Pub 1
Pub 1
Pub 1
Treatment
Introduction
Cancer and hypertension, two formidable adversaries of human health, have increasingly
been recognized for their interconnectedness. Cancer patients undergoing treatment often
face the daunting challenge of managing not only their primary disease but also the
emergence or exacerbation of high blood pressure (hypertension). This article delves into the
intricate relationship between cancer and hypertension, exploring the underlying
mechanisms, prevalence, impact on treatment outcomes, and strategies for effective
management.
Cancer and hypertension share common risk factors, such as obesity, sedentary lifestyle, and
aging. Moreover, certain cancer treatments, including chemotherapy agents and targeted
therapies, can directly contribute to the development of hypertension. For instance, vascular
endothelial growth factor (VEGF) inhibitors, commonly used in cancer treatment, can disrupt
normal vascular function, leading to elevated blood pressure.
The prevalence of hypertension among cancer patients varies depending on factors such as
cancer type, treatment modalities, and patient demographics. Studies have reported
significantly higher rates of hypertension in cancer patients compared to the general
population. For instance, research indicates that up to 75% of patients receiving certain
targeted therapies develop hypertension during treatment.
7
2024, IRJEdT Volume: 06, Issue: 04 | April-2024
the risk of cardiovascular complications, such as heart failure and stroke, which can further
impede cancer treatment and diminish quality of life.
1. Endothelial Dysfunction: Cancer and its treatment can impair endothelial function,
leading to vasoconstriction and increased peripheral resistance, thereby elevating
blood pressure.
2. Renin-Angiotensin-Aldosterone System (RAAS) Dysregulation: Disruption of the
RAAS, either by cancer itself or by certain treatments, can result in sodium retention
and arterial vasoconstriction, contributing to hypertension.
3. Sympathetic Nervous System Activation: Cancer-related stress and treatment-
induced toxicity can stimulate sympathetic nervous system activity, leading to
heightened vascular tone and blood pressure elevation.
4. Inflammation and Oxidative Stress: Chronic inflammation and oxidative stress,
hallmark features of cancer, can promote endothelial dysfunction and vascular
remodeling, predisposing to hypertension.
Management Strategies
8
2024, IRJEdT Volume: 06, Issue: 04 | April-2024
3. Pharmacological Interventions: Antihypertensive medications, including
angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers
(ARBs), calcium channel blockers, and diuretics, may be prescribed to achieve blood
pressure goals while minimizing interference with cancer therapy.
4. Individualized Treatment Approaches: Tailoring treatment regimens to individual
patient characteristics, including cancer type, stage, comorbidities, and treatment
regimen, is essential for optimizing therapeutic efficacy and minimizing adverse
effects.
5. Collaborative Care: Close collaboration between oncologists, cardiologists, primary
care physicians, and other healthcare providers is crucial for integrated management
of hypertension and cancer, ensuring comprehensive patient care and optimal
treatment outcomes.
Conclusion
Reference
9
2024, IRJEdT Volume: 06, Issue: 04 | April-2024
4. Izzedine H, Ederhy S, Goldwasser F et al. Management of hypertension in angiogenesis
inhibitor-treated patients. Ann Oncol 2009;20:807–15. 10.1093/annonc/mdn713
5. Kim CS, Han K-D, Choi HS et al. Association of hypertension and blood pressure with
kidney cancer risk: a nationwide population-based cohort study. Hypertension
2020;75:1439–46. 10.1161/HYPERTENSIONAHA.120.14820
6. Sanfilippo KM, Mctigue KM, Fidler CJ et al. Hypertension and obesity and the risk of
kidney cancer in 2 large cohorts of US men and women. Hypertension 2014;63:934–41.
10.1161/HYPERTENSIONAHA.113.02953
7. Stocks T, Van Hemelrijck M, Manjer J et al. Blood pressure and risk of cancer incidence
and mortality in the Metabolic Syndrome and Cancer Project. Hypertension 2012;59:802–10.
10.1161/HYPERTENSIONAHA.111.189258
8. Gunasekaran PM, Chertow GM, Bhalla V et al. Current status of angiotensin receptor
blocker recalls. Hypertension 2019;74:1275–8. 10.1161/HYPERTENSIONAHA.119.13955
10. Touyz RM, Herrmann SMS, Herrmann J. Vascular toxicities with VEGF inhibitor
therapies-focus on hypertension and arterial thrombotic events. J Am Soc Hypertens
2018;12:409–25. 10.1016/j.jash.2018.03.
12. Pandey AK, Singhi EK, Arroyo JP et al. Mechanisms of VEGF (vascular endothelial
growth factor) inhibitor-associated hypertension and vascular disease. Hypertension
2018;71:e1–8. 10.1161/HYPERTENSIONAHA.117.10271
13. Izzedine H, Mangier M, Ory V et al. Expression patterns of RelA and c-mip are
associated with different glomerular diseases following anti-VEGF therapy. Kidney Int
2014;85:457–70. 10.1038/ki.2013.344
10
2024, IRJEdT Volume: 06, Issue: 04 | April-2024
14. van Dorst DCH, Kabadayi S, Oomen-de Hoop E et al. Treatment and implications of
vascular endothelial growth factor inhibitor-induced blood pressure rise: a clinical cohort
study. J Am Heart Assoc 2023;12:e028050.
15. Cohen JB, Geara AS, Hogan JJ et al. Hypertension in cancer patients and survivors:
epidemiology, diagnosis, and management. JACC CardioOncol 2019;1:238–51.
10.1016/j.jaccao.2019.11.009
16. Knijnenburg SL, Jaspers MW, Van Der Pal HJ et al. Renal dysfunction and elevated
blood pressure in long-term childhood cancer survivors. Clin J Am Soc Nephrol
2012;7:1416–27. 10.2215/CJN.09620911 .
11
2024, IRJEdT Volume: 06, Issue: 04 | April-2024