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.
Nicole Prescott, Victoria Eichten, Vishal Ahuja et al.· American Journal of Cardiolo...· 0 citations
BACKGROUND
Cancer and heart failure (HF) frequently coexist due to population ageing and improved survival for both conditions. HF is a well-recognised complication of oncologic therapies and a potential association between HF and subsequent cancer incidence has been recently noticed. We therefore conducted a meta-analysis to quantify cancer incidence and mortality in patients with and without HF.
METHODS
Databases were searched from inception to 15 February 2026. Data from observational studies and randomised trials on individuals with and without HF and reporting cancer incidence and/or mortality during follow-up were included. The main outcome of interest was the incidence of any cancer; secondary outcomes included site-specific cancer incidence (lung, colorectal, breast, and prostate) and all-cause, cardiovascular, and cancer-related mortality.
RESULTS
Twelve studies comprising 8,979,195 individuals were included. HF was associated with a higher incidence of cancer (hazard ratio [HR] 1.33, 95% confidence interval [CI] 1.14-1.54), with substantial heterogeneity (I2 = 99.7%). Cancer site-specific analyses showed increased incidences of lung (HR 1.70, 95% CI 1.26-2.29), colorectal (HR 1.28, 95% CI 1.11-1.48), and breast (HR 1.19, 95% CI 1.04-1.37), but not prostate, cancer. Effect estimates varied according to analytical strategy: matched HF and non-HF cohorts reported higher risk estimates than those using covariate adjustment without matching. Mortality data were sparse and heterogeneous.
CONCLUSIONS
HF is associated with a higher incidence of cancer, although with marked heterogeneity among studies and cancer types. Mortality and cause of death were rarely reported. The observed HF-cancer association is influenced by statistical methodology, shared risk factors, differences in surveillance intensity and cancer type, that confound analyses investigating possible causal biological links. More granular and harmonised studies are required.
L. Sanasi, A. Iaconelli, Danila Azzolina et al.· European Journal of Heart Fa...· 0 citations
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