Deborah is 56 years old, smokes half a pack of cigarettes a day, and is overweight. Her friend wants her to come to a local women's fitness class she attends to once a week

Question

She knows Deborah's dad had died an acute myocardial infarction when he was 56, and she fears, seeing Deborah's lifestyle, the same fate awaits her friend. What she did not know was that Deborah had also been to her doctor for her annual physical where she was told her LDLs were 180 mg/dL, HDLs were 36 mg/dL, and cholesterol was 239 mg/dL.

What are Deborah's known risk factors for coronary heart disease?

Deborah's doctor referred her to a dietician for strict dietary therapy, hoping the intervention would raise her HDL and lower her LDL and cholesterol levels. Why is diet modification necessary to control and moderate the lipids indicated?

Deborah's doctor also gave her pamphlets describing strategies to stop smoking and a list of exercise ideas she might want to try. How is smoking thought to contribute to atherosclerotic plaque formation? Why would exercise have a positive effect on Deborah's lipid profile?

Atherosclerosis is thought to be an inflammatory disorder. What is the role of macrophages in the formation of atherosclerotic plaques? What is the significance of elevated serum hs-CRP levels in at-risk individuals?

Answer 1

being overweight, smoking, family history of heart disease, and low serum HDL and high serum LDL levels.

An excessive caloric intake lowers HDL levels. Elevated serum cholesterol levels are affected not only by dietary intake of cholesterol but also by a diet high in saturated fats. Hypercholesterolemia results in increased VLDL and LDL levels in the blood. Trans fat is emerging as the most potent atherogenic lipid, and limiting dietary levels of this fat is important in managing the at-risk patient.

Smoking is thought to contribute to oxidative processes in the lumen of vessels and consequent damage to the endothelium. Furthermore, smoking is thought to magnify endothelial dysfunction when it is already present in predisposed individuals. Finally, smoking decreases circulating levels of HDL. Unlike smoking, exercise increases serum HDL levels. High levels of HDL are inversely related to the development of atherosclerosis and coronary artery disease. These lipoproteins clear cholesterol from atheromatous plaques and move them to the liver for excretion from the body. It is believed they also inhibit the cellular uptake of LDL.

Monocytes migrate to the subendothelial space in blood vessels and become macrophages. Once activated, macrophages release free radicals to oxidize LDL. Oxidized LDL subsequently destroys endothelial tissue. Macrophages also ingest oxidized LDL and form foam cells, a feature common to all atherosclerotic changes. Finally, macrophages promote the proliferation of smooth muscle cells and the deposition of the extracellular matrix at the lesion site.
Elevated levels of hs-CRP (a protein involved in the acute-phase inflammatory response) indicate systemic inflammation. It is now considered a major risk factor marker for cardiovascular disease.