TY - JOUR
T1 - Cardiac mechanics and dysfunction with anthracyclines in the community
T2 - Results from the PREDICT study
AU - Narayan, Hari K.
AU - Wei, Wei
AU - Feng, Ziding
AU - Lenihan, Daniel
AU - Plappert, Ted
AU - Englefield, Virginia
AU - Fisch, Michael
AU - Ky, Bonnie
N1 - Funding Information:
Funding This study was supported by the NCI U10 CA 189828-02, U10 CA 045809-25, and an NCI Echocardiography Supplement. BK was supported by NHLBI R01-HL118018 and NHLBI K23-HL095661. HKN was supported by NICHD T32-HD060550. WW was supported by NIH P30 CA016672.
Funding Information:
This study was supported by the NCI U10 CA 189828-02, U10 CA 045809-25, and an NCI Echocardiography Supplement. BK was supported by NHLBI R01-HL118018 and NHLBI K23-HL095661. HKN was supported by NICHD T32-HD060550. WW was supported by NIH P30 CA016672.
PY - 2017
Y1 - 2017
N2 - Background: Our objective was to determine the relevance of changes in myocardial mechanics in diagnosing and predicting cancer therapeutics-related cardiac dysfunction (CTRCD) in a community-based population treated with anthracyclines. Methods: Quantitative measures of cardiac mechanics were derived from 493 echocardiograms in 165 participants enrolled in the PREDICT study (A Multicenter Study in Patients Undergoing AnthRacycline-Based Chemotherapy to Assess the Effectiveness of Using Biomarkers to Detect and Identify Cardiotoxicity and Describe Treatment). Echocardiograms were obtained primarily at baseline (prior to anthracyclines), 6 and 12 months. Predictors included changes in strain; strain rate; indices of contractile function derived from the end-systolic pressure-volume relationship (end-systolic elastance (Eessb) and the left ventricular (LV) volume at an end-systolic pressure of 100 mm Hg (V100)); total arterial load (effective arterial elastance (Ea)) and ventricular-arterial coupling (Ea/Eessb). Logistic regression models determined the diagnostic and prognostic associations of changes in these measures and CTRCD, defined as a LV ejection fraction decline ≥10 to <50%. Results: By 12 months, 31 participants developed CTRCD. Longitudinal and circumferential strain and strain rate, V100, Ea, and Ea/Eessb each demonstrated significant diagnostic associations, with a 1-7% increased odds of CTRCD (p<0.05). Changes in longitudinal strain rate (area under the curve (AUC) 0.719 (95% CI 0.595 to 0.843)), V100 (AUC 0.796 (95% CI 0.686 to 0.903)) and Ea (AUC 0.742 (95% CI 0.632 to 0.852)) from baseline to 6 months were individually predictive of CTRCD at 12 months. Conclusions: Changes in non-invasively derived measures of myocardial mechanics are diagnostic and predictive of cardiac dysfunction with anthracycline chemotherapy in community populations. Our findings support the non-invasive assessment of measures of myocardial mechanics more broadly in clinical practice and emphasise the role of serial assessments of these measures during and after cardiotoxic cancer therapy.
AB - Background: Our objective was to determine the relevance of changes in myocardial mechanics in diagnosing and predicting cancer therapeutics-related cardiac dysfunction (CTRCD) in a community-based population treated with anthracyclines. Methods: Quantitative measures of cardiac mechanics were derived from 493 echocardiograms in 165 participants enrolled in the PREDICT study (A Multicenter Study in Patients Undergoing AnthRacycline-Based Chemotherapy to Assess the Effectiveness of Using Biomarkers to Detect and Identify Cardiotoxicity and Describe Treatment). Echocardiograms were obtained primarily at baseline (prior to anthracyclines), 6 and 12 months. Predictors included changes in strain; strain rate; indices of contractile function derived from the end-systolic pressure-volume relationship (end-systolic elastance (Eessb) and the left ventricular (LV) volume at an end-systolic pressure of 100 mm Hg (V100)); total arterial load (effective arterial elastance (Ea)) and ventricular-arterial coupling (Ea/Eessb). Logistic regression models determined the diagnostic and prognostic associations of changes in these measures and CTRCD, defined as a LV ejection fraction decline ≥10 to <50%. Results: By 12 months, 31 participants developed CTRCD. Longitudinal and circumferential strain and strain rate, V100, Ea, and Ea/Eessb each demonstrated significant diagnostic associations, with a 1-7% increased odds of CTRCD (p<0.05). Changes in longitudinal strain rate (area under the curve (AUC) 0.719 (95% CI 0.595 to 0.843)), V100 (AUC 0.796 (95% CI 0.686 to 0.903)) and Ea (AUC 0.742 (95% CI 0.632 to 0.852)) from baseline to 6 months were individually predictive of CTRCD at 12 months. Conclusions: Changes in non-invasively derived measures of myocardial mechanics are diagnostic and predictive of cardiac dysfunction with anthracycline chemotherapy in community populations. Our findings support the non-invasive assessment of measures of myocardial mechanics more broadly in clinical practice and emphasise the role of serial assessments of these measures during and after cardiotoxic cancer therapy.
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U2 - 10.1136/openhrt-2016-000524
DO - 10.1136/openhrt-2016-000524
M3 - Article
C2 - 28123764
AN - SCOPUS:85019853861
SN - 2053-3624
VL - 4
JO - Open Heart
JF - Open Heart
IS - 1
M1 - e000524
ER -