Tafamidis for the treatment of transthyretin cardiac amyloidosis (ATTR-CM) - Real-world data from a tertiary center
Abstract Introduction Tafamidis 61mg was shown to be the first treatment to reduce cardiovascular hospitalizations and to improve survival in patients with Transthyretin Amyloid Cardiomyopathy (ATTR-CM). Real-world data on the efficacy of transthyretin (TTR) stabilizers in patients with Heart Failur...
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| Veröffentlicht in: | European heart journal 2024-10, Vol.45 (Supplement_1) |
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| creator | Carvalho, R Rocha, B Maltes, S Cunha, G Marques, A Laranjeira, T Brizido, C Adragao, P Mendes, M Aguiar, C |
| description | Abstract
Introduction
Tafamidis 61mg was shown to be the first treatment to reduce cardiovascular hospitalizations and to improve survival in patients with Transthyretin Amyloid Cardiomyopathy (ATTR-CM). Real-world data on the efficacy of transthyretin (TTR) stabilizers in patients with Heart Failure (HF) due to ATTR-CM is scarce.
Purpose
We aimed to assess the use of tafamidis in our center, that features a dedicated Cardiomyopathy Clinic.
Methods
We conducted an all-comers single-centre prospective study of consecutive patients with symptomatic HF due to ATTR-CM followed up to November 2023. As per site protocol, the diagnosis was established according to the ESC algorithm and all patients were assessed at least twice yearly. Disease management plans include HF treatment tailored to ATTR-CM (CHAD-STOP) and treatment with disease-modifying tafamidis 61mg. The latter is considered in patients who meet the local protocol criteria, including key inclusion criteria - NYHA class I-II - and none of the exclusion criteria - e.g. estimated glomerular filtration rate (GFR) |
| doi_str_mv | 10.1093/eurheartj/ehae666.1040 |
| format | Article |
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Introduction
Tafamidis 61mg was shown to be the first treatment to reduce cardiovascular hospitalizations and to improve survival in patients with Transthyretin Amyloid Cardiomyopathy (ATTR-CM). Real-world data on the efficacy of transthyretin (TTR) stabilizers in patients with Heart Failure (HF) due to ATTR-CM is scarce.
Purpose
We aimed to assess the use of tafamidis in our center, that features a dedicated Cardiomyopathy Clinic.
Methods
We conducted an all-comers single-centre prospective study of consecutive patients with symptomatic HF due to ATTR-CM followed up to November 2023. As per site protocol, the diagnosis was established according to the ESC algorithm and all patients were assessed at least twice yearly. Disease management plans include HF treatment tailored to ATTR-CM (CHAD-STOP) and treatment with disease-modifying tafamidis 61mg. The latter is considered in patients who meet the local protocol criteria, including key inclusion criteria - NYHA class I-II - and none of the exclusion criteria - e.g. estimated glomerular filtration rate (GFR) <25mL/min. The primary endpoint was time to cardiovascular hospitalization or all-cause death.
Results
A total 226 ATTR-CM patients were identified, of whom 181 had a follow-up of at least 6 months and were included in the analysis (mean age 84 ± 7 years; 81% males, 16% hATTR-CM). Overall, there were 84 patients treated with tafamidis. Compared to non-treated patients, those receiving tafamidis were younger (mean age 83 vs. 86 years, p=0.007), more often with a lower NYHA functional class (e.g., NYHA I-II: 92 vs. 62%; p<0.001), scored higher on performance scales (e.g., Karnovsky >70: 67 vs 33%; p<0.001), and had less comorbidities (e.g., GFR: 40 vs. 30mL/min; p<0.001). Over a median follow-up of 16 months, 68 (37.6%) patients met the primary endpoint (49.5% vs. 22.6%, respectively; p<0.001). In multivariate analysis, treatment with tafamidis was an independent predictor of the primary endpoint (HR 0.24; 95%CI 0.13-0.43; p<0.001), adjusted for NYHA functional class (HR for NYHA I-II vs. III-IV: 0.54; 95%CI 0.32-0.92; p=0.023), NT-proBNP (HR 1.83; 95%CI 1.09-3.08; p=0.023) and high-sensitivity Troponin T (HR per 10 units: 1.01; 95%CI 1.01-1.02; p=0.024). These findings were consistent in multivariate analysis with any combination of the prior variables with either creatinine, GFR, albumin, or TTR type (wild-type vs. mutated). These results were primarily driven due to association of tafamidis treatment with increased survival.
