Abstract

Smoking is one of the biggest public health threats worldwide, and it has been widely acknowledged as a traditional hazard for the progression of cardiovascular disease. Apolipoprotein-E (APO-E) has proinflammatory qualities; however, the link between APO-E genetic variation and inflammation remains controversial. We investigated the association between APO-E genotype and inflammation and the risk of premature coronary heart disease (CHD) in smokers versus non-smokers. We studied 300 South Indian subjects, including 100 healthy non-smokers, 100 smokers with CHD, and 100 smokers with diabetes and CHD. The APO-E gene was genotyped using an allele-specific polymerase chain reaction method (PCR) that was adapted to use with a TaqMan probe for real-time PCR. The study’s findings suggest that the E3/E3 genotypes were among the most frequent in the study population, whereas E2/E2 was the least prevalent. After controlling for clinical variables, patients with the E3/E4 genotype had lower levels of serum high-density lipoprotein, higher total cholesterol, triglyceride, low-density lipoprotein (LDL), APO-E, high-sensitive C-reactive protein, and matrix metalloproteinase-9 and were statistically significant (“p-value”

Key words: Apolipoprotein-E, Coronary heart disease Inflammation, Smoking, Diabetes mellitus