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The Wait for High-Sensitivity Troponin Is Over—Proceed Cautiously Impact of the US Food and Drug Administration–Approved Sex-Specific Cutoff Values for High-Sensitivity Cardiac Troponin T to Diagnose Myocardial Infarction Clinical Outcomes Following Intravascular Imaging-Guided Versus Coronary Angiography–Guided Percutaneous Coronary Intervention With Stent Implantation: A Systematic Review and Bayesian Network Meta-Analysis of 31 Studies and 17,882 Patients Good response to tolvaptan shortens hospitalization in patients with congestive heart failure Revision: prognostic impact of baseline glucose levels in acute myocardial infarction complicated by cardiogenic shock-a substudy of the IABP-SHOCK II-trial Usefulness of longitudinal reconstructed optical coherence tomography images for predicting the need for the reverse wire technique during coronary bifurcation interventions Cardiac Implantable Electronic Devices in Patients With Left Ventricular Assist Systems Wearable Cardioverter-Defibrillator after Myocardial Infarction Use of Risk Assessment Tools to Guide Decision-Making in the Primary Prevention of Atherosclerotic Cardiovascular Disease A Special Report From the American Heart Association and American College of Cardiology What's new in the Fourth Universal Definition of Myocardial infarction?
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Clinical Trial2018 Mar;11(3):e004408.

JOURNAL：Circ Heart Fail. Article Link

Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma

Catino AB, Hubbard RA, Ky B et al. Keywords: VEGF TKI; blood pressure; carcinoma, renal cell; cardio-oncology; cardiotoxicity; hypertension; ventricular dysfunction

ABSTRACT

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.

© 2018 American Heart Association, Inc.
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