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Heart failure and cardiomyopathies
Original research article
Cardiac mechanics and dysfunction with anthracyclines in the community: results from the PREDICT study
  1. Hari K Narayan1,
  2. Wei Wei2,
  3. Ziding Feng2,
  4. Daniel Lenihan3,
  5. Ted Plappert4,
  6. Virginia Englefield4,
  7. Michael Fisch5 and
  8. Bonnie Ky4,6
  1. 1Division of Cardiology, Department of Pediatrics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
  2. 2Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  3. 3Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  4. 4Department of Medicine, Division of Cardiovascular Medicine, The University of Pennsylvania, Philadelphia, Pennsylvania, USA
  5. 5Department of General Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  6. 6Department of Biostatistics and Epidemiology, The University of Pennsylvania, Philadelphia, Pennsylvania, USA
  1. Correspondence to Dr Bonnie Ky; bonnie.ky{at}uphs.upenn.edu

Abstract

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.

Trial registration number NCT01032278; Pre-results.

  • HEART FAILURE

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/openhrt-2016-000524

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    Footnotes

    • Contributors BK designed the echocardiography study, monitored data collection, wrote the statistical analysis plan, analysed the data and drafted and revised the manuscript. She is guarantor. HKN wrote the statistical analysis plan, analysed the data and drafted and revised the manuscript. WW and ZF analysed the data and drafted and revised the manuscript. TP and VE performed data collection and analyses of all echocardiograms and critically reviewed and revised the manuscript. DL and MF conceived the parent study, implemented the trial, monitored data collection and critically reviewed and revised the manuscript. All authors provided final approval of the manuscript.

    • 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.

    • Competing interests None declared.

    • Ethics approval Institutional Review Board of each participating centre.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data sharing statement No additional data are available.