Anti-VEGF Therapy–Induced Accelerated Atherosclerosis

Bevacizumab is an antiangiogenic monoclonal antibody used in several primary and secondary central nervous system malignancies to reduce refractory cerebral edema. However, long-term therapy may lead to accelerated atherosclerosis through endothelial dysfunction and proteinuria-driven hyperlipidemia. A 27-year-old man with neurofibromatosis type 2 on long-term bevacizumab presented with progressively worsening chest pain and subsequently experienced ventricular fibrillation arrest. Emergent angiography identified an anomalous right coronary artery occlusion causing an inferior ST-segment elevation myocardial infarction and demonstrated left coronary atherosclerotic disease. He underwent successful percutaneous coronary intervention and guideline-based therapy for heart failure with reduced ejection fraction. Bevacizumab-induced endothelial injury and hyperlipidemia were implicated in premature coronary artery disease. This case underscores the interplay between inhibition of angiogenesis and early coronary atherosclerosis, highlighting the importance of nitric oxide derangement and proteinuria-induced dyslipidemia. Clinicians must remain vigilant about cardiovascular complications in young patients on long-term bevacizumab. Bevacizumab may accelerate atherosclerosis; early detection and risk factor reduction including lipid control and tight blood pressure management are crucial.