Background: Sunitinib, used widely in metastatic renal cell carcinoma, can result in hypertension, left ventricular dysfunction, and heart failure. However, the relationships between vascular function and cardiac dysfunction with sunitinib are poorly understood.

Methods and Results: In a multicenter prospective study of 84 metastatic renal cell carcinoma patients, echocardiography, arterial tonometry, and BNP (B-type natriuretic peptide) measures were performed at baseline and at 3.5, 15, and 33 weeks after sunitinib initiation, correlating with sunitinib cycles 1, 3, and 6. Mean change in vascular function parameters and 95% confidence intervals were calculated. Linear regression models were used to estimate associations between vascular function and left ventricular ejection fraction, longitudinal strain, diastolic function (E/e′), and BNP. After 3.5 weeks of sunitinib, mean systolic blood pressure increased by 9.5 mm Hg (95% confidence interval, 2.0–17.1; P=0.02) and diastolic blood pressure by 7.2 mm Hg (95% confidence interval, 4.3–10.0; P<0.001) across all participants. Sunitinib resulted in increases in large artery stiffness (carotid–femoral pulse wave velocity) and resistive load (total peripheral resistance and arterial elastance; all P<0.05) and changes in pulsatile load (total arterial compliance and wave reflection). There were no statistically significant associations between vascular function and systolic dysfunction (left ventricular ejection fraction and longitudinal strain). However, baseline total peripheral resistance, arterial elastance, and aortic impedance were associated with worsening diastolic function and filling pressures over time.

Conclusions: In patients with metastatic renal cell carcinoma, sunitinib resulted in early, significant increases in blood pressure, arterial stiffness, and resistive and pulsatile load within 3.5 weeks of treatment. Baseline vascular function parameters were associated with worsening diastolic but not systolic function.

背景：舒尼替尼广泛用于转移性肾细胞癌，可导致高血压，左心功能不全和心力衰竭。然而，舒尼替尼的血管功能与心脏功能障碍之间的关系知之甚少。

方法和结果：在一项对84例转移性肾细胞癌患者的多中心前瞻性研究中，在基线和舒尼替尼启动后3.5周，15周和33周进行了超声心动图，动脉眼压测量和BNP（B型利尿钠肽）测量。使用舒尼替尼周期1、3和6。计算了血管功能参数的平均变化和95％的置信区间。线性回归模型用于估计血管功能与左心室射血分数，纵向应变，舒张功能（E / e'）和BNP之间的关联。舒尼替尼治疗3.5周后，平均收缩压增加9.5 mm Hg（95％置信区间2.0-17.1；P = 0.02），舒张压增加7.2 mm Hg（95％置信区间4.3-10.0）。P <0.001）。舒尼替尼导致大动脉僵硬度（颈动脉-股动脉脉搏波速度）和阻力负荷（总外周阻力和动脉弹性；所有P <0.05）增加，脉动负荷变化（总动脉顺应性和波反射）。血管功能和收缩功能障碍（左心室射血分数和纵向应变）之间无统计学意义的关联。然而，随着时间的推移，基线总外周阻力，动脉弹性和主动脉阻抗与舒张功能恶化和充盈压相关。

结论：在转移性肾细胞癌患者中，舒尼替尼在治疗后3.5周内导致血压，动脉僵硬度以及抵抗力和脉搏负荷的早期显着升高。基线血管功能参数与舒张功能恶化相关，而与收缩功能无关。