Related Experiment Videos
Studies of low density lipoprotein molecular weight in human beings with coronary artery disease
Insights
Low density lipoprotein molecular weight (LDL MW) is lower in coronary artery disease (CAD) patients. However, this difference disappears when adjusting for triglyceride levels, suggesting triglycerides influence LDL MW in CAD.
Area of Science:
- Cardiovascular Science
- Lipid Metabolism
- Biochemistry
Background:
- Low density lipoprotein molecular weight (LDL MW) has shown a positive correlation with coronary artery disease (CAD) in nonhuman primates.
- Investigating this correlation in human subjects is crucial for understanding CAD pathogenesis.
Purpose of the Study:
- To evaluate the relationship between LDL MW and CAD in human volunteers.
- To determine the influence of plasma triglyceride levels on the association between LDL MW and CAD.
Main Methods:
- Measured LDL MW in 93 volunteers (46 CAD patients, 47 controls) undergoing coronary angiography.
- Utilized covariance adjustment for plasma triglyceride levels.
- Employed density gradient ultracentrifugation to characterize LDL in a subset of volunteers.
Main Results:
- CAD patients exhibited lower LDL MW compared to controls (P < 0.001).
- LDL MW decreased with increasing plasma triglyceride levels.
- After adjusting for triglyceride, no significant LDL MW difference was observed between CAD patients and controls.
- LDL mean hydrated density was inversely related to LDL MW and increased with triglyceride levels.
Conclusions:
- The initial observed difference in LDL MW between CAD patients and controls is likely confounded by elevated plasma triglyceride levels.
- Triglyceride concentration significantly impacts LDL MW and density, independent of coronary artery status.
- Further research into LDL heterogeneity and its role in CAD is warranted.
Abstract:
Low density lipoprotein molecular weight (LDL MW) correlates positively with coronary artery disease in cholesterol-fed nonhuman primates. To evaluate this in human beings with coronary artery disease (CAD) we measured LDL MW in 93 volunteers undergoing coronary angiography (47 controls and 46 CAD patients). LDL MW of CAD patients was less than that of controls (patients, 2.79 +/- 0.17 g/mumol; controls, 2.93 +/- 0.19 g/mumol; P less than 0.001). However, LDL MW decreased as plasma triglyceride increased and concentrations of triglyceride were greater in CAD patients than in controls. Since decreased LDL MW is likely to result, in part, from increased plasma triglyceride concentrations, we attempted to determine the effect of triglyceride on the relation of LDL MW to CAD in this study. After covariance adjustment for triglyceride, there was no LDL MW difference between CAD patients and controls. Because LDL heterogeneity has been identified in other studies and was apparent on inspection of agarose column profiles of LDL of these volunteers, we sought differences in the profiles that might distinguish coronary disease cases from controls. No differences could be found. In addition, we used density gradient ultracentrifugation to characterize LDL in more detail in a subset of volunteers who had a wide range of plasma triglyceride concentrations (50 mg/dl to 900 mg/dl). LDL mean hydrated density was inversely related to LDL MW and increased as triglyceride increased. The increase in peak density was reflected in an increase in percent of total protein in LDL found to have d greater than 1.045 g/ml and a decrease in protein in LDL of d 1.035-1.040 g/ml. These interrelationships were not apparently influenced by coronary artery status.