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Treating arteries instead of risk factors: a paradigm change in management of atherosclerosis
J David Spence1, Daniel G Hackam
1Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, 1400 Western Road, London, ON Canada N6G 2V2. dspence@robarts.ca
Insights
A new approach to treating atherosclerosis by directly targeting arterial plaque led to plaque regression in patients. This method, focusing on arteries rather than just risk factors, reversed progression trends observed previously.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Medical Imaging
Background:
- Atherosclerosis was historically considered a progressive disease.
- A paradigm shift occurred in 2003, moving from treating risk factors to directly treating arteries.
Purpose of the Study:
- To evaluate the proportion of patients experiencing plaque progression versus regression before and after the implementation of a new treatment strategy.
- To assess the impact of directly treating arterial plaque on atherosclerosis progression.
Main Methods:
- Carotid total plaque area was measured using ultrasound for serial assessments.
- Patients were treated according to consensus guidelines before 2003.
- After 2003, intensive treatment was applied to patients with plaque progression, aiming for halting or regression.
Main Results:
- The study included 4,378 patients with serial plaque measurements between 1997 and 2007.
- Before 2003, approximately 50% of patients showed plaque progression and 25% regression; this trend reversed by 2005.
- Post-2003, plaque progression significantly decreased, with patients showing regression having lower LDL cholesterol levels.
Conclusions:
- Directly treating arteries, analogous to measuring blood pressure for hypertension, is crucial for managing atherosclerosis.
- A clinical trial is being designed to further validate this artery-focused treatment approach.
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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