Abstract 17397: Cardiac Dysfunction Resulting From Therapeutic Inhibition of the Vascular Endothelial Growth Factor Signaling Pathway in Cancer Patients
Background: Inhibitors of the vascular endothelial growth factor signaling pathway (VSP) are increasingly used in cancer treatments. VSP inhibitor therapy is frequently associated with blood pressure (BP) elevation and, rarely, with new-onset cardiomyopathy and heart failure. The extent to which VSP inhibitor therapy may lead to asymptomatic changes in cardiac structure and function is unknown.
Methods: 37 patients (aged 58.3±9.8 years, 76% men) with solid tumors (73% renal cell carcinoma) underwent ≥2 (2.6±0.8) serial echocardiograms before and after initiation of VSP inhibitor therapy. Multivariable longitudinal regression was used to determine change in LV measures during therapy.
Results: At baseline, before starting VSP inhibitor therapy, all patients had normal measures of cardiac structure and function: LV mass (204±62 g), EF (64±8%), and average E’ (0.11±0.03 m/s). During the follow up period (52±35 weeks), BP increased from 131±14/79±11 mmHg to 142±16/89±13 mmHg (P<0.001). There were no significant changes in LV mass, wall thickness, EF, or conventional measures of diastolic function (Table ). However, changes in LV systolic function were detected based on measures of myocardial deformation, including worse global longitudinal and transverse strain, and paradoxically ‘better’ circumferential and radial strain rate (Table ).
Conclusions: Patients started on VSP inhibitor therapy experience a decline in global longitudinal strain and a paradoxical improvement in circumferential strain. This pattern of altered LV function is similar to that described in hypertensive heart disease, despite the lack of concurrent change in LV mass or wall thickness. Further research is needed to investigate the mechanisms underlying these findings. These results also reinforce the need for close monitoring of cardiac function during VSP inhibitor therapy.
- © 2013 by American Heart Association, Inc.