Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma

Catino, Anna; Hubbard, Rebecca A.; Chirinos, Julio A.; Townsend, Ray; Keefe, Stephen Michael; Haas, Naomi B.; Puzanov, Igor; Fang, James C.; Agarwal, Neeraj; Hyman, David M.; Smith, Amanda M.; Gordon, M.S.; Plappert, Theodore; Englefield, Virginia; Narayan, Vivek; Ewer, Steven M.; ElAmm, Chantal; Lenihan, Daniel J.; Ky, Bonnie

doi:10.1161/circheartfailure.117.004408

Cited by 38 publications

(31 citation statements)

References 47 publications

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“…In this study renin and aldosterone levels did not change after sorafenib initiation; however, vascular stiffness did increase. These results were confirmed by Catino et al ( 35 ), who demonstrated increases in arterial stiffness, resistance, and pulsatile load in the setting of sunitinib use. Although the absence of an increase in renin and aldosterone may indicate that the RAAS system is not involved in VEGFi-mediated hypertension, this finding may not fully eliminate the possibility of a relative imbalance between VEGF and RAAS such that the absence of a compensatory decrease in renin and aldosterone after VEGFi administration could possibly play a role in VEGFi-mediated hypertension.…”

Section: Discussionsupporting

confidence: 70%

Renin-Angiotensin-Aldosterone System Modulates Blood Pressure Response During Vascular Endothelial Growth Factor Receptor Inhibition

Bottinor

Shuey

Manouchehri

et al. 2019

JACC: CardioOncology

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OBJECTIVES This study postulated that antihypertensive therapy with renin-angiotensin-aldosterone system (RAAS) inhibition may mitigate vascular endothelial growth factor inhibitor (VEGFi)–mediated increases in blood pressure more effectively than other antihypertensive medications in patients receiving VEGFi therapy. BACKGROUND VEGFi therapy is commonly used in the treatment of cancer. One common side effect of VEGFi therapy is elevated blood pressure. Evidence suggests that the RAAS may be involved in VEGFi-mediated increases in blood pressure. METHODS This retrospective cohort analysis was performed using a de-identified version of the electronic health record at Vanderbilt University Medical Center in Nashville, Tennessee. Subjects with cancer who were exposed to VEGFi therapy were identified, and blood pressure and medication data were extracted. Changes in mean systolic and diastolic blood pressure in response to VEGFi therapy in patients receiving RAAS inhibitor (RAASi) therapy before VEGFi initiation were compared with changes in mean systolic and diastolic blood pressure in patients not receiving RAASi therapy before VEGFi initiation. RESULTS Mean systolic and diastolic blood pressure rose in both groups after VEGFi use; however, patients who had RAASi therapy before VEGFi initiation had a significantly lower increase in systolic blood pressure as compared with patients with no RAASi therapy (2.46 mm Hg [95% confidence interval: 0.7 to 4.2] compared with 4.56 mm Hg [95% confidence interval: 3.5 to 5.6], respectively; p = 0.034). CONCLUSIONS In a real-world clinical population, RAASi therapy before VEGFi initiation may ameliorate VEGFi-mediated increases in blood pressure. Randomized clinical trials are needed to further our understanding of the role of RAASi therapy in VEGFi-mediated increases in blood pressure. (J Am Coll Cardiol CardioOnc 2019;1:14–23)

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Section: Discussionsupporting

confidence: 70%

Renin-Angiotensin-Aldosterone System Modulates Blood Pressure Response During Vascular Endothelial Growth Factor Receptor Inhibition

Bottinor

Shuey

Manouchehri

et al. 2019

JACC: CardioOncology

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“…A study in 84 patients with metastatic RCC demonstrated that sunitinib increased large artery stiffness within the first weeks of therapy, as measured by increased carotid-femoral pulse wave velocity. 124 This increase in vascular stiffness was also observed after 3 weeks of sorafenib treatment in another clinical study. 125 Nonetheless, the exact contribution of vascular stiffness to the prohypertensive effects of VEGFI remains unclear, as it could both be a cause and consequence of hypertension.…”

