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
New-onset atrial fibrillation (AF) is common among acutely hospitalized patients and is associated with increased risks of stroke and mortality. However, anticoagulation in this setting involves a temporal tradeoff between early bleeding during recovery and potential long-term stroke prevention, and data guiding direct oral anticoagulant (DOAC) initiation at discharge remain limited. We conducted a retrospective cohort study of adults with newly diagnosed AF identified between 3 days before hospital admission and hospital discharge within the Baylor Scott & White Health system (July 2020-June 2024), comparing patients initiated on DOAC therapy at discharge with those who were not. Outcomes included major adverse cardiovascular events (MACE: all-cause death, non-fatal myocardial infarction, or ischemic stroke/transient ischemic attack) and net adverse clinical events (NACE: MACE or major bleeding) at 30 days and 3 years. Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs), and landmark cumulative incidence analyses assessed temporal trends after discharge. Among 16,641 patients (mean age 75.1 years; 41.8% women), 7,181 (43.2%) were discharged on a DOAC. In adjusted analyses, DOAC use was associated with lower risk of 3-year MACE (HR 0.61; 95% CI 0.58-0.65; p<0.001) and NACE (HR 0.64; 95% CI 0.61-0.68; p<0.001) compared with those not receiving DOAC therapy. Landmark analyses showed consistent reductions in MACE at both 30 days (HR 0.61; 95% CI 0.57-0.65) and 3 years (HR 0.68; 95% CI 0.62-0.74). Patients treated with DOACs had a lower risk of NACE at both 30 days (HR 0.65; 95% CI 0.61-0.69) and 3 years (HR 0.67; 95% CI 0.62-0.73). Overall, DOAC initiation at discharge in patients with newly diagnosed AF identified between 3 days before hospital admission and hospital discharge was associated with lower early and long-term ischemic risk, with lower rates of both MACE and NACE observed at 30 days and 3 years, underscoring the need for individualized decision-making regarding anticoagulation during acute hospitalization.
Matthew Cervantes, Tariq Jamal Siddiqi, Anand Gupta et al.· American Journal of Cardiolo...· 0 citations
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