reported that there is no correlation between the LA diameter and PWD in patients with rheumatic mitral stenosis [6]. This controversy may be explained by the predominance of fibrosis of the left atrial wall change due to rheumatic process in addition to pressure and diameter changes of left atrium. Since the clinical manifestation of rheumatic mitral stenosis takes 10–20 years after the acute rheumatic fever attack, it can be expected that this relatively long period may results in much more fibrotic changes in left atrial tissue. Both the anatomic and hemodynamic changes in the left atrium as left atrial dilatation, increased left atrial pressure and left atrial fibrosis caused by left ventricular dysfunction may be the underlying cause of prolonged P-wave duration and increased PWD in patients with dilated cardiomyopathy compared to control subjects.

P-wave duration and PWD have been reported to be influenced by the autonomic tone, which induces changes in the velocity of impulse propagation [19]. Sympathetic activity has been well known to be elevated in patients with dilated cardiomyopathy [20]. Tukek et al. [21] have reported that increased sympathetic activity causes a significant elevation in PWD. Therefore, increased PWD in patients with dilated cardiomyopathy might be partly related to an elevation in sympathetic activity.

The effects of left ventricular dysfunction on the left atrial pathology (macro- and microstructural) and neuroendocrine activity and their effects on intracardiac hemodynamics and atrial electrophysiology may be the underlying mechanisms responsible for increased P-wave duration and PWD in patients with dilated cardiomyopathy.

In summary, although maximum P-wave duration and PWD have been found to be increased in patients with dilated cardiomyopathy compared to healthy control subjects, there is no long-term prospective study to evaluate the clinical significance of increased PWD in patients with dilated cardiomyopathy. Clearly, further prospective studies which include larger series and long term follow-up will have to be conducted to clarify the clinical utility of PWD in patients with dilated cardiomyopathy.


   References
Top
 Abstract
 1. Introduction
 2. Material and method
 3. Results
 4. Discussion
 References
 

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