Conclusion
The use of tafamidis in a cohort of patients with symptomatic HF and ATTR-CM was shown to be independently associated with reduced cardiovascular hospitalization or all-cause death. The effect had a similar magnitude of effect to that of the ATTR-ACT trial, suggesting that our local protocol based on the key criteria from this trial may allow for appropriate patient selection.]]></description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehae666.1040</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><ispartof>European heart journal, 2024-10, Vol.45 (Supplement_1)</ispartof><rights>The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com. 2024</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Carvalho, R</creatorcontrib><creatorcontrib>Rocha, B</creatorcontrib><creatorcontrib>Maltes, S</creatorcontrib><creatorcontrib>Cunha, G</creatorcontrib><creatorcontrib>Marques, A</creatorcontrib><creatorcontrib>Laranjeira, T</creatorcontrib><creatorcontrib>Brizido, C</creatorcontrib><creatorcontrib>Adragao, P</creatorcontrib><creatorcontrib>Mendes, M</creatorcontrib><creatorcontrib>Aguiar, C</creatorcontrib><title>Tafamidis for the treatment of transthyretin cardiac amyloidosis (ATTR-CM) - Real-world data from a tertiary center</title><title>European heart journal</title><description><![CDATA[Abstract
Introduction
Tafamidis 61mg was shown to be the first treatment to reduce cardiovascular hospitalizations and to improve survival in patients with Transthyretin Amyloid Cardiomyopathy (ATTR-CM). Real-world data on the efficacy of transthyretin (TTR) stabilizers in patients with Heart Failure (HF) due to ATTR-CM is scarce.
Purpose
We aimed to assess the use of tafamidis in our center, that features a dedicated Cardiomyopathy Clinic.
Methods
We conducted an all-comers single-centre prospective study of consecutive patients with symptomatic HF due to ATTR-CM followed up to November 2023. As per site protocol, the diagnosis was established according to the ESC algorithm and all patients were assessed at least twice yearly. Disease management plans include HF treatment tailored to ATTR-CM (CHAD-STOP) and treatment with disease-modifying tafamidis 61mg. The latter is considered in patients who meet the local protocol criteria, including key inclusion criteria - NYHA class I-II - and none of the exclusion criteria - e.g. estimated glomerular filtration rate (GFR) <25mL/min. The primary endpoint was time to cardiovascular hospitalization or all-cause death.
Results
A total 226 ATTR-CM patients were identified, of whom 181 had a follow-up of at least 6 months and were included in the analysis (mean age 84 ± 7 years; 81% males, 16% hATTR-CM). Overall, there were 84 patients treated with tafamidis. Compared to non-treated patients, those receiving tafamidis were younger (mean age 83 vs. 86 years, p=0.007), more often with a lower NYHA functional class (e.g., NYHA I-II: 92 vs. 62%; p<0.001), scored higher on performance scales (e.g., Karnovsky >70: 67 vs 33%; p<0.001), and had less comorbidities (e.g., GFR: 40 vs. 30mL/min; p<0.001). Over a median follow-up of 16 months, 68 (37.6%) patients met the primary endpoint (49.5% vs. 22.6%, respectively; p<0.001). In multivariate analysis, treatment with tafamidis was an independent predictor of the primary endpoint (HR 0.24; 95%CI 0.13-0.43; p<0.001), adjusted for NYHA functional class (HR for NYHA I-II vs. III-IV: 0.54; 95%CI 0.32-0.92; p=0.023), NT-proBNP (HR 1.83; 95%CI 1.09-3.08; p=0.023) and high-sensitivity Troponin T (HR per 10 units: 1.01; 95%CI 1.01-1.02; p=0.024). These findings were consistent in multivariate analysis with any combination of the prior variables with either creatinine, GFR, albumin, or TTR type (wild-type vs. mutated). These results were primarily driven due to association of tafamidis treatment with increased survival.
Conclusion
The use of tafamidis in a cohort of patients with symptomatic HF and ATTR-CM was shown to be independently associated with reduced cardiovascular hospitalization or all-cause death. The effect had a similar magnitude of effect to that of the ATTR-ACT trial, suggesting that our local protocol based on the key criteria from this trial may allow for appropriate patient selection.]]