Cancer patients face an increased risk of developing coronary artery disease (CAD), primarily due to the following factors:
- Cancer and CAD share common risk factors, such as smoking, obesity, hypertension, and diabetes.
- Pro-inflammatory factors produced by tumor cells promote plaque formation.
- Pro-coagulant factors produced by tumors contribute to a hypercoagulable state.
- Cancer treatments can induce CAD through various mechanisms.
Pathogenesis
Common cancer therapies that may lead to CAD include antimetabolites, antimicrotubule agents, platinum-based drugs, antitumor antibiotics, VEGF inhibitors, multi-target tyrosine kinase inhibitors, aromatase inhibitors, anti-androgen/anti-estrogen drugs, gonadotropin-releasing hormone analogs/antagonists, immunomodulatory agents (e.g., lenalidomide), and immune checkpoint inhibitors (ICIs). The primary mechanisms by which these therapies induce CAD include coronary endothelial injury, coronary vasospasm, and acute thrombosis.
Radiotherapy can also induce CAD, with mechanisms including coronary endothelial damage, inflammatory responses, oxidative stress, accelerated atherosclerosis, microthrombosis formation, and plaque rupture. Radiotherapy-induced coronary lesions are often located at the proximal segments or the ostia of coronary arteries.
Clinical Manifestations
The symptoms, signs, auxiliary examinations, and diagnostic criteria for cancer therapy-associated CAD are similar to those for atherosclerotic coronary artery disease. However, it is important to note that symptoms such as chest discomfort or tightness in cancer patients with concurrent CAD can be easily confused with tumor-related syndromes, complicating early diagnosis.
Treatment
The treatment of CAD in cancer patients is generally similar to that in the general population, as detailed in atherosclerotic coronary artery disease. However, certain unique considerations and challenges exist in treatment strategies:
When cancer therapy is suspected to be the trigger for acute coronary syndrome (ACS), temporary discontinuation of cancer therapy is recommended.
For cancer patients with persistent ischemic symptoms or ACS despite optimized medical therapy, individualized coronary revascularization should be considered if the expected survival exceeds six months. For patients with a life expectancy of less than six months or those with a high risk of hemorrhage, conservative medical therapy is preferred.
For cancer patients undergoing percutaneous coronary intervention (PCI) for ACS who also have a high risk of hemorrhage, such as those with thrombocytopenia, the duration of dual antiplatelet therapy should be shortened.
Alongside optimizing secondary prevention medications for CAD, efforts should be made to address cancer-related ischemic triggers, such as anemia, infection, and hypoxia.