Gene polymorphisms in APOE, NOS3, and LIPC genes may be risk factors for cardiac adverse events after primary CABG

We investigated 192 CABG patients (18% female, age: 60.9 ± 7.4 years). Clinically cardiac adverse events were defined as need for reoperation (n = 88; 46%), reintervention (n = 58; 30%), or angina (n = 89; 46%). Mean follow-up time measured 10.1 ± 5.1 years. Gene polymorphisms (ApoE, NOS3, LIPC, CETP, SERPINE-1, Prothrombin) were investigated separately and combined (gene risk profile).Among classical risk factors, arterial hypertension and hypercholesterinemia significantly influenced CAD progression. Single ApoE, NOS3 and LIPC polymorphisms provided limited information. Patients missing the most common ApoE ε3 allele (5,2%), showed recurrent symptoms (p = 0,077) and had more frequently reintervention (p = 0,001). NOS3 a allele was associated with a significant increase for reintervention (p = 0,041) and recurrent symptoms (p = 0,042).Homozygous LIPC patients had a higher reoperation rate (p = 0.049).A gene risk profile enabled us to discriminate between faster and slower occurrence of cardiac adverse events (p = 0.0012).Single APOE, LIPC and NOS3 polymorphisms permitted limited prognosis of cardiac adverse events in patients after CABG. Risk profile, in contrast, allowed for risk stratification.Coronary artery disease (CAD) is a multifactorial disorder, accounts for roughly one-half of all cardiovascular deaths, and is a major cause of morbidity and mortality. Classical risk factors for CAD such as smoking or alterations in lipid metabolism are well known for decades to increase the incidence [1,2]. Patient counselling and medical therapy of risk factors have become the basis for secondary CAD prevention after primary coronary artery bypass grafting (CABG). Appearance of cardiac adverse events after primary CABG is frequent and leads to recurrent angina, myocardial infarction, and the need for reintervention.Apolipoproteins play a major role in lipid metabolism. They transfer water insoluble lipids in their soluble state and enable lipid transport mechanisms. Furt