From the Division of Cardiovascular Medicine (A.B.C., J.C.F.) and Division of Oncology (N.A.), Department of Medicine, University of Utah, Salt Lake City; Department of Biostatistics, Epidemiology and Informatics (R.A.H., B.K.), Division of Cardiology (J.A.C., D.H., A.M.S., T.P., V.E., B.K.), Division of Hematology and Oncology (S.K., N.B.H., V.N.), and Division of Nephrology (R.T.), Department of Medicine, and Abramson Cancer Center (S.K., N.B.H., V.N., B.K.), University of Pennsylvania, Philadelphia; Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY (I.P.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (S.E.); Division of Cardiovascular Medicine, Department of Medicine, University Hospitals Case Medical Center, Cleveland, OH (C.E.); Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN (M.G.); and Division of Cardiology, Department of Medicine, Washington University in St Louis, MO (D.L.).
Circ Heart Fail. 2018 Mar;11(3):e004408. doi: 10.1161/CIRCHEARTFAILURE.117.004408.
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.
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; =0.02) and diastolic blood pressure by 7.2 mm Hg (95% confidence interval, 4.3-10.0; <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 <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.
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.
舒尼替尼广泛用于转移性肾细胞癌的治疗，可能导致高血压、左心室功能障碍和心力衰竭。然而，舒尼替尼与血管功能和心脏功能障碍之间的关系尚不清楚。
在一项针对 84 例转移性肾细胞癌患者的多中心前瞻性研究中，在舒尼替尼开始治疗后的 3.5、15 和 33 周进行了超声心动图、动脉张力测定和 BNP（B 型利钠肽）测量，并与舒尼替尼的第 1、3 和 6 个周期相关联。计算了血管功能参数的平均变化及其 95%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 之间的相关性。在舒尼替尼治疗 3.5 周后，所有参与者的收缩压平均升高 9.5mmHg（95%置信区间，2.0-17.1；=0.02），舒张压平均升高 7.2mmHg（95%置信区间，4.3-10.0；<0.001）。舒尼替尼导致大动脉僵硬度（颈股脉搏波速度）和阻力负荷（总外周阻力和动脉弹性；均<0.05）增加以及脉动负荷（总动脉顺应性和波反射）变化。血管功能与收缩功能障碍（左心室射血分数和纵向应变）之间没有统计学显著相关性。然而，基线总外周阻力、动脉弹性和主动脉阻抗与随时间恶化的舒张功能和充盈压相关。
在转移性肾细胞癌患者中，舒尼替尼在治疗开始后 3.5 周内导致血压、动脉僵硬度以及阻力和脉动负荷显著早期增加。基线血管功能参数与舒张功能恶化但与收缩功能障碍无关。
