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Low-Dose Aspirin Discontinuation and Risk of Cardiovascular Events: A Swedish Nationwide, Population-Based Cohort Study Targeting the Immune System in Atherosclerosis: JACC State-of-the-Art Review Door to Balloon Time: Is There a Point That Is Too Short? Nonculprit Stenosis Evaluation Using Instantaneous Wave-Free Ratio in Patients With ST-Segment Elevation Myocardial Infarction Bare metal versus drug eluting stents for ST-segment elevation myocardial infarction in the TOTAL trial Comparison of Outcomes of Patients With ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention Analyzed by Age Groups (<75, 75 to 85, and >85 Years); (Results from the Bremen STEMI Registry) Location of the culprit coronary lesion and its association with delay in door-to-balloon time (from a multicenter registry of primary percutaneous coronary intervention) Volume brings value Percutaneous coronary intervention reduces mortality in myocardial infarction patients with comorbidities: Implications for elderly patients with diabetes or kidney disease Remote ischaemic conditioning and healthcare system delay in patients with ST-segment elevation 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.