></description><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqNkE1Lw0AQhhdRsFb_guxRD6s72WSaPZbiF1SEkoO3ME0mJCXplt0t0n9vSotnTy_vwPMyPELcg34Cbc0z733L5OPmmVtiRBzPqb4QE8iSRFlMs0sx0WAzhZh_X4ubEDZa6xwBJyIU1NDQ1V2QjfMytiyjZ4oDb6N0zVhoG2J78By7razI1x1VkoZD77rahRF7mBfFSi0-H6WSK6Ze_Tjf17KmSLLxbpAkI_vYkT_IalxlfyuuGuoD351zKorXl2LxrpZfbx-L-VJVudUKUk5mBtZZjqTRotHERgPmPENbV2OsTQWcoQWNeYZJimAJawNpZgxYMxV4mq28C8FzU-58N4xvlKDLo7nyz1x5NlcezY0gnEC33_2X-QV70HYq</recordid><startdate>20241028</startdate><enddate>20241028</enddate><creator>Carvalho, R</creator><creator>Rocha, B</creator><creator>Maltes, S</creator><creator>Cunha, G</creator><creator>Marques, A</creator><creator>Laranjeira, T</creator><creator>Brizido, C</creator><creator>Adragao, P</creator><creator>Mendes, M</creator><creator>Aguiar, C</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20241028</creationdate><title>Tafamidis for the treatment of transthyretin cardiac amyloidosis (ATTR-CM) - Real-world data from a tertiary center</title><author>Carvalho, R ; Rocha, B ; Maltes, S ; Cunha, G ; Marques, A ; Laranjeira, T ; Brizido, C ; Adragao, P ; Mendes, M ; Aguiar, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c890-14e2731b586a069630ae30168e769dc8e7b3c1e56910685624619a6d314533193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carvalho, R</creatorcontrib><creatorcontrib>Rocha, B</creatorcontrib><creatorcontrib>Maltes, S</creatorcontrib><creatorcontrib>Cunha, G</creatorcontrib><creatorcontrib>Marques, A</creatorcontrib><creatorcontrib>Laranjeira, T</creatorcontrib><creatorcontrib>Brizido, C</creatorcontrib><creatorcontrib>Adragao, P</creatorcontrib><creatorcontrib>Mendes, M</creatorcontrib><creatorcontrib>Aguiar, C</creatorcontrib><collection>CrossRef</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carvalho, R</au><au>Rocha, B</au><au>Maltes, S</au><au>Cunha, G</au><au>Marques, A</au><au>Laranjeira, T</au><au>Brizido, C</au><au>Adragao, P</au><au>Mendes, M</au><au>Aguiar, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tafamidis for the treatment of transthyretin cardiac amyloidosis (ATTR-CM) - Real-world data from a tertiary center</atitle><jtitle>European heart journal</jtitle><date>2024-10-28</date><risdate>2024</risdate><volume>45</volume><issue>Supplement_1</issue><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract><![CDATA[Abstract
Introduction
Tafamidis 61mg was shown to be the first treatment to reduce cardiovascular hospitalizations and to improve survival in patients with Transthyretin Amyloid Cardiomyopathy (ATTR-CM). Real-world data on the efficacy of transthyretin (TTR) stabilizers in patients with Heart Failure (HF) due to ATTR-CM is scarce.
Purpose
We aimed to assess the use of tafamidis in our center, that features a dedicated Cardiomyopathy Clinic.
Methods
We conducted an all-comers single-centre prospective study of consecutive patients with symptomatic HF due to ATTR-CM followed up to November 2023. As per site protocol, the diagnosis was established according to the ESC algorithm and all patients were assessed at least twice yearly. Disease management plans include HF treatment tailored to ATTR-CM (CHAD-STOP) and treatment with disease-modifying tafamidis 61mg. The latter is considered in patients who meet the local protocol criteria, including key inclusion criteria - NYHA class I-II - and none of the exclusion criteria - e.g. estimated glomerular filtration rate (GFR) <25mL/min. The primary endpoint was time to cardiovascular hospitalization or all-cause death.
Results
A total 226 ATTR-CM patients were identified, of whom 181 had a follow-up of at least 6 months and were included in the analysis (mean age 84 ± 7 years; 81% males, 16% hATTR-CM). Overall, there were 84 patients treated with tafamidis. Compared to non-treated patients, those receiving tafamidis were younger (mean age 83 vs. 86 years, p=0.007), more often with a lower NYHA functional class (e.g., NYHA I-II: 92 vs. 62%; p<0.001), scored higher on performance scales (e.g., Karnovsky >70: 67 vs 33%; p<0.001), and had less comorbidities (e.g., GFR: 40 vs. 30mL/min; p<0.001). Over a median follow-up of 16 months, 68 (37.6%) patients met the primary endpoint (49.5% vs. 22.6%, respectively; p<0.001). In multivariate analysis, treatment with tafamidis was an independent predictor of the primary endpoint (HR 0.24; 95%CI 0.13-0.43; p<0.001), adjusted for NYHA functional class (HR for NYHA I-II vs. III-IV: 0.54; 95%CI 0.32-0.92; p=0.023), NT-proBNP (HR 1.83; 95%CI 1.09-3.08; p=0.023) and high-sensitivity Troponin T (HR per 10 units: 1.01; 95%CI 1.01-1.02; p=0.024). These findings were consistent in multivariate analysis with any combination of the prior variables with either creatinine, GFR, albumin, or TTR type (wild-type vs. mutated). These results were primarily driven due to association of tafamidis treatment with increased survival.
Conclusion
The use of tafamidis in a cohort of patients with symptomatic HF and ATTR-CM was shown to be independently associated with reduced cardiovascular hospitalization or all-cause death. The effect had a similar magnitude of effect to that of the ATTR-ACT trial, suggesting that our local protocol based on the key criteria from this trial may allow for appropriate patient selection.]]></abstract><cop>US</cop><pub>Oxford University Press</pub><doi>10.1093/eurheartj/ehae666.1040</doi></addata></record> |
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| source | Oxford Journals |
| title | Tafamidis for the treatment of transthyretin cardiac amyloidosis (ATTR-CM) - Real-world data from a tertiary center |
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