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High-Sensitivity Troponin and The Application of Risk Stratification Thresholds in Patients with Suspected Acute Coronary Syndrome Open sesame technique in percutaneous coronary intervention for ST-elevation myocardial infarction Multivessel PCI Guided by FFR or Angiography for Myocardial Infarction Optimal medical therapy vs. coronary revascularization for patients presenting with chronic total occlusion: A meta-analysis of randomized controlled trials and propensity score adjusted studies Deficiency of GATA3-Positive Macrophages Improves Cardiac Function Following Myocardial Infarction or Pressure Overload Hypertrophy Fractional flow reserve vs. angiography in guiding management to optimize outcomes in non-ST-segment elevation myocardial infarction: the British Heart Foundation FAMOUS-NSTEMI randomized trial The year in cardiovascular medicine 2020: acute coronary syndromes and intensive cardiac care New AHA/ACC/HRS Guidance on Sudden Cardiac Death Prevention 2017 AHA/ACC Clinical Performance and Quality Measures for Adults With ST-Elevation and Non–ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Performance Measures Imaging Coronary Anatomy and Reducing Myocardial Infarction

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.