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. 2017 Apr 13;12(4):e0175544.
doi: 10.1371/journal.pone.0175544. eCollection 2017.

Anthracyclines induce early changes in left ventricular systolic and diastolic function: A single centre study

Affiliations

Anthracyclines induce early changes in left ventricular systolic and diastolic function: A single centre study

Anita Boyd et al. PLoS One. .

Abstract

Aims: 2 dimensional (2D) strain analysis detects subclinical left ventricular (LV) systolic dysfunction. Our aim was to evaluate changes in LV systolic and diastolic function in breast cancer patients early after anthracycline chemotherapy, and to identify predisposing factors.

Methods and results: 140 patients were assessed by detailed echocardiography before and within seven days post treatment. LV ejection fraction (LVEF), global longitudinal strain (GLS), strain rate and radial and circumferential strain were assessed. Additionally, left atrial volumes and LV diastolic parameters were evaluated. LVEF although reduced after treatment, remained within the normal range (60±3% vs. 59±3%, p = 0.04). Triplane GLS was significantly reduced after treatment (-20.0±1.6% vs. -19.1±1.8%, p<0.001). Subclinical LV dysfunction (>11% reduction in GLS compared to before therapy) occurred in 22% (29/135). Impaired diastolic function grade significantly increased from 46% to 57% (p<0.001) after treatment. Furthermore, diastolic dysfunction was more common in the subgroup group with reduced systolic GLS compared to those without changes in GLS (30% vs. 11%; p = 0.04). No risk factors or clinical parameters were associated with the development of subclinical LV dysfunction; however the percentage change in early diastolic strain rate and the E velocity were independent predictors of >11% reduction in GLS.

Conclusion: Twenty two percent of patients had subclinical LV dysfunction by GLS, whilst none had cardiotoxicity defined by LVEF, demonstrating that GLS is more sensitive for detection of subclinical LV systolic dysfunction immediately after anthracycline therapy. Diastolic dysfunction increased, particularly in the group with reduced GLS, demonstrating the close pathophysiological relationship between systolic and diastolic function.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Global longitudinal strain.
Peak systolic negative deflection from six segments (basal, mid and apical) from each view A. Four chamber view–septal and lateral walls; B. Two chamber view–inferior and anterior walls and C. Long axis view–posterior and anteroseptal walls. X-axis = Time (s); Y-axis = Strain (%).
Fig 2
Fig 2. Strain rate.
Systolic strain rate (Ssr), early diastolic strain rate (Esr) and late diastolic strain rate (Esr). X-axis = Time (s); Y-axis = Strain rate (s-1).
Fig 3
Fig 3. Radial and circumferential strain.
A. Radial strain (peak systolic positive deflection) and B. Circumferential strain (peak systolic negative deflection) from the parasternal short axis view at the level of the papillary muscles (septal, anteroseptal, anterior, lateral, posterior, inferior segments). X-axis = Time (s); Y-axis = Strain (%).
Fig 4
Fig 4. Bullseye map of GLS after anthracycline therapy.
A. in the group with subclinical LV dysfunction (reduction in GLS>11%) and B. in the group without subclinical LV dysfunction. * p<0.05 compared to before anthracycline therapy.

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