J David Spence1, Karla Solo2. 1. From the Divisions of Neurology and Clinical Pharmacology, Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute (J.D.S.) and Department of Epidemiology and Biostatistics (K.S.), Western University, London, ON, Canada. dspence@robarts.ca. 2. From the Divisions of Neurology and Clinical Pharmacology, Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute (J.D.S.) and Department of Epidemiology and Biostatistics (K.S.), Western University, London, ON, Canada.
Abstract
BACKGROUND AND PURPOSE: Recent studies indicate that patients with lower levels of low-density lipoprotein cholesterol (LDL-C) have greater regression of coronary plaque. In 2002, we found that carotid plaque progression doubled cardiovascular risk. In 2003, we therefore implemented a new approach, treating arteries instead of risk factors. Since then, we have seen many patients with carotid plaque progression despite very low levels of LDL-C, suggesting other causes of atherosclerosis. We studied the relationship of achieved LDL-C and change in LDL-C to progression/regression of atherosclerosis, before and after 2003. METHODS: All 4512 patients in our clinic database with at least 2 measurements of LDL-C and carotid total plaque area approximately a year apart and complete data for analyses (n=2025 before and 2487 after December 31, 2003) were included in the study. RESULTS: Baseline total plaque area was significantly higher after 2003 (129.56±134.32 versus 113.33±121.52 mm2; P<0.0001), and plaque progression was significantly less after 2003 (2.94±37.11 versus 12.62±43.24 mm2; P<0.0001). Many patients with LDL-C <1.8 mm had plaque progression (47.5%), and change in LDL-C was not correlated with plaque progression/regression. Increasing age and serum creatinine contributed to resistant atherosclerosis. CONCLUSIONS: Many patients have Resistant Atherosclerosis, failing to achieve regression of atherosclerosis despite low levels of LDL-C. Instead of relying on LDL-C, measuring plaque burden may be a more useful way of assessing individual response to therapy, particularly in resistant atherosclerosis.
BACKGROUND AND PURPOSE: Recent studies indicate that patients with lower levels of low-density lipoprotein cholesterol (LDL-C) have greater regression of coronary plaque. In 2002, we found that carotid plaque progression doubled cardiovascular risk. In 2003, we therefore implemented a new approach, treating arteries instead of risk factors. Since then, we have seen many patients with carotid plaque progression despite very low levels of LDL-C, suggesting other causes of atherosclerosis. We studied the relationship of achieved LDL-C and change in LDL-C to progression/regression of atherosclerosis, before and after 2003. METHODS: All 4512 patients in our clinic database with at least 2 measurements of LDL-C and carotid total plaque area approximately a year apart and complete data for analyses (n=2025 before and 2487 after December 31, 2003) were included in the study. RESULTS: Baseline total plaque area was significantly higher after 2003 (129.56±134.32 versus 113.33±121.52 mm2; P<0.0001), and plaque progression was significantly less after 2003 (2.94±37.11 versus 12.62±43.24 mm2; P<0.0001). Many patients with LDL-C <1.8 mm had plaque progression (47.5%), and change in LDL-C was not correlated with plaque progression/regression. Increasing age and serum creatinine contributed to resistant atherosclerosis. CONCLUSIONS: Many patients have Resistant Atherosclerosis, failing to achieve regression of atherosclerosis despite low levels of LDL-C. Instead of relying on LDL-C, measuring plaque burden may be a more useful way of assessing individual response to therapy, particularly in resistant atherosclerosis.
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