Diana A Gorog1, Nabeel Ahmed, Graham J Davies. 1. Division of Cardiology, Imperial College School of Medicine at Hammersmith Hospital, London, UK. diana.gorg@kcl.ac.uk
Abstract
BACKGROUND: The concept that oxidised low-density lipoprotein (LDL), not native LDL, plays a major role in atherogenesis is gaining support. Lipid hydroperoxides in plasma are carried almost exclusively in LDL and reflect oxidised LDL. Previously, elevated plasma lipid hydroperoxides were reported in coronary artery disease (CAD) patients following bypass surgery. To determine whether the increased lipid hydroperoxide was related to bypass or reflected ongoing atherosclerosis, plasma lipid hydroperoxide was measured in acute myocardial infarction (AMI) and stable angina. METHODS: Patients with AMI (n=39) and stable angina (n=40) were compared with matched controls. Lipids and lipoproteins were selectively removed from plasma by absorption to Liposorb gel. Lipid hydroperoxide concentration in the gel was measured by a sensitive triiodide spectrophotometric technique. RESULTS: Lipid hydroperoxide levels in AMI and stable angina were elevated (3.47+/-0.21 micromol/l, P<.001 and 3.76+/-0.24 micromol/l, P<.001) compared to controls (2.18+/-0.13 micromol/l). Previously, a concentration >3 mol/l was considered pathological. Using this criterion, we detected pathological lipid hydroperoxide concentrations in 10.3% of controls, 57.5% of AMI and 61.5% of angina patients. CONCLUSION: Plasma lipid hydroperoxide levels are significantly elevated in AMI and angina. This is not attributable to previous cardiopulmonary bypass but to the presence of atherosclerotic disease and is likely to play a role in atherogenesis.
BACKGROUND: The concept that oxidised low-density lipoprotein (LDL), not native LDL, plays a major role in atherogenesis is gaining support. Lipid hydroperoxides in plasma are carried almost exclusively in LDL and reflect oxidised LDL. Previously, elevated plasma lipid hydroperoxides were reported in coronary artery disease (CAD) patients following bypass surgery. To determine whether the increased lipid hydroperoxide was related to bypass or reflected ongoing atherosclerosis, plasma lipid hydroperoxide was measured in acute myocardial infarction (AMI) and stable angina. METHODS:Patients with AMI (n=39) and stable angina (n=40) were compared with matched controls. Lipids and lipoproteins were selectively removed from plasma by absorption to Liposorb gel. Lipid hydroperoxide concentration in the gel was measured by a sensitive triiodide spectrophotometric technique. RESULTS:Lipid hydroperoxide levels in AMI and stable angina were elevated (3.47+/-0.21 micromol/l, P<.001 and 3.76+/-0.24 micromol/l, P<.001) compared to controls (2.18+/-0.13 micromol/l). Previously, a concentration >3 mol/l was considered pathological. Using this criterion, we detected pathological lipid hydroperoxide concentrations in 10.3% of controls, 57.5% of AMI and 61.5% of anginapatients. CONCLUSION: Plasma lipid hydroperoxide levels are significantly elevated in AMI and angina. This is not attributable to previous cardiopulmonary bypass but to the presence of atherosclerotic disease and is likely to play a role in atherogenesis.