化疗患者中最令人担忧的心脏毒性是心血管变化。为了增进对心脏毒性的理解，我们研究了如下问题：1)基于蒽环类化疗药物导致心脏功能障碍的患者是否有增加的交感神经活动和下降的运动能力；2) 这些反应是否类似于其他病因引起的心力衰竭患者的表现。研究对象包括16例基于蒽环类化疗药物导致的心力衰竭患者（心射血分数降低型）合并或未合并胸部放射治疗(HFrEFCA)、10例心力衰竭患者（心射血分数降低型），不与癌症治疗相关（HFrEF），以及16例年龄和身体质量指数匹配的健康对照组。测量了左室射血分数（LFEF，超声心动图）、峰值氧耗（peak V̇O2，心肺运动试验）、肌肉交感神经活动（MSNA，微神经图）和前臂血流（FBF，静脉阻塞血容积检测法）。我们发现，HFrEFCA患者的峰值氧耗和LVEF明显低于对照组（P<0.0001），但与HFrEF患者相似。HFrEFCA患者的交感神经活动爆发频率和发生率明显高于对照组（P<0.0001）。HFrEF患者与HFrEFCA患者之间无显著差异。峰值氧耗与MSNA爆发频率呈负相关 (r=-0.53, P=0.002)和发生率呈负相关(r=-0.38, P=0.01)，与LVEF呈正相关(r=0.71, P<0.0001)。综上所述，我们得出结论：由于蒽环类化疗药物导致的心力衰竭患者存在交感神经过度激活和运动能力下降。而且，这些生理变化类似于HFrEF患者。

Cardiotoxicity is the most worrying cardiovascular alteration in patients treated with chemotherapy. To improve the understanding regarding the cardiotoxicity, we studied whether: 1) patients with cardiac dysfunction related to anthracycline-based chemotherapy have augmented sympathetic nerve activity and decreased exercise capacity and 2) these responses are similar to those observed in patients with heart failure caused by other etiologies. Sixteen patients with heart failure with reduced ejection fraction related to anthracycline-based chemotherapy with or without chest radiation (HFrEFCA), 10 patients with heart failure with reduced ejection not related to cancer therapy (HFrEF), and 16 age-and body mass index (BMI)-matched healthy controls were studied. Left ventricular ejection fraction (LFEF, Echocardiography), peak oxygen consumption (peak V̇O2, cardiopulmonary exercise test), muscle sympathetic nerve activity (MSNA, microneurography) and forearm blood flow (FBF, venous occlusion plethysmography) were measured. We found that peak oxygen consumption peak V̇O2 and LVEF were significantly reduced in patients with HFrEFCA compared to controls (P<0.0001) but similar to those found in HFrEFCA patients. The sympathetic nerve activity burst frequency and incidence were significantly higher in patients with HFrEFCA than in controls (P<0.0001). No differences were found between HFrEF and HFrEFCA patients. Peak V̇O2 was inversely associated with MSNA burst frequency (r=-0.53, P=0.002) and burst incidence (r=-0.38, P=0.01), and directly associated with LVEF (r=0.71, P<0.0001). Taken together, we conclude that patients who develop heart failure due to anthracycline-based chemotherapy have sympathetic neural overdrive and reduced exercise capacity. In addition, these physiological changes are similar to those observed in patients with HFrEF.