Lipidparadox bij kanker: LDL-C dekt de lading niet voor cardiovasculair risico

Cardiovascular disease has emerged as a leading cause of morbidity and mortality among patients with cancer, yet conventional lipid-based risk assessment remains poorly suited to this population. Growing evidence supports a cancer-associated lipid paradox, in which atherosclerotic events occur frequently despite low or well-controlled low-density lipoprotein cholesterol (LDL-C) levels. This paradox reflects the convergence of systemic inflammation, immune activation, hypercoagulability, tumor-driven metabolic reprogramming, and therapy-related vascular injury. Collectively, these processes decouple circulating lipid concentrations from cardiovascular risk. Cancer therapies including anthracyclines, immune checkpoint inhibitors, human epidermal growth factor receptor 2-targeted agents androgen-deprivation therapy, and thoracic radiation promote endothelial dysfunction, atherosclerotic plaque inflammation, and instability through mechanisms largely independent of LDL-C burden. Concurrent reductions in circulating cholesterol related to cancer metabolism, cachexia, and treatment effects may further obscure the residual cardiovascular risk in cancer patients. Lipoprotein(a) has also emerged as a potential mediator of inflammation and thrombosis-driven risk that is not captured by standard lipid metrics. This review synthesizes mechanistic, angiographic, and clinical evidence underpinning the lipid paradox in cancer, evaluates contemporary lipid-lowering strategies, and proposes a precision cardio-oncology framework that moves beyond LDL-centric paradigms toward a dynamic longitudinal risk-based prevention. Such an approach is essential to reduce cardiovascular events and to ultimately improve long-term outcomes in cancer survivors.