Table of Contents

ABSTRACT

Analysis via Mendelian randomization at the genome level can provide convincing evidence that tobacco intake contributes to coronary disease (CAD) and risk of myocardial infarction (MI). The association between cigarettes per day and age of smoking initiation and the risk of CAD and MI might be weak due to limited statistical power. A reducing trend of genomic DNA methylation in atheromatous plaque samples obtained from humans, ApoE−/−mice fed a high-fat diet, and New Zealand rabbits fed a high-cholesterol diet, with these changes being associated with the severity of atherosclerosis. Another expert found a notable decrease in the methylation levels of peripheral blood leukocytes in patients with atherosclerosis. Later studies have validated the correlation between the genomic methylation of peripheral blood cells and CAD. It may be proposed that DNA methylation may be a reactive epigenetic mechanism that links genetic predisposition to CAD and MI with exposure to tobacco intake. These results of smoking initiation indicated an overall association between smoking and an increased risk of MI. It was supported by subsequent epi-genetic Mendelian randomization analysis, not affecting overall conclusions.

Keywords: Epigenetics, genetics, inflammation, heart disease smoking