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Authors:

Harleen Jaggi, BS, MT (ASCP), CLS (NCA)

Ellen Hope Kearns, MS, SH(ASCP)H

Quest Diagnostics Inc., San Juan Capistrano, CA, and

Division of Health Sciences, School of Health, California State University Dominguez Hills

Risk Factors in Coronary Artery Disease

Discussion: Nonstandard CAD Biochemical Risk Factors


There are some non-standard CAD risk factors such as lipoprotein (a), homocysteine, and LDL subparticles.[12] Table 4 describes the non-standard CAD risk factors.

These risk factors are not part of a typical lipid panel. These tests should be performed when the patient has two or more coronary artery disease risk factors.

Table 4: Non-standard CAD risk factors
Non-standard CAD Risk Factor Significance
Lipoprotein(a)
  • Lipoprotein(a) or Lp(a) is a cholesterol-rich plasma lipoprotein with a structure very similar to low density lipoprotein.
  • Increased levels of Lp(a) are associated with high risk for atherothrombotic cardiovascular disease.
Homocysteine
  • Homocysteine is sulphur containing amino acid and is derived from dietary methionine.
  • Hyperhomocysteinemia is a risk factor for development of cardiovascular disease.
  • It is associated with other cardiovascular risk factors like male gender, old age, smoking, high blood pressure, elevated cholesterol and lack of exercise.
LDL subparticles
  • Low density lipoprotein (LDL) consists of discrete subparticles which vary in buoyant density, size, and lipid and protein composition. These subparticles have different effects on the development of atherosclerosis.
  • LDL subparticle diameter decreases with increasing density.
  • LDL subparticles are categorized based on size as follows:

large buoyant (pattern A) with sizes greater than or equal to 26.4 nm

small, dense (pattern B) with size less than or equal to 25.7 nm.

LDL subparticles between 25.8 - 26.3 nm are intermediate pattern.

Presence of small dense particles of pattern B creates a three-fold CAD risk. The prevalence of these patterns in the general population is approximately 70% for pattern A, 10-15% intermediate and 15-20% pattern B.[15]

The hypothesis regarding the atherosclerotic properties of small dense LDL particles is that as LDL particles enter the arterial vessel walls they become oxidized. Oxidized LDL particles form foam cells during atherogenesis.[12] Oxidized LDL is phagocytized by macrophages. Macrophages become filled with oxidized LDL and form foam cells. These foam cells are observed in early atherosclerotic lesions. The foam cells ultimately lead to formation of atherosclerotic plaque, which can make the affected coronary artery susceptible to abnormal vasoconstriction, which can lead to angina.[12] Studies have shown that the oxidative metabolism of LDL demonstrates a link between hyperlipidemia and development of atherosclerosis.[12,] [14]

Studies have shown that the LDL subclass pattern B is associated with other risk factors like male gender, [16] increased levels of triglycerides and apolipoprotein a and decreased levels of HDL.[14] LDL subclass pattern doesn't have a strong relationship with LDL cholesterol concentration.[14]

It has also been shown that patients with small dense LDL appear to receive the largest benefit from lipid-lowering treatment by converting small dense LDL to more buoyant LDL.[14] This conversion can be achieved by weight loss, diet restriction, and regular exercise. These hygienic measures will lower total cholesterol, triglycerides, and LDL-C, and will increase the size of LDL subparticles and HDL cholesterol levels.


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Last Update: Jan 4 2011