J David Spence1, Daniel G Hackam. 1. Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, 1400 Western Road, London, ON Canada N6G 2V2. dspence@robarts.ca
Abstract
BACKGROUND AND PURPOSE: Until recently, atherosclerosis was thought to be inexorably progressive. Beginning in 2001 and implemented in our vascular prevention clinics by 2003, we have been treating arteries rather than risk factors. We studied the proportion of patients with plaque progression vs regression before and after this change in paradigm. METHODS: Carotid total plaque area was measured by ultrasound at baseline and during follow-up. Before 2003, patients were treated according to consensus guidelines. After 2003, patients with plaque progression were treated more intensively, with the explicit goal of halting plaque progression or achieving regression. RESULTS: Four thousand three-hundred seventy-eight patients had serial plaque measurements in a given year between 1997 and 2007; 47% were female. Mean age at time of referral was 60 (SD, 15); this increased steeply (from age 50 to 62 years over the first 5 years) as we focused on stroke prevention. The annual rate of plaque progression increased steeply as the clinic populations aged but then abruptly decreased after implementation of the new approach to therapy. Before 2003, approximately half the patients had plaque progression and approximately 25% had regression; by 2005, this had reversed. Changes in plasma lipids show that the differences were attributable to plaque measurement, not simply more intensive therapy for all patients. By 2007, patients with progression had lower levels of low-density lipoprotein than those with regression. CONCLUSIONS: Treating arteries without measuring plaque would be like treating hypertension without measuring blood pressure. A clinical trial to test this approach is being designed.
BACKGROUND AND PURPOSE: Until recently, atherosclerosis was thought to be inexorably progressive. Beginning in 2001 and implemented in our vascular prevention clinics by 2003, we have been treating arteries rather than risk factors. We studied the proportion of patients with plaque progression vs regression before and after this change in paradigm. METHODS: Carotid total plaque area was measured by ultrasound at baseline and during follow-up. Before 2003, patients were treated according to consensus guidelines. After 2003, patients with plaque progression were treated more intensively, with the explicit goal of halting plaque progression or achieving regression. RESULTS: Four thousand three-hundred seventy-eight patients had serial plaque measurements in a given year between 1997 and 2007; 47% were female. Mean age at time of referral was 60 (SD, 15); this increased steeply (from age 50 to 62 years over the first 5 years) as we focused on stroke prevention. The annual rate of plaque progression increased steeply as the clinic populations aged but then abruptly decreased after implementation of the new approach to therapy. Before 2003, approximately half the patients had plaque progression and approximately 25% had regression; by 2005, this had reversed. Changes in plasma lipids show that the differences were attributable to plaque measurement, not simply more intensive therapy for all patients. By 2007, patients with progression had lower levels of low-density lipoprotein than those with regression. CONCLUSIONS: Treating arteries without measuring plaque would be like treating hypertension without measuring blood pressure. A clinical trial to test this approach is being designed.
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