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

Anthracyclines induce early changes in left ventricular systolic and diastolic function: A single centre study.
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DOI:
10.1371/journal.pone.0175544
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发表时间:
2017
期刊:
影响因子:
3.7
通讯作者:
Thomas L
Thomas L
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Boyd A;Stoodley P;Richards D;Hui R;Harnett P;Vo K;Marwick T;Thomas L

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二维(2D)应变分析检测亚临床左心室(LV)收缩功能障碍。我们的目的是评估乳腺癌患者在蒽环类药物化疗后早期左室收缩和舒张功能的变化,并确定易感因素。140例患者在治疗前和治疗后7天内通过详细的超声心动图进行评估。评估左室弹射分数(LVEF)、整体纵向应变(GLS)、应变率以及径向和周向应变。此外,评估左房容积和左室舒张参数。治疗后LVEF虽降低,但仍在正常范围内(60±3% vs. 59±3%,p = 0.04)。治疗后三平面GLS显著降低(-20.0±1.6% vs -19.1±1.8%,p<0.001)。亚临床左室功能障碍(与治疗前相比GLS降低11%)发生率为22%(29/135)。治疗后舒张功能受损等级从46%显著增加到57% (p<0.001)。此外,与GLS无变化的亚组相比,收缩期GLS降低的亚组中舒张功能障碍更常见(30% vs 11%; p = 0.04)。无危险因素或临床参数与亚临床左室功能障碍的发生相关;然而,舒张早期应变率和E速的百分比变化是GLS降低11%的独立预测因子。通过GLS, 22%的患者出现亚临床左室功能障碍,而没有患者出现LVEF定义的心脏毒性,这表明GLS对蒽环类药物治疗后立即检测亚临床左室收缩功能障碍更敏感。舒张功能障碍增加,特别是在GLS降低组,表明收缩和舒张功能之间存在密切的病理生理关系。
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. 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. 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.