Suspected Denosumab-Associated Acute Coronary Syndrome
Matthew Maharaj1, Arun Katwaroo1, Priya Ramcharan2
1Department of Medicine, North West Regional Health Authority, Port of Spain, Trinidad and Tobago.
Insights
Denosumab, a monoclonal antibody targeting RANKL, may increase the risk of acute coronary syndrome. This case report highlights a potential link between denosumab treatment and myocardial infarction in a patient without traditional cardiovascular risk factors.
Area of Science:
- Cardiology
- Oncology
- Pharmacology
Background:
- Denosumab, a monoclonal antibody targeting receptor activator of nuclear factor-κB ligand (RANKL), is used for bone diseases and giant cell tumors.
- Emerging evidence suggests RANKL inhibition may affect cardiovascular health through various pathways.
Purpose of the Study:
- To report a case of acute coronary syndrome in a patient treated with denosumab.
- To explore the potential association between denosumab and myocardial infarction.
Main Methods:
- Case report of a 48-year-old man with recurrent giant cell tumors treated with denosumab.
- Clinical presentation, coronary angiography, and treatment of ST-elevation acute coronary syndrome.
- Review of potential biological mechanisms linking RANKL inhibition to atherothrombotic events.
Main Results:
- The patient developed an anterior ST-elevation acute coronary syndrome shortly after receiving denosumab.
- Coronary angiography showed thrombotic occlusion of the left anterior descending artery.
- The event occurred in the absence of traditional cardiometabolic risk factors.
Conclusions:
- A denosumab-associated myocardial infarction was considered the most probable cause of the patient's acute coronary syndrome.
- This case suggests a potential link between denosumab and atherothrombotic cardiovascular events.
- Further research is warranted to investigate the cardiovascular safety of denosumab.
Abstract:
Denosumab, a monoclonal antibody (mAb) targeting receptor activator of nuclear factor-κB ligand (RANKL), is commonly used in managing metabolic bone diseases and giant cell tumors (GCTs) of bone. Growing evidence suggests that RANKL inhibition may influence cardiovascular health by impacting endothelial function, inflammatory pathways, vascular smooth muscle cell behavior, and systemic calcium regulation. We report a case of a 48-year-old Caribbean-South Asian man with recurrent GCTs who received three subcutaneous doses of denosumab and soon thereafter developed an anterior ST-elevation acute coronary syndrome (STE-ACS). The patient had no traditional cardiometabolic risk factors. Coronary angiography revealed thrombotic occlusion of the proximal left anterior descending artery (LAD), which was successfully treated with primary percutaneous coronary intervention (PPCI) and guideline-directed medical therapy (GDMT). Given the lack of modifiable risk factors, a significant family history, and biologically plausible mechanisms linking RANKL inhibition to atherothrombotic events, a denosumab-associated myocardial infarction was considered the most probable cause.
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