Abstract
Coronary artery disease (CAD) is a leading cause of death worldwide. The death rate is decreasing in developed countries due to awareness, but the disease burden is increasing in developing countries. Pakistan is a country with high prevalence of CAD. The serum lipids have long been implicated in the development of CAD by the deposition of mainly LDL on endothelial lining resulting in atherosclerosis. Progression to CAD involves environmental as well as genetic factors. The genetic component is due to the contribution from various low to modest effect size variants in many genes. Common variants have been used to construct a genetic risk score (GRS) to calculate the risk of future CAD. In conclusion, lifestyle interventions in concert with the knowledge of genetic predisposition based on family history and use of population data may one day lead to the development of personalized medicine for the treatment and prevention of CAD.
Highlights
Coronary artery disease (CAD) is a multifactorial chronic disorder of coronary arteries progressing silently and usually has established to an advance stage by the time symptoms start appearing
CAD, a fatty material known as plaque deposits inside the coronary arteries which narrows their lumen and restricts flow of blood to myocardial muscles, the process is known as atherosclerosis
The proportion of circulating OX low-density lipoprotein cholesterol (LDL-C) is low compared to OX LDLC present in the vessel endothelium, an increase in the amount of circulatory OX LDL-C is an indicator of oxidative stress and a CAD risk factor
Summary
Coronary artery disease (CAD) is a multifactorial chronic disorder of coronary arteries progressing silently and usually has established to an advance stage by the time symptoms start appearing. In. CAD, a fatty material known as plaque deposits inside the coronary arteries which narrows their lumen and restricts flow of blood to myocardial muscles, the process is known as atherosclerosis. Atherosclerotic plaques are characterised by the accumulation of necrotised tissue, calcification of dead necrotic material, deposition of oxidized lipids, aggregation of foam cells and other cell types like smooth muscle cells, endothelial cells, dendritic cells, T lymphocytes and a fibrous cap. Born with clear coronary arteries having wide lumen, the first streaks of fatty material may appear in the teenagers but the disease is asymptomatic until the plaque has grown enough to compromise the flow of blood.
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