Effect of Percutaneous Transvenous Mitral Commissurotomy on Left Atrial Appendage Function: An Immediate and 6-Month Follow-Up Transesophageal Doppler Study

Abstract

The left atrial appendage (LAA) is a common site of thrombus formation and is the source of systemic thromboembolism in patients with rheumatic mitral stenosis. LAA contractile dysfunction is a common finding in these patients. The aim of this study was to assess immediate and 6-month follow-up LAA function by transesophageal Doppler echocardiography in patients who underwent percutaneous transvenous mitral commissurotomy (PTMC). Forty-seven consecutive patients with symptomatic critical mitral stenosis who underwent PTMC were enrolled. All had underwent transthoracic and transesophageal echocardiography before, 24 hours after, and 6 months after PTMC. Pulse Doppler velocities of the LAA were measured, including peak early diastolic (E wave), peak late diastolic (A wave), and peak systolic (S wave). The corresponding tissue Doppler velocities of the LAA, including peak early diastolic (E(LAA)), peak late diastolic (A(LAA)), and peak systolic (S(LAA)), were also measured. LAA ejection fraction was measured using the modified Simpson's method. The mean age of the 47 enrolled patients was 31.7 ± 10.26 years. Thirty-eight patients were in sinus rhythm, and the remaining nine were in atrial fibrillation. PTMC was successful in all patients. The pulse Doppler velocities of the LAA at baseline, after PTMC, and at 6-month follow-up were as follows: for the E wave, 15.29 ± 2.26, 17.02 ± 2.25, and 17.97 ± 2.55 cm/sec, respectively (P < .001); for the A wave 22.45 ± 4.11, 24.19 ± 4.21, and 25.99 ± 4.51 cm/sec, respectively (P < .001); and for the S wave, 28.52 ± 4.37, 31.45 ± 5.37, and 33.06 ± 4.99 cm/sec, respectively (P < .001). The corresponding tissue Doppler velocities of LAA were as follows: for E(LAA), 4.65 ± 0.91, 5.28 ± 0.85, and 5.80 ± 0.84 cm/sec, respectively (P < .001); for A(LAA), 6.67 ± 1.12, 7.33 ± 1.17, and 7.88 ± 1.22 cm/sec, respectively (P < .001); and for S(LAA), 4.67 ± 1.12, 5.52 ± 1.18, 6.07 ± 1.11 cm/sec, respectively (P < .001). There was a nonsignificant increase in LAA ejection fraction (48.97 ± 8.14% vs 52.3 ± 13.76% vs 52.11 ± 16.3%, respectively, P= .052). On subgroup analysis between patients in sinus rhythm and those with atrial fibrillation, there was no significant difference for LAA ejection fraction and pulse and tissue Doppler velocities. Very good intraclass correlation of the LAA parameters was also observed for the reproducibility of the data. The present study shows contractile dysfunction of the LAA in patients with critical mitral stenosis, which significantly improved after PTMC, and a further improvement was observed at 6-month follow-up. Favorable 6-month improvements in LAA parameters suggest continuous structural remodeling of the LAA after PTMC, which is clinically attributed to the absence of thromboembolism. Although there was an improvement in LAA function, it was far below the normal range, suggesting a need for continuous long-term monitoring and management of thromboembolism in these patients.