Section: Anticancer Therapy and Hypertensionsupporting

confidence: 53%

Hypertension and Prohypertensive Antineoplastic Therapies in Cancer Patients

Dorst

Dobbin

Neves

et al. 2021

Circulation Research

104

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The development of a wide range of novel antineoplastic therapies has improved the prognosis for patients with a wide range of malignancies, which has increased the number of cancer survivors substantially. Despite the oncological benefit, cancer survivors are exposed to short- and long-term adverse cardiovascular toxicities associated with anticancer therapies. Systemic hypertension, the most common comorbidity among cancer patients, is a major contributor to the increased risk for developing these adverse cardiovascular events. Cancer and hypertension have common risk factors, have overlapping pathophysiological mechanisms and hypertension may also be a risk factor for some tumor types. Many cancer therapies have prohypertensive effects. Although some of the mechanisms by which these antineoplastic agents lead to hypertension have been characterized, further preclinical and clinical studies are required to investigate the exact pathophysiology and the optimal management of hypertension associated with anticancer therapy. In this way, monitoring and management of hypertension before, during, and after cancer treatment can be improved to minimize cardiovascular risks. This is vital to optimize cardiovascular health in patients with cancer and survivors, and to ensure that advances in terms of cancer survivorship do not come at the expense of increased cardiovascular toxicities.

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“…139 Dihydropyridine calcium channel blockers, such as nifedipine and amlodipine, are direct vasodilators and may be very useful in complex BP control of these patients, although they are negative inotropes. 140 However, the non-dihydropyridine calcium channel blockers (diltiazem and verapamil) are typically contraindicated, since they are inducers of cytochrome P450 3A4 (CYP3A4) resulting in increased VEGF inhibitor drug levels. 141 Factors that can contribute to BP elevation need to be addressed, such as obstructive sleep apnoea, excessive alcohol consumption, nonsteroidal anti-inflammatory drugs, adrenal steroid hormones, erythropoietin, oral contraceptive hormones and sympathomimetics, such as methylphenidate.…”

Section: Annals Of Oncologymentioning

confidence: 99%

Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations

et al. 2020

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Cancer and cardiovascular (CV) disease are the most prevalent diseases in the developed world. Evidence increasingly shows that these conditions are interlinked through common risk factors, coincident in an ageing population, and are connected biologically through some deleterious effects of anticancer treatment on CV health. Anticancer therapies can cause a wide spectrum of short-and long-term cardiotoxic effects. An explosion of novel cancer therapies has revolutionised this field and dramatically altered cancer prognosis. Nevertheless, these new therapies have introduced unexpected CV complications beyond heart failure. Common CV toxicities related to cancer therapy are defined, along with suggested strategies for prevention, detection and treatment. This ESMO consensus article proposes to define CV toxicities related to cancer or its therapies and provide guidance regarding prevention, screening, monitoring and treatment of CV toxicity. The majority of anticancer therapies are associated with some CV toxicity, ranging from asymptomatic and transient to more clinically significant and long-lasting cardiac events. It is critical however, that concerns about potential CV damage resulting from anticancer therapies should be weighed against the potential benefits of cancer therapy, including benefits in overall survival. CV disease in patients with cancer is complex and treatment needs to be individualised. The scope of cardio-oncology is wide and includes prevention, detection, monitoring and treatment of CV toxicity related to cancer therapy, and also ensuring the safe development of future novel cancer treatments that minimise the impact on CV health. It is anticipated that the management strategies discussed herein will be suitable for the majority of patients. Nonetheless, the clinical judgment of physicians remains extremely important; hence, when using these best clinical practices to inform treatment options and decisions, practitioners should also consider the individual circumstances of their patients on a case-by-case basis.

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Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma

Cited by 38 publications

References 47 publications

Renin-Angiotensin-Aldosterone System Modulates Blood Pressure Response During Vascular Endothelial Growth Factor Receptor Inhibition

Renin-Angiotensin-Aldosterone System Modulates Blood Pressure Response During Vascular Endothelial Growth Factor Receptor Inhibition

Hypertension and Prohypertensive Antineoplastic Therapies in Cancer Patients

Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations

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