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Lipoprotein lipase activity is associated with severity of angina pectoris. REGRESS Study Group

J J Kastelein1, J W Jukema, A H Zwinderman

  • 1Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.

Circulation
|October 4, 2000
PubMed

Insights

Lipoprotein lipase (LPL) activity and mass are linked to cardiovascular disease severity. Lower LPL levels correlate with increased angina and ischemia, suggesting LPL influences coronary artery disease risk.

Area of Science:

  • Cardiovascular Science
  • Lipid Metabolism
  • Enzymology

Background:

  • Elevated triglyceride-rich lipoproteins are a significant risk factor for cardiovascular disease.
  • Lipoprotein lipase (LPL) activity is critical for clearing these lipoproteins, potentially modulating cardiovascular risk.

Purpose of the Study:

  • To investigate the relationship between LPL activity and mass and the severity of ischemia in male coronary artery disease patients.
  • To assess the association between LPL levels and clinical indicators of ischemia, such as angina pectoris and silent ischemia.

Main Methods:

  • Measured postheparin LPL activity and mass in a cohort of male coronary artery disease patients from the REGRESS trial.
  • Assessed angina severity using NYHA classification and silent ischemia via 24-hour ambulatory ECG monitoring.
  • Analyzed correlations between LPL levels, angina class, and ischemic burden.

Main Results:

  • Patients in lower LPL activity quartiles reported more severe angina (47% class III/IV vs. 29% in highest quartile, P=0.002).
  • Lower LPL activity quartiles exhibited a higher total ischemic burden on ECG monitoring (36.5+/-104.1 mm x min vs. 14.8+/-38.8 mm x min, P=0.001).
  • Strong correlation found between LPL activity and mass (r=0.70, P<0.0001); LPL mass associated with NYHA class (P=0.012).

Conclusions:

  • A significant relationship exists between LPL mass/activity and ischemia severity (angina class, ECG).
  • LPL appears to influence coronary artery disease risk through both catalytic and noncatalytic mechanisms.
Abstract

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