Key result
Patients who developed hypertension during VEGFR-TKI treatment experienced a significant decrease in left ventricular ejection fraction from 70.7% to 68.3% (p=0.03) and a decrease in E/e' from 11.9 to 10.3 (p=0.02).
Why the study?
VEGFR-TKIs cause adverse cardiovascular events such as hypertension and left ventricular failure, prompting investigation into the relationship between hypertension onset and cardiac diastolic dysfunction during VEGFR-TKI use.
Does the development of hypertension during VEGFR-TKI therapy associate with deterioration of left ventricular systolic and diastolic function?
Cohort (n=54)
No
Does the development of hypertension during VEGFR-TKI therapy associate with deterioration of left ventricular systolic and diastolic function?
Absolute Event Rate: 68.3% vs 70.7%
p-value: p=0.03
VEGFR-TKI-induced hypertension is associated with significant reductions in left ventricular ejection fraction and changes in diastolic function, highlighting the need for early echocardiographic monitoring and antihypertensive treatment.
Hypertension during VEGFR-TKI therapy may signal need for echocardiographic monitoring; leaves open whether BP control prevents systolic decline.
Vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor (VEGFR-TKI), an oral molecular targeted drug, reportedly causes serious adverse cardiovascular events such as hypertension and left ventricular failure. The association between VEGFR-TKI-induced hypertension and heart failure with preserved left ventricular ejection fraction (LVEF) (HFpEF) has been previously studied. Therefore, we investigated the relationship between hypertension onset and associated cardiac diastolic dysfunction due to VEGFR-TKI use. Patients who used VEGFR-TKIs (target drugs: sunitinib, axitinib, sorafenib, pazopanib, and cabozantinib) at the Department of Urology, Hokkaido Cancer Center were recruited between May 2009 and October 2021 and were divided into two groups based on whether their blood pressure was elevated during VEGFR-TKI use. The markers of left ventricular diastolic function (E/A, Dct (ms), mean E/e, septal e') and left ventricular systolic function (LVEF, LVDd, and LVDs) were evaluated. LVEF and mean E/e in the elevated blood pressure group (n = 41) showed significant changes before and after treatment. LVEF values (contractile function markers) in the TKI-HT (+) group significantly decreased from 70.7% ± 6.8% before treatment to 68.3% ± 7.8% after treatment (p = 0.03). Conversely, no significant difference was observed for any ventricular systolic function marker in the TKI-HT (−) group. E/e (diastolic function marker) in the TKI-HT (+) group significantly decreased from 11.9% ± 3.6% before treatment to 10.3% ± 3.0% after treatment (p = 0.02). However, no change was observed in any ventricular diastolic function marker in the TKI-HT (−) group. The results of this study suggest that cardiac function may be affected in patients using VEGFR-TKI. Furthermore, appropriate antihypertensive treatment and early monitoring with regular echocardiography, even in asymptomatic patients, may help prevent VEGFR-TKI-induced deterioration of systolic and diastolic function.
No takes yet. Share an insight, caveat, or question.
Hashino et al. (2023) conducted a cohort in Renal cell carcinoma (n=54). VEGFR-TKI-induced hypertension vs. Baseline (before treatment) and patients without VEGFR-TKI-induced hypertension was evaluated on Left Ventricular Ejection Fraction (LVEF) before and after treatment in the TKI-HT (+) group (p=0.03). Patients who developed hypertension during VEGFR-TKI treatment experienced a significant decrease in left ventricular ejection fraction from 70.7% to 68.3% (p=0.03) and a decrease in E/e' from 11.9 to 10.3 (p=0.02).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: