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Congestive Heart Failure

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Atrial Fibrillation and the Prognostic Performance of Biomarkers in Heart Failure Risk of Mortality Following Catheter Ablation of Atrial Fibrillation Cardiac resynchronization therapy with a defibrillator (CRTd) in failing heart patients with type 2 diabetes mellitus and treated by glucagon-like peptide 1 receptor agonists (GLP-1 RA) therapy vs. conventional hypoglycemic drugs: arrhythmic burden, hospitalizations for heart failure, and CRTd responders rate sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Frequency, predictors, and prognosis of ejection fraction improvement in heart failure: an echocardiogram-based registry study Vericiguat in Patients with Heart Failure and Reduced Ejection Fraction Novel percutaneous interventional therapies in heart failure with preserved ejection fraction: an integrative review Economic and Quality-of-Life Outcomes of Natriuretic Peptide–Guided Therapy for Heart Failure Unexpectedly Low Natriuretic Peptide Levels in Patients With Heart Failure
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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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