BACKGROUND: The electrical activity of atria can be demonstrated by P waves on surface electrocardiogram (ECG). Atrial electromechanical delay (AEMD) measured with tissue Doppler imaging (TDI) echocardiography can be a useful non-invasive method for evaluating atrial conduction features. We investigated whether AEMD is prolonged in patients with chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS: Study consisted of 41 (15 female, 26 male, mean age 62 + 12 years) patients with COPD and 41 healthy subjects. Pulmonary function tests,12 lead surface ECG and echocardiographic examination were performed and recorded. P wave changes on surface ECG, minimum (P (min)) and maximum (P (max)) duration of P wave and its difference as P wave dispersion (P (wd)) were measured and recorded. Atrial electromechanic delay (AEMD) was calculated from colored-TDI recordings. RESULTS: Pulmonary functions were significantly lower in COPD group than the control group as expected. Right atrial areas and pulmonary arterial systolic pressures (PAP) were significantly higher in COPD group than the controls (right atrial area: 11.9 ± 3.4 cm(2) and 8.2 ± 2.2 cm(2), p < 0.0001 and PAP: 38.4 ± 12.2 and 19.0 ± 3.2 mmHg p < 0.0001, respectively). P wave intervals on surface ECG were significantly increased in COPD patients than the control group (P (max): 105 ± 11 and 90 ± 12 ms, p < 0.0001; P (min): 60 ± 12 and 51 ± 10 ms, p = 0.003 and P (wd): 39 ± 10 and 31 ± 7 ms, p < 0.0001). According to the AEMD measurements from different sites by TDI, there was a significant delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave in patients with COPD when compared with controls measured from tricuspid lateral septal annulus (TAEMD) (COPD: 41.3 ± 9.8 ms, control: 36 ± 4.5 ms; p = 0.005). There was a positive correlation between TAEMD and right atrial area (r = 0.63, p < 0.0001) and also between TAEMD and PASP (r = 0.43, p < 0.0005) and a negative correlation between TAEMD and forced expiratory volume (FEV1) (r = -0.44, p = 0.04). CONCLUSIONS: Right atrial electromechanical delay is significantly prolonged in patients with COPD. The right atrial area, PAP and FEV1 levels are important factors of this prolonged delay. Also the duration of atrial depolarization is significantly prolonged and propagation of depolarization is inhomogeneous in patients with COPD. These may be the underlying mechanisms to explain the atrial premature beats, multifocal atrial tachycardia, atrial flutter and fibrillation often seen in patients with COPD secondary to these changes.
BACKGROUND: The electrical activity of atria can be demonstrated by P waves on surface electrocardiogram (ECG). Atrial electromechanical delay (AEMD) measured with tissue Doppler imaging (TDI) echocardiography can be a useful non-invasive method for evaluating atrial conduction features. We investigated whether AEMD is prolonged in patients with chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS: Study consisted of 41 (15 female, 26 male, mean age 62 + 12 years) patients with COPD and 41 healthy subjects. Pulmonary function tests,12 lead surface ECG and echocardiographic examination were performed and recorded. P wave changes on surface ECG, minimum (P (min)) and maximum (P (max)) duration of P wave and its difference as P wave dispersion (P (wd)) were measured and recorded. Atrial electromechanic delay (AEMD) was calculated from colored-TDI recordings. RESULTS: Pulmonary functions were significantly lower in COPD group than the control group as expected. Right atrial areas and pulmonary arterial systolic pressures (PAP) were significantly higher in COPD group than the controls (right atrial area: 11.9 ± 3.4 cm(2) and 8.2 ± 2.2 cm(2), p < 0.0001 and PAP: 38.4 ± 12.2 and 19.0 ± 3.2 mmHg p < 0.0001, respectively). P wave intervals on surface ECG were significantly increased in COPDpatients than the control group (P (max): 105 ± 11 and 90 ± 12 ms, p < 0.0001; P (min): 60 ± 12 and 51 ± 10 ms, p = 0.003 and P (wd): 39 ± 10 and 31 ± 7 ms, p < 0.0001). According to the AEMD measurements from different sites by TDI, there was a significant delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave in patients with COPD when compared with controls measured from tricuspid lateral septal annulus (TAEMD) (COPD: 41.3 ± 9.8 ms, control: 36 ± 4.5 ms; p = 0.005). There was a positive correlation between TAEMD and right atrial area (r = 0.63, p < 0.0001) and also between TAEMD and PASP (r = 0.43, p < 0.0005) and a negative correlation between TAEMD and forced expiratory volume (FEV1) (r = -0.44, p = 0.04). CONCLUSIONS: Right atrial electromechanical delay is significantly prolonged in patients with COPD. The right atrial area, PAP and FEV1 levels are important factors of this prolonged delay. Also the duration of atrial depolarization is significantly prolonged and propagation of depolarization is inhomogeneous in patients with COPD. These may be the underlying mechanisms to explain the atrial premature beats, multifocal atrial tachycardia, atrial flutter and fibrillation often seen in patients with COPD secondary to these changes.
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