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Tissue Doppler echocardiographic evidence of atrial mechanical dysfunction in coronary artery disease. | LitMetric

AI Article Synopsis

  • Atrial function is essential for heart health and can be affected by coronary artery disease (CAD), which this study aimed to investigate using tissue Doppler echocardiography (TDI).
  • Patients with CAD (118 subjects) showed significantly decreased atrial contraction velocities in both the left and right atria compared to healthy controls (100 subjects).
  • This impairment in atrial contractile function was noted even in patients with preserved systolic function and mild diastolic dysfunction, suggesting that TDI may provide a more accurate assessment of atrial mechanics than traditional methods.

Article Abstract

Background: Atrial function is an integral part of cardiac function which is often neglected. The presence of coronary artery disease (CAD) may impair atrial function. This study investigated if atrial mechanical dysfunction was present in patients with CAD by tissue Doppler echocardiography (TDI).

Methods: Echocardiography with TDI was performed in 118 patients with CAD, and compared with 100 normal controls with comparable age and heart rate. Regional atrial function was assessed at the left (LA) and right (RA) atrial free wall and inter-atrial septum (IAS). The peak regional atrial contraction velocity of (V(A)) and the timing of mechanical events were compared.

Results: The V(A) in the LA (5.0+/-2.6 Vs 7.7+/-2.6 cm/s), IAS (4.8+/-1.7 Vs 5.7+/-1.5 cm/s) and RA (6.8+/-3.1 Vs 9.2+/-2.9 cm/s) were significantly decreased in patients with CAD when compared with controls (all p<0.001). Patients with impaired systolic function (ejection fraction50% (both p<0.001); and were lower in those with restrictive filling pattern (RFP) than non-RFP of diastolic dysfunction (both p<0.05). The V(A) in all the subgroups was lower than controls. In contrast, transmitral atrial velocity was unable to reveal any abnormality except in the subgroup with a RFP. The LA dimension, area and volume were increased in the disease groups, but were largely unchanged in the RA despite abnormal V(A). The physiological inter-atrial delay for the onset and peak atrial contraction between the RA and LA were unaffected by CAD.

Conclusions: The atrial contractile function in both atria was impaired in the presence of CAD, especially in the LA. This was detected even in patients with preserved systolic function or mild diastolic dysfunction such as non-RFP. Direct assessment of atrial velocity by TDI may better reflect atrial mechanical function than transmitral atrial velocity.

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Source
http://dx.doi.org/10.1016/j.ijcard.2004.12.077DOI Listing

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