Reciprocal Mechanisms Linking Cancer and Cardiovascular Disease: Emerging Paradigms in Onco-Cardiology

BACKGROUND: There is a dual causal relationship between cancer and Cardiovascular Disease (CVD) due to similar risk factors and overlapping convergent molecular mechanisms. Factors such as hypertension, diabetes, dyslipidemia, obesity, smoking, and inactivity overlap with chronic inflammation, oxidative stress, endothelial dysfunction, and stromal transformation, coupling atherogenesis with tumour growth. NF- κB and JAK/STAT signalling, as well as the destabilisation of the plaque and angiogenesis, rely on pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), which also facilitate immune escape and fibrotic remodelling. Clonal hematopoiesis (DNMT3A, TET2 defects) is a myeloid inflammation amplifier that links ageing of hematopoiesis to vascular damage and cancer-proneness. Exosomal microRNAs in tumour-derived extracellular vesicles, however, can remodel endothelial tone and immunity, and cancer-induced cachexia hastens cardiac wasting and repair. OBJECTIVE: This study aims to explore the standard molecular mechanisms that underlie CVD-cancer interaction and to describe the diagnostic, imaging, and therapeutic approaches to allow both early diagnosis and effective cardioprotection without undermining anticancer responses. METHOD: This study undertook a narrative literature review by systematically searching the websites of PubMed (MEDLINE), Web of Science, and ScienceDirect between January 2010 and December 2025 using the keywords and terms shared molecular mechanisms, clinical interactions, and therapeutic, with cardiovascular disease and cancer. RESULTS: Cancer treatment causes cardiovascular risk: anthracycline and trastuzumab damage cardiomyocytes, VEGF-pathway blockers trigger hypertension and endothelial dysfunction, and immune blockers may lead to myocarditis and other adverse outcomes. Epidemiological research makes a bidirectional risk assertion by confirming that cancer survivors are at increased risk of CVD and that heart failure patients are at increased risk of cancer. Multimodality imaging (strain echocardiography, cardiac MRI, PET) and biomarker panels (troponins, natriuretic peptides, cytokines, circulating miRNAs) are used as integrative techniques to detect subclinical injury and cardioprotection and sustain anticancer efficacy. CONCLUSION: Inflammation, metabolic dysregulation, and thrombosis are the intersections between CVD and cancer. Specific approaches to address these pathways, combined with biomarker-based surveillance and the promotion of oncology-cardiology care, could lead to earlier diagnosis, less toxic treatments, and better longterm outcomes.