J. David Spence, Professor of Neurology and Clinical Pharmacology, and Director, Stroke Prevention & Atherosclerosis Research Centre (SPARC)
Why I Became a Scientist
My research work is a continual process of learning from my patients, and then taking those lessons back, not only to my clinic, but also to the clinics of physicians worldwide. As an individual physician I have only been able to see about 20,000 patients and prevent about 6,000 strokes. My research and teaching, however, by helping other physicians do a better job of stroke prevention, will achieve much more. Furthermore, the fun of doing research makes me a better physician because I am still excited about my work. After more than 30 years of clinical practice I would probably not be so enthusiastic if I weren’t doing my research.
Research Summary
Atherosclerosis is the process that underlies heart attacks and a large proportion of strokes. Areas of thickening in the artery wall, called plaques, lead to heart attacks when they rupture and block arteries. Measurement of 2-dimensional carotid plaque area was developed in our lab by Maria DiCicco in 1990. We were the first to show that carotid total plaque area (TPA), and the progression of TPA strongly predicted the risk of strokes, heart attacks and death. In 1995, with Dr. Aaron Fenster, we began to study 3-dimensional carotid plaque volume. With Dr. Fenster and Dr. Grace Parraga we have shown that 3-dimensional measurements of atherosclerosis can evaluate effects of therapies for atherosclerosis much more efficiently than earlier methods. At SPARC, our work is about using ultrasound measurements of atherosclerosis for patient management, genetic research and evaluation of new therapies, to reduce the burden of atherosclerosis in our aging population.
Research Questions and Disease Implications
Can measuring carotid plaque improve preventive therapy in vascular clinics, by motivating patients to comply with their therapy, and motivating physicians to prescribe more intensive therapy?
Reduction of heart attacks and strokes, and reduction of dementia resulting from strokes.
What are the genetic variants that account for extremes of atherosclerosis? Why do some patients have excessive atherosclerosis not explained by traditional risk factors, while others with high levels of risk factors have no plaque?
Finding genetic variants that protect against atherosclerosis, and that cause excessive atherosclerosis, will lead to new therapies to reduce heart attacks, strokes and dementia.
What are the best ways to efficiently evaluate new therapies for atherosclerosis? In how few patients and in how short a time can new therapies be reliably be shown to be effective?
This will accelerate the development of new therapies so they can be used to help patients at risk of heart attacks, strokes and dementia.
Education
• B.A., University of Western Ontario 1965
• M.D., University of Western Ontario 1970
• M.B.A., University of Toronto 1991
Training
• Internship in Internal Medicine University of Western Ontario 1971
• Residency in Neurology and Internal Medicine at University of Western Ontario, leading to FRCPC Internal Medicine 1974, FRCPC Neurology 1976
• Fellowship in Clinical Pharmacology at the Cardiovascular Research Institute, University of California at San Francisco, 1974-76.
Awards
• Francis McNaughton Young Investigator Award, Canadian Neurological Society 1974
• Research Award, Canadian Hypertension Society
• Dean’s Honour List, University of Toronto Executive MBA, 1991
• Stroke Recovery Association Clifford J. Goodall Award of Merit, 1998
• Fellow of the Canadian Academy of Health Sciences, 2008
Publications
• Spence JD. Intensive management of risk factors for accelerated atherosclerosis: the role of multiple interventions. Curr Neurol Neurosci Rep. 2007; 7:42-8.
• Egger M, Spence JD, Fenster A, Parraga G. Validation of 3D ultrasound vessel wall volume: an imaging phenotype of carotid atherosclerosis. Ultrasound Med Biol. 2007 Jun;33(6):905-14.
• Spence JD. Homocysteine-lowering therapy: a role in stroke prevention? Lancet Neurology 2007;7: 830-838.
• Klein JH, Hegele RA, Hackam DG, Koschinsky ML, Huff MW, Spence JD. Lipoprotein(a) Is Associated Differentially With Carotid Stenosis, Occlusion, and Total Plaque Area. Arterioscler Thromb Vasc Biol. 2008 Oct;28(10):1851-6
• Ozdemir AO, Tamayo A, Munoz C, Dias B, Spence JD. Cryptogenic stroke and patent foramen ovale: Clinical clues to paradoxical embolism. Journal of the Neurological Sciences 2008; 275: 121–127
• Bhavsar S, Nimigan A, Hackam DG, O'Gorman DB, Gan BS, Spence JD. Keloid scarring, but not Dupuytren's contracture, is associated with unexplained carotid atherosclerosis. Clin Invest Med. 2009 Apr 1;32(2):E95-102.
Contact Information
Stroke Prevention & Atherosclerosis Research Centre
1400 Western Road, London, ON N6G 2V2
Phone 519-663-3113; Fax 519-663-3018
Email dspence@robarts.ca