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

*geplaatst 2026-08-30 · Cholesterol · The American journal of cardiology · doi 10.1016/j.amjcard.2026.08.022 · https://hartvaat.nl/2026/08/21/lipidparadox-bij-kanker-ldl-c-dekt-de-lading-niet-voor-cardiovasculair-risico/*

Deze review beschrijft de 'lipidparadox' bij kankerpatiënten, waarbij atherosclerotische events vaak voorkomen ondanks gecontroleerde LDL-C-waarden. Systemische ontsteking, therapie-gerelateerde vaatbeschadiging en tumor-metabolisme ontkoppelen de lipidenconcentraties van het werkelijke cardiovasculaire risico. Voor de klinische praktijk betekent dit dat een puur LDL-C-gestuurde preventie ontoereikend is en dat een dynamisch, op longitudinale risicobeoordeling gebaseerd cardio-oncologie-profiel nodig is om hart- en vaatcomplicaties bij kankeroverlevenden te voorkomen.

## English: The Cancer-Associated Lipid Paradox: Implications for Cardiovascular Risk and Lipid Management.

This review explores the cancer-associated lipid paradox, where cardiovascular events frequently occur despite low or well-controlled LDL-C levels in oncology patients. Systemic inflammation, treatment-related vascular injury, and tumor-driven metabolic shifts decouple circulating lipid concentrations from actual cardiovascular risk. Clinicians should recognize that LDL-centric prevention strategies are insufficient for cancer survivors, necessitating a dynamic, longitudinal risk-assessment framework in cardio-oncology to better mitigate cardiovascular morbidity.

## Abstract (original, from the publication)

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.

Auteurs: Nicole Prescott, Victoria J Eichten, Vishal Ahuja, Courtney M Campbell, Anand Gupta, Catherine A Raver, Michael D Duncan, Javed Butler, Byron Cryer, Ronan J Kelly, Subhash Banerjee

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Bron: The American journal of cardiology, https://doi.org/10.1016/j.amjcard.2026.08.022. Bijgewerkt 2026-08-23T01:16:29Z. Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.