Key result
Anti-VEGFR therapy significantly increased peripheral systolic blood pressure (+13 mm Hg, P<0.001) and central systolic blood pressure (+14 mm Hg, P<0.001) over 6 weeks.
Why the study?
Do anti-VEGFR drugs alter central blood pressure and cardiovascular function in patients with solid tumors?
Observational (n=29)
Do anti-VEGFR drugs alter central blood pressure and cardiovascular function in patients with solid tumors?
p-value: p=<0.001
Anti-VEGFR therapy causes early, reversible increases in blood pressure and arterial stiffness, alongside persistent subclinical alterations in left ventricular systolic and diastolic function.
May warrant BP monitoring with anti-VEGFR therapy; leaves open long-term cardiovascular consequences and optimal management.
BACKGROUND: In the last 2 decades, new drugs that oppose the effects of vascular endothelial growth factor receptor (VEGFR), and thus angiogenesis, have considerably improved treatment of solid tumors. These anti-VEGFR drugs, however, are burdened by several side effects, particularly relevant on heart and vessels. The aim of this study was to analyze the changes in cardiovascular structure and function associated with use of anti-VEGFR drugs. METHODS: Twenty-nine patients (27 affected by renal and 2 by thyroid cancer), received treatment with anti-VEGFR drugs. Brachial blood pressure (BP), central BP, carotid-femoral pulse wave velocity (cfPWV), augmentation index (Aix), and several echocardiographic markers of systolic and diastolic left ventricular functions including global longitudinal strain were measured before starting treatment (T0), after 2 (T1), and 6 weeks (T2) of treatment. RESULTS: Anti-VEGFR treatment was accompanied by a significant increase of both peripheral (systolic BP +13±15.5mm Hg, diastolic BP +7.1±9.3mm Hg, P < 0.001) and central BP (systolic BP +14±14.2mm Hg, diastolic BP +7.3±10.4mm Hg, P < 0.001) and a significant raise of cfPWV (+1.3±1.8 m/sec, P = 0.003). There was also a significant alteration of markers of diastolic and subclinical left ventricular systolic function, including global longitudinal strain (-19.9±3.8% at T0, -17.8±2.6% at T2, P < 0.05). All the changes were already evident at T1, worsened at T2 in patients who maintained oncological treatment, but disappeared at T2 in patients in whom treatment was stopped. CONCLUSIONS: All the changes regarding BP and cfPWV appear early after treatment initiation and seem to be reversible if treatment is stopped, instead diastolic and systolic left ventricular function are persistently altered by anti-VEGFR drugs.
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Moreo et al. (2015) conducted an observational in Renal and thyroid cancer (n=29). Anti-VEGFR drugs vs. Baseline was evaluated on Changes in cardiovascular structure and function including blood pressure, pulse wave velocity, and echocardiographic markers (p=<0.001). Anti-VEGFR therapy significantly increased peripheral systolic blood pressure (+13 mm Hg, P<0.001) and central systolic blood pressure (+14 mm Hg, P<0.001) over 6 weeks.
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