TY - JOUR
T1 - Renin-angiotensin system blockade therapy after transcatheter aortic valve implantation
AU - Ochiai, Tomoki
AU - Saito, Shigeru
AU - Yamanaka, Futoshi
AU - Shishido, Koki
AU - Tanaka, Yutaka
AU - Yamabe, Tsuyoshi
AU - Shirai, Shinichi
AU - Tada, Norio
AU - Araki, Motoharu
AU - Naganuma, Toru
AU - Watanabe, Yusuke
AU - Yamamoto, Masanori
AU - Hayashida, Kentaro
N1 - Publisher Copyright:
© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
PY - 2018/4
Y1 - 2018/4
N2 - Objective The persistence of left ventricular (LV) hypertrophy is associated with poor clinical outcomes after transcatheter aortic valve implantation (TAVI) for aortic stenosis. However, the optimal medical therapy after TAVI remains unknown. We investigated the effect of renin 'angiotensin system (RAS) blockade therapy on LV hypertrophy and mortality in patients undergoing TAVI. Methods Between October 2013 and April 2016, 1215 patients undergoing TAVI were prospectively enrolled in the Optimized CathEter vAlvular iNtervention (OCEAN)-TAVI registry. This cohort was stratified according to the postoperative usage of RAS blockade therapy with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs). Patients with at least two prescriptions dispensed 180 days apart after TAVI and at least a 6-month follow-up constituted the RAS blockade group (n=371), while those not prescribed any ACE inhibitors or ARBs after TAVI were included in the no RAS blockade group (n=189). Results At 6 months postoperatively, the RAS blockade group had significantly greater LV mass index regression than the no RAS blockade group ('9±24% vs '2±25%, p=0.024). Kaplan-Meier analysis revealed a significantly lower cumulative 2-year mortality in the RAS blockade than that in the no RAS blockade group (7.5% vs 12.5%; log-rank test, p=0.031). After adjusting for confounding factors, RAS blockade therapy was associated with significantly lower all-cause mortality (HR, 0.45; 95% CI 0.22 to 0.91; p=0.025). Conclusions Postoperative RAS blockade therapy is associated with greater LV mass index regression and reduced all-cause mortality. These data need to be confirmed by a prospective randomised controlled outcome trial.
AB - Objective The persistence of left ventricular (LV) hypertrophy is associated with poor clinical outcomes after transcatheter aortic valve implantation (TAVI) for aortic stenosis. However, the optimal medical therapy after TAVI remains unknown. We investigated the effect of renin 'angiotensin system (RAS) blockade therapy on LV hypertrophy and mortality in patients undergoing TAVI. Methods Between October 2013 and April 2016, 1215 patients undergoing TAVI were prospectively enrolled in the Optimized CathEter vAlvular iNtervention (OCEAN)-TAVI registry. This cohort was stratified according to the postoperative usage of RAS blockade therapy with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs). Patients with at least two prescriptions dispensed 180 days apart after TAVI and at least a 6-month follow-up constituted the RAS blockade group (n=371), while those not prescribed any ACE inhibitors or ARBs after TAVI were included in the no RAS blockade group (n=189). Results At 6 months postoperatively, the RAS blockade group had significantly greater LV mass index regression than the no RAS blockade group ('9±24% vs '2±25%, p=0.024). Kaplan-Meier analysis revealed a significantly lower cumulative 2-year mortality in the RAS blockade than that in the no RAS blockade group (7.5% vs 12.5%; log-rank test, p=0.031). After adjusting for confounding factors, RAS blockade therapy was associated with significantly lower all-cause mortality (HR, 0.45; 95% CI 0.22 to 0.91; p=0.025). Conclusions Postoperative RAS blockade therapy is associated with greater LV mass index regression and reduced all-cause mortality. These data need to be confirmed by a prospective randomised controlled outcome trial.
KW - angiotensin receptor blockers
KW - angiotensin-converting enzyme inhibitors
KW - aortic valve stenosis
KW - renin-angiotensin system
KW - transcatheter aortic valve replacement
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U2 - 10.1136/heartjnl-2017-311738
DO - 10.1136/heartjnl-2017-311738
M3 - Article
C2 - 28986405
AN - SCOPUS:85044822998
SN - 1355-6037
VL - 104
SP - 644
EP - 651
JO - Heart
JF - Heart
IS - 8
ER -