From the Research
Patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency are at increased risk of cardiac complications, including coronary artery disease, arrhythmias, and heart failure, primarily due to oxidative stress and hemolysis, as evidenced by recent studies 1, 2. The main cardiac concerns in G6PD-deficient patients include:
- Increased risk of coronary artery disease
- Arrhythmias
- Heart failure, particularly during hemolytic episodes When G6PD-deficient patients experience hemolysis, the resulting anemia can lead to increased cardiac workload and oxygen demand, potentially triggering or worsening cardiac symptoms. Additionally, these patients may have impaired endothelial function and increased arterial stiffness, contributing to hypertension and atherosclerosis. Certain medications commonly used for cardiac conditions, such as quinidine, procainamide, and some ACE inhibitors, can trigger hemolysis in G6PD-deficient patients and should be avoided, as noted in studies 3, 4. During acute hemolytic episodes, cardiac monitoring is recommended, especially in patients with pre-existing heart disease. The underlying mechanism involves reduced antioxidant capacity due to G6PD deficiency, leading to increased oxidative damage to cardiac tissues and blood vessels, as discussed in 1, 2. This oxidative stress can accelerate atherosclerosis and contribute to myocardial injury over time, particularly when exacerbated by triggers like certain medications, infections, or fava bean consumption. It is essential to consider G6PD deficiency in patients who experience acute hemolysis after exposure to known oxidative medications, infection, or ingestion of fava beans, and to use alternative medications when possible, as suggested in 4, 2.