Abstract
Cardiovascular disease is a major cause of morbidity and mortality in patients with cancer and in cancer survivors. Lipoprotein(a) [Lp(a)] is a largely genetically determined causal risk factor for atherosclerotic cardiovascular disease and calcific aortic valve disease, acting through proatherogenic, proinflammatory, and potentially prothrombotic pathways. These mechanisms may be relevant in cancer, where inflammation, hypercoagulability, metabolic disturbances, and treatment-related cardiovascular toxicity increase cardiovascular risk. Observational studies have also linked circulating Lp(a) to tumor characteristics, disease stage, or prognosis in several malignancies. However, these findings are heterogeneous, often derived from small, retrospective, or single-center cohorts, and do not establish a causal role for Lp(a) in cancer development or progression. Evidence relating Lp(a) specifically to cancer therapy-related cardiovascular toxicity remains limited, and a prospective biomarker cohort found no association between baseline Lp(a) and major adverse cardiovascular events. This review summarizes the biology and measurement of Lp(a), critically evaluates its reported oncological associations, and examines its relevance in cardio-oncology. Currently, Lp(a) should be interpreted primarily as part of comprehensive cardiovascular risk assessment rather than as a cancer-specific or cardiotoxicity biomarker. Prospective, treatment-specific studies are needed to determine whether Lp(a) improves risk prediction or represents an actionable therapeutic target in this population.