Assessment of atrial conduction in patients with scleroderma by tissue Doppler echocardiography and P wave dispersion.

BACKGROUND Atrial conduction abnormalities in patients with scleroderma have not been evaluated in terms of P wave duration, P wave dispersion (P(d)) and electromechanical coupling measured by tissue Doppler echocardiography. METHODS Twenty-four patients with scleroderma and 24 control subjects underwent resting electrocardiogram (ECG), M mode and tissue Doppler echocardiography. The P wave duration was calculated in all leads of the surface ECG. The difference between the maximum (P(max)) and minimum P wave duration was calculated and defined as P(d). Interatrial and intraatrial electromechanical delays were measured with tissue Doppler tissue echocardiography. RESULTS The left ventricular dimensions, fractional shortening, and left atrial diameter did not differ between the patients and the controls. P(d) and P(max) were significantly higher in patients with scleroderma compared with controls: 51 +/- 17 versus 28 +/- 7 ms (p < 0.01) and 109 +/- 10 versus 93 +/- 6 ms (p < 0.01), respectively. There was a delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave (A wave; PA) obtained by tissue Doppler echocardiography in patients with scleroderma compared with controls measured at lateral septal annulus (lateral PA; 122 +/- 8 vs. 105 +/- 7 ms, p = 0.001), septal mitral annulus (104 +/- 11 vs. 93 +/- 10 ms, p = 0.01) and tricuspid annulus (right ventricular PA; 71 +/- 9 vs. 64 +/- 7 ms, p = 0.05). Interatrial conduction time (lateral PA - right ventricular PA) was delayed in patients with scleroderma compared with controls (88 +/- 13 vs. 76 +/- 11 ms, p = 0.01). A positive correlation was detected between interatrial electromechanical delay (lateral PA - right ventricular PA) and P(d) (r = 0.5, p = 0.03). CONCLUSION Atrial conduction abnormalities as estimated with P(d) and P(max) are significantly higher in patients with scleroderma compared with controls. There is a delay in both intraatrial and interatrial electromechanical coupling intervals in patients with scleroderma.