P3580Impact of glucose-6-phosphate dehydrogenase deficiency on the extent and severity of coronary atherosclerosis in patients with acute coronary syndrome

Abstract

Abstract Background Studies in animal models and humans suggested that glucose-6-phosphate dehydrogenase (G6PD) deficiency, a genetically inherited condition causing haemolytic anemia, may be considered a risk factor for cardiovascular disease. It is currently unknown whether enzymatic activity may impact the extent and severity of coronary atherosclerosis in patients with acute myocardial infarction. This hypothesis was tested in a cohort of acute coronary syndrome (ACS) patients undergoing invasive management from Northern Sardinia, where the population prevalence of G6PD deficiency is the highest in the Mediterranean area. Methods The study was based on a prospective single-centre registry of consecutive ACS patients undergoing coronary angiography and subsequent percutaneous revascularization between January 2017 and December 2018, in which G6PD activity has been measured quantitatively using a biochemical assay based on G6PD/6GPD ratio in erythrocytes. Subjects were defined as deficient when the ratio was <0.80. The primary endpoint of the study was the severity of coronary artery disease as assessed by the SYNTAX I score at baseline angiography. Results Among the 466 enrolled patients, 41 (9%) showed G6PD deficiency. Patients with G6PD deficiency were less likely to have a history of dyslipidemia (27% vs 50%; p=0.005) or diabetes (12% vs 21%; p=0.105). As expected, at admission patients with deficiency had lower hemoglobin level (12.1 vs 13.7 g/dL; p=0.005) as compared with those without. By angiography, SYNTAX score resulted as 19±9 and 16±9 (p=0.039) in patients with and without G6PD deficiency; while the number of diseased (with >50% stenosis) vessels was 1.9 vs 1.6 (p=0.089) in the 2 study groups. Left main disease was detected in 15% and 7% (p=0.06) patients, respectively. G6PD deficiency emerged as an independent predictor of high SYNTAX score (OR=2.16, 95% CI 1.1–4.5; p=0.037). Angioplasty with coronary stenting of the culprit vessel was performed in all patients, while GP IIb/IIIa inhibitors were used in 30% and 14% (p=0.009) of patients with and without G6PD deficiency. Finally, in-hospital events were similar between the 2 study groups. Conclusions An increased extent and severity of coronary artery disease was observed in ACS patients with G6PD deficiency as compared with those without, despite the lower prevalence of “classic” cardiovascular risk factors.