TY - JOUR
T1 - Effect of Percutaneous Edge-to-Edge Repair on Mitral Valve Area and Its Association With Pulmonary Hypertension and Outcomes
AU - Utsunomiya, Hiroto
AU - Itabashi, Yuji
AU - Kobayashi, Sayuki
AU - Rader, Florian
AU - Hussaini, Asma
AU - Makar, Moody
AU - Trento, Alfredo
AU - Siegel, Robert J.
AU - Kar, Saibal
AU - Shiota, Takahiro
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/8/15
Y1 - 2017/8/15
N2 - Percutaneous edge-to-edge repair using the MitraClip system causes reduction in mitral valve area (MVA). However, its clinical impact is not fully elucidated. This study assessed the impact of postprocedural MVA reduction on pulmonary hypertension and outcomes. A total of 92 patients with grades 3 to 4 + mitral regurgitation (MR) who underwent MitraClip therapy were retrospectively reviewed. Using intraprocedural, 3-dimensional transesophageal echocardiography, postprocedural MVA was obtained by 2 optimized planes through the medial and lateral orifices of the repaired valve. MVA was reduced by 60.1% immediately after MitraClip procedure (p <0.001). Postprocedural MVA correlated moderately with mean transmitral pressure gradient (TMPG) in the majority of patients (r = −0.56, p <0.001), but discordance of MVA and TMPG was observed in 40% of patients. In multivariable linear regression analysis, postprocedural MVA ≤1.94 cm2 was independently associated with a blunted decrease in systolic pulmonary artery pressure at 1-month follow-up (β-estimate −4.63, 95% confidence interval −9.71 to −0.15, p = 0.042). Postprocedural MVA ≤1.94 cm2 was an independent predictor of all-cause mortality and heart failure hospitalization after MitraClip (hazard ratio 4.28, 95% confidence interval 1.56 to 11.7, p = 0.005) even after adjustment for age, gender, atrial fibrillation, cause of MR, left ventricular systolic function, pre-existing pulmonary hypertension, and residual MR. After further adjustment for TMPG ≥5 mm Hg, postprocedural MVA ≤1.94 cm2 remained predictive for adverse outcomes (p = 0.048). In conclusion, the intraprocedural assessment of MVA by 3-dimensional transesophageal echocardiography can predict hemodynamic response and postprocedural prognosis after MitraClip therapy.
AB - Percutaneous edge-to-edge repair using the MitraClip system causes reduction in mitral valve area (MVA). However, its clinical impact is not fully elucidated. This study assessed the impact of postprocedural MVA reduction on pulmonary hypertension and outcomes. A total of 92 patients with grades 3 to 4 + mitral regurgitation (MR) who underwent MitraClip therapy were retrospectively reviewed. Using intraprocedural, 3-dimensional transesophageal echocardiography, postprocedural MVA was obtained by 2 optimized planes through the medial and lateral orifices of the repaired valve. MVA was reduced by 60.1% immediately after MitraClip procedure (p <0.001). Postprocedural MVA correlated moderately with mean transmitral pressure gradient (TMPG) in the majority of patients (r = −0.56, p <0.001), but discordance of MVA and TMPG was observed in 40% of patients. In multivariable linear regression analysis, postprocedural MVA ≤1.94 cm2 was independently associated with a blunted decrease in systolic pulmonary artery pressure at 1-month follow-up (β-estimate −4.63, 95% confidence interval −9.71 to −0.15, p = 0.042). Postprocedural MVA ≤1.94 cm2 was an independent predictor of all-cause mortality and heart failure hospitalization after MitraClip (hazard ratio 4.28, 95% confidence interval 1.56 to 11.7, p = 0.005) even after adjustment for age, gender, atrial fibrillation, cause of MR, left ventricular systolic function, pre-existing pulmonary hypertension, and residual MR. After further adjustment for TMPG ≥5 mm Hg, postprocedural MVA ≤1.94 cm2 remained predictive for adverse outcomes (p = 0.048). In conclusion, the intraprocedural assessment of MVA by 3-dimensional transesophageal echocardiography can predict hemodynamic response and postprocedural prognosis after MitraClip therapy.
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U2 - 10.1016/j.amjcard.2017.05.036
DO - 10.1016/j.amjcard.2017.05.036
M3 - Article
C2 - 28673638
AN - SCOPUS:85021651399
SN - 0002-9149
VL - 120
SP - 662
EP - 669
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 4
ER -