Anthracycline Therapy Is Associated With Cardiomyocyte Atrophy and Preclinical Manifestations of Heart Disease
The goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy. Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specific...
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| Veröffentlicht in: | JACC. Cardiovascular imaging 2018-08, Vol.11 (8), p.1045-1055 |
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| creator | Ferreira de Souza, Thiago Quinaglia A.C. Silva, Thiago Osorio Costa, Felipe Shah, Ravi Neilan, Tomas G. Velloso, Lício Nadruz, Wilson Brenelli, Fabricio Sposito, Andrei Carvalho Matos-Souza, Jose Roberto Cendes, Fernando Coelho, Otávio Rizzi Jerosch-Herold, Michael Coelho-Filho, Otavio Rizzi |
| description | The goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy.
Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.
A total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.
At baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p 10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.
A decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036)
[Display omitted] |
| doi_str_mv | 10.1016/j.jcmg.2018.05.012 |
| format | Article |
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Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.
A total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.
At baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p < 0.001), and mean ECV had increased by 0.037 to 0.36 ± 0.04 (p = 0.004), while mean τic had decreased by 62 ms to 119 ± 54 ms (p = 0.004). Myocardial edema peaked at about 146 to 231 days (p < 0.001). LV mass index was associated with τic (β = 4.1 ± 1.5 g/m2 per 100-ms increase in τic, p = 0.007) but not with ECV. Cardiac troponin T (mean 4.6 ± 1.4 pg/ml at baseline) increased significantly after anthracycline treatment (p < 0.001). Total LV cardiomyocyte mass, estimated as: (1 − ECV) × LV mass, declined more rapidly after anthracycline therapy, with peak cardiac troponin T >10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.
A decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036)
[Display omitted]</description><identifier>ISSN: 1936-878X</identifier><identifier>EISSN: 1876-7591</identifier><identifier>DOI: 10.1016/j.jcmg.2018.05.012</identifier><identifier>PMID: 30092965</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>anthracycline ; cardiac troponin T ; fibrosis ; left ventricular remodeling ; magnetic resonance imaging ; T1 mapping techniques</subject><ispartof>JACC. Cardiovascular imaging, 2018-08, Vol.11 (8), p.1045-1055</ispartof><rights>2018 American College of Cardiology Foundation</rights><rights>Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-ef10b9d3434b8860de5228ddcaea134dfad201320b4796261edac9dd20604e183</citedby><cites>FETCH-LOGICAL-c455t-ef10b9d3434b8860de5228ddcaea134dfad201320b4796261edac9dd20604e183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1936878X18304479$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30092965$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferreira de Souza, Thiago</creatorcontrib><creatorcontrib>Quinaglia A.C. Silva, Thiago</creatorcontrib><creatorcontrib>Osorio Costa, Felipe</creatorcontrib><creatorcontrib>Shah, Ravi</creatorcontrib><creatorcontrib>Neilan, Tomas G.</creatorcontrib><creatorcontrib>Velloso, Lício</creatorcontrib><creatorcontrib>Nadruz, Wilson</creatorcontrib><creatorcontrib>Brenelli, Fabricio</creatorcontrib><creatorcontrib>Sposito, Andrei Carvalho</creatorcontrib><creatorcontrib>Matos-Souza, Jose Roberto</creatorcontrib><creatorcontrib>Cendes, Fernando</creatorcontrib><creatorcontrib>Coelho, Otávio Rizzi</creatorcontrib><creatorcontrib>Jerosch-Herold, Michael</creatorcontrib><creatorcontrib>Coelho-Filho, Otavio Rizzi</creatorcontrib><title>Anthracycline Therapy Is Associated With Cardiomyocyte Atrophy and Preclinical Manifestations of Heart Disease</title><title>JACC. Cardiovascular imaging</title><addtitle>JACC Cardiovasc Imaging</addtitle><description>The goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy.
Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.
A total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.
At baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p < 0.001), and mean ECV had increased by 0.037 to 0.36 ± 0.04 (p = 0.004), while mean τic had decreased by 62 ms to 119 ± 54 ms (p = 0.004). Myocardial edema peaked at about 146 to 231 days (p < 0.001). LV mass index was associated with τic (β = 4.1 ± 1.5 g/m2 per 100-ms increase in τic, p = 0.007) but not with ECV. Cardiac troponin T (mean 4.6 ± 1.4 pg/ml at baseline) increased significantly after anthracycline treatment (p < 0.001). Total LV cardiomyocyte mass, estimated as: (1 − ECV) × LV mass, declined more rapidly after anthracycline therapy, with peak cardiac troponin T >10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.
A decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036)
[Display omitted]</description><subject>anthracycline</subject><subject>cardiac troponin T</subject><subject>fibrosis</subject><subject>left ventricular remodeling</subject><subject>magnetic resonance imaging</subject><subject>T1 mapping techniques</subject><issn>1936-878X</issn><issn>1876-7591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kc1u1DAUhSNERUvhBVggL9kk9U_iJBJCGk2hrdQKFkWws-7YN41HSTzYnkp5G56FJ6ujKVXZsLJln3Pse74se8dowSiTZ9tiq8e7glPWFLQqKOMvshPW1DKvq5a9TPtWyLypm5_H2esQtpRKKsv6VXYsKG15K6uTzK2m2HvQsx7shOS2Rw-7mVwFsgrBaQsRDflhY0_W4I114-z0HJGsone7fiYwGfLN4-K2GgZyA5PtMESI1k2BuI5cIvj45_e5DQgB32RHHQwB3z6up9n3L59v15f59deLq_XqOtdlVcUcO0Y3rRGlKDdNI6nBivPGGA0ITJSmA5PGFpxuyrqVXDI0oFuTDiUtkTXiNPt0yN3tNyMajVP0MKidtyP4WTmw6t-byfbqzt0ryVopqiXgw2OAd7_2aSI12qBxGGBCtw-K0ya1zAUXScoPUu1dCB67p2cYVQsptVULKbWQUrRSiVQyvX_-wSfLXzRJ8PEgwFTTvUWvgrY4aTQ29R2VcfZ_-Q_boqjJ</recordid><startdate>201808</startdate><enddate>201808</enddate><creator>Ferreira de Souza, Thiago</creator><creator>Quinaglia A.C. 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Cardiovascular imaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ferreira de Souza, Thiago</au><au>Quinaglia A.C. Silva, Thiago</au><au>Osorio Costa, Felipe</au><au>Shah, Ravi</au><au>Neilan, Tomas G.</au><au>Velloso, Lício</au><au>Nadruz, Wilson</au><au>Brenelli, Fabricio</au><au>Sposito, Andrei Carvalho</au><au>Matos-Souza, Jose Roberto</au><au>Cendes, Fernando</au><au>Coelho, Otávio Rizzi</au><au>Jerosch-Herold, Michael</au><au>Coelho-Filho, Otavio Rizzi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anthracycline Therapy Is Associated With Cardiomyocyte Atrophy and Preclinical Manifestations of Heart Disease</atitle><jtitle>JACC. Cardiovascular imaging</jtitle><addtitle>JACC Cardiovasc Imaging</addtitle><date>2018-08</date><risdate>2018</risdate><volume>11</volume><issue>8</issue><spage>1045</spage><epage>1055</epage><pages>1045-1055</pages><issn>1936-878X</issn><eissn>1876-7591</eissn><abstract>The goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy.
Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.
A total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.
At baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p < 0.001), and mean ECV had increased by 0.037 to 0.36 ± 0.04 (p = 0.004), while mean τic had decreased by 62 ms to 119 ± 54 ms (p = 0.004). Myocardial edema peaked at about 146 to 231 days (p < 0.001). LV mass index was associated with τic (β = 4.1 ± 1.5 g/m2 per 100-ms increase in τic, p = 0.007) but not with ECV. Cardiac troponin T (mean 4.6 ± 1.4 pg/ml at baseline) increased significantly after anthracycline treatment (p < 0.001). Total LV cardiomyocyte mass, estimated as: (1 − ECV) × LV mass, declined more rapidly after anthracycline therapy, with peak cardiac troponin T >10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.
A decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036)
[Display omitted]</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30092965</pmid><doi>10.1016/j.jcmg.2018.05.012</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | anthracycline cardiac troponin T fibrosis left ventricular remodeling magnetic resonance imaging T1 mapping techniques |
| title | Anthracycline Therapy Is Associated With Cardiomyocyte Atrophy and Preclinical Manifestations of Heart Disease |
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