TY - JOUR
T1 - Unveiling outcomes in coexisting severe aortic stenosis and transthyretin cardiac amyloidosis
AU - Rosenblum, Hannah
AU - Masri, Ahmad
AU - Narotsky, David L.
AU - Goldsmith, Jeff
AU - Hamid, Nadira
AU - Hahn, Rebecca T.
AU - Kodali, Susheel
AU - Vahl, Torsten
AU - Nazif, Tamim
AU - Khalique, Omar K.
AU - Bokhari, Sabahat
AU - Soman, Prem
AU - Cavalcante, João L.
AU - Maurer, Mathew S.
AU - Castaño, Adam
N1 - Funding Information:
Dr. Rosenblum is supported by the National Institutes of Health T32 HL007854. Dr. Masri has research grants from Pfizer and Akcea (paid to OHSU). Dr. Maurer reports grant support from National Institutes of Health [R01HL139671–01], [R21AG058348] and [K24AG036778], consulting income from Pfizer, GSK, EIdos, Prothena, Akcea and Alnylam, and institution received clinical trial funding from Pfizer, Prothena, Eidos and Alnylam.
Funding Information:
Dr. Rosenblum is supported by the National Institutes of Health T32 HL007854. Dr. Masri has research grants from Pfizer and Akcea (paid to OHSU). Dr. Maurer reports grant support from National Institutes of Health [R01HL139671?01], [R21AG058348] and [K24AG036778], consulting income from Pfizer, GSK, EIdos, Prothena, Akcea and Alnylam, and institution received clinical trial funding from Pfizer, Prothena, Eidos and Alnylam. Conflict of interest: R.T.H. reports speaker fees from Boston Scientific Corporation and Baylis Medical; consulting for Abbott Structural, Edwards Lifesciences, Medtronic, Navigate, Philips Healthcare and Siemens Healthcare; equity with Navigate; non-financial support from 3mensio; and is the Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored trials, for which she receives no direct industry compensation. T.N. reports honoraria and consulting for Edwards LifeSciences, Medtronic, and Boston Scientific. P.S. reports grant support from Pfizer. At the time of the majority of this writing and manuscript development, A.C. was Assistant Professor of Medicine and Co-Director of the Columbia University Center for Cardiac Amyloidosis; he is now a full-time employee of Pfizer Inc. All other authors have nothing to disclose.
Funding Information:
: R.T.H. reports speaker fees from Boston Scientific Corporation and Baylis Medical; consulting for Abbott Structural, Edwards Lifesciences, Medtronic, Navigate, Philips Healthcare and Siemens Healthcare; equity with Navigate; non‐financial support from 3mensio; and is the Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry‐sponsored trials, for which she receives no direct industry compensation. T.N. reports honoraria and consulting for Edwards LifeSciences, Medtronic, and Boston Scientific. P.S. reports grant support from Pfizer. At the time of the majority of this writing and manuscript development, A.C. was Assistant Professor of Medicine and Co‐Director of the Columbia University Center for Cardiac Amyloidosis; he is now a full‐time employee of Pfizer Inc. All other authors have nothing to disclose. Conflict of interest
Publisher Copyright:
© 2020 European Society of Cardiology
PY - 2021/2
Y1 - 2021/2
N2 - Aims: Advances in diagnostic imaging have increased the recognition of coexisting transthyretin cardiac amyloidosis (ATTR-CA) and severe aortic stenosis (AS), with a reported prevalence between 8–16%. In this prospective study, we aimed to evaluate the implications of ATTR-CA on outcomes after transcatheter aortic valve replacement (TAVR). Methods and results: At two academic centres, we screened patients with severe AS undergoing TAVR for ATTR-CA. Using Kaplan–Meier analysis, we compared survival free from death and a combined endpoint of death and first heart failure hospitalization between patients with and without ATTR-CA. Cox proportional-hazards models were used to determine the association of ATTR-CA with these endpoints. The rate of heart failure hospitalization was compared amongst those with and without ATTR-CA. Overall, 204 patients (83 years, 65% male, Society of Thoracic Surgeons score 6.6%, 72% New York Heart Association class III/IV) were included, 27 (13%) with ATTR-CA. Over a median follow-up of 2.04 years, there was no difference in mortality (log rank, P = 0.99) or the combined endpoint (log rank, P = 0.79) between patients with and without ATTR-CA. In Cox proportional-hazards models, the presence of ATTR-CA was not associated with death. However, patients with ATTR-CA had increased rates of heart failure hospitalization at 1 year (0.372 vs. 0.114 events/person-year, P < 0.004) and 3 years (0.199 vs. 0.111 events/person-year, P = 0.087) following TAVR. Conclusion: In moderate-risk patients with severe AS undergoing TAVR, there was a 13% prevalence of ATTR-CA, which did not affect mortality. The observed increase in heart failure hospitalization following TAVR in those with ATTR-CA suggests the consequences of the underlying infiltrative myopathy.
AB - Aims: Advances in diagnostic imaging have increased the recognition of coexisting transthyretin cardiac amyloidosis (ATTR-CA) and severe aortic stenosis (AS), with a reported prevalence between 8–16%. In this prospective study, we aimed to evaluate the implications of ATTR-CA on outcomes after transcatheter aortic valve replacement (TAVR). Methods and results: At two academic centres, we screened patients with severe AS undergoing TAVR for ATTR-CA. Using Kaplan–Meier analysis, we compared survival free from death and a combined endpoint of death and first heart failure hospitalization between patients with and without ATTR-CA. Cox proportional-hazards models were used to determine the association of ATTR-CA with these endpoints. The rate of heart failure hospitalization was compared amongst those with and without ATTR-CA. Overall, 204 patients (83 years, 65% male, Society of Thoracic Surgeons score 6.6%, 72% New York Heart Association class III/IV) were included, 27 (13%) with ATTR-CA. Over a median follow-up of 2.04 years, there was no difference in mortality (log rank, P = 0.99) or the combined endpoint (log rank, P = 0.79) between patients with and without ATTR-CA. In Cox proportional-hazards models, the presence of ATTR-CA was not associated with death. However, patients with ATTR-CA had increased rates of heart failure hospitalization at 1 year (0.372 vs. 0.114 events/person-year, P < 0.004) and 3 years (0.199 vs. 0.111 events/person-year, P = 0.087) following TAVR. Conclusion: In moderate-risk patients with severe AS undergoing TAVR, there was a 13% prevalence of ATTR-CA, which did not affect mortality. The observed increase in heart failure hospitalization following TAVR in those with ATTR-CA suggests the consequences of the underlying infiltrative myopathy.
KW - Cardiac amyloidosis
KW - Severe aortic stenosis
KW - Transcatheter aortic valve replacement
KW - Transthyretin cardiac amyloidosis
UR - http://www.scopus.com/inward/record.url?scp=85090305838&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85090305838&partnerID=8YFLogxK
U2 - 10.1002/ejhf.1974
DO - 10.1002/ejhf.1974
M3 - Article
C2 - 32729170
AN - SCOPUS:85090305838
VL - 23
SP - 250
EP - 258
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
SN - 1388-9842
IS - 2
ER -