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(Circulation. 2000;102:1629.)
© 2000 American Heart Association, Inc.

Clinical Investigation and Reports

Lipoprotein Lipase Activity Is Associated With Severity of Angina Pectoris

John J. P. Kastelein, MD, PhD; J. Wouter Jukema, MD, PhD; Aeilko H. Zwinderman, PhD; Suzanne Clee, MD; Ad J. van Boven, MD, PhD; Hans Jansen, PhD; Ton J. Rabelink, MD, PhD; Ron J. G. Peters, MD, PhD; Kong I. Lie, MD, PhD; George Liu, PhD; Albert V. G. Bruschke, MD, PhD; Michael R. Hayden, MD, PhD; for the REGRESS Study Group

From the Departments of Vascular Medicine (J.J.P.K.) and Cardiology (R.J.G.P., K.I.L.), Academic Medical Center, Amsterdam; Departments of Cardiology (J.W.J., A.V.G.B.) and Biostatistics (A.H.Z.), Leiden University Medical Center, Leiden; Interuniversity Cardiology Institute of the Netherlands (J.W.J., A.H.Z., A.V.G.B.), Utrecht; Department of Cardiology, University Hospital Groningen, Groningen (A.J.v.B.); Department of Biochemistry, University Hospital Rotterdam, Rotterdam (H.J.); Department of Nephrology and Hypertension, University Hospital Utrecht, Utrecht (T.J.R.), the Netherlands; and Centre for Molecular Medicine and Therapeutics, University of British Columbia (S.C., M.R.H.), Vancouver, Canada.

Correspondence to John J.P. Kastelein, Academic Medical Center, Department of Vascular Medicine, G1-146, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands. E-mail e.vandongen{at}amc.uva.nl

Background—Raised triglyceride-rich lipoproteins significantly increase the risk for cardiovascular disease. Variation in the activity of the enzyme lipoprotein lipase (LPL), which is crucial in the removal of these lipoproteins, may therefore modulate this risk.

Methods and Results—Postheparin levels of LPL activity and mass were measured in a large cohort of male coronary artery disease patients participating in the Regression Growth Evaluation Statin Study (REGRESS), a lipid-lowering regression trial. In addition, the relationships between LPL activity and mass and severity of angina pectoris according to the NYHA classification and silent ischemia on 24-hour ambulatory ECG monitoring were assessed. Patients in different LPL activity quartiles and mass had different severities of angina; a total of 47% of patients in the lowest LPL quartile reported class III or IV angina. In contrast, only 29% in the highest activity quartile (P=0.002) had severe angina. These parameters were supported by ambulatory ECG results, for which the total ischemic burden in the lowest LPL activity quartile was 36.5±104.1 mmxmin compared with 14.8±38.8 mmxmin in the highest quartile of LPL activity (P=0.001). LPL activity levels were strongly correlated with LPL mass (r=0.70, P<0.0001). A significant association between the LPL protein mass and NYHA class (P=0.012) was also demonstrated.

Conclusions—We have demonstrated a significant relationship between LPL mass and activity and severity of ischemia as defined by angina class and ambulatory ECG. These results suggest that LPL influences risk for coronary artery disease by both catalytic and noncatalytic mechanisms.

Key Words: angina • ischemia • lipoproteins

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