Abstract
ABSTRACT
Cancer and hypertension (HTN) frequently coexist, and their relationship is increasingly recognized as a clinically relevant intersection between oncology and cardiovascular medicine. However, the extent to which this association reflects shared risk factors, common biological mechanisms, or treatment‐related effects remains incompletely understood. In this narrative review, we focus specifically on the cancer–HTN interface and summarize epidemiological evidence while considering the potential influence of age, obesity, metabolic syndrome, dietary patterns, and psychosocial factors. We further discuss overlapping mechanisms, including chronic inflammation, renin–angiotensin–aldosterone system activation, calcium signaling abnormalities, activation of the sympathetic nervous system, metabolic dysregulation, dysbiosis of the gut microbiota and genetic and epigenetic alterations. Particular attention is given to the bidirectional interactions between cancer therapies and HTN, as well as the heterogeneous evidence concerning potential associations between antihypertensive medications and cancer outcomes. We also summarize the clinical assessment and management of cancer therapy‐related HTN, including Common Terminology Criteria for Adverse Events grading, blood pressure monitoring, cardiovascular risk assessment, and current recommendations from the European Society of Hypertension (ESH) and American Heart Association. Emerging issues, including immune checkpoint inhibitor‐associated cardiovascular toxicity, the potential role of cardiac biomarkers such as troponin and natriuretic peptides, and the prognostic significance of treatment‐induced HTN across different tumor types, are also discussed. Overall, the available evidence supports an important clinical interplay between cancer and HTN but does not establish a uniform causal relationship. Future prospective studies integrating tumor biology, cardiovascular risk factors, treatment exposure, and longitudinal blood pressure (BP) assessment are needed to clarify these interactions and improve individualized cardio‐oncology care.