Abstract
BACKGROUND: 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. CASE SUMMARY: 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. DISCUSSION: 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. TAKE-HOME MESSAGE: Bevacizumab may accelerate atherosclerosis; early detection and risk factor reduction including lipid control and tight blood pressure management are crucial.