Michael Allard

Cardiovascular Pathologist
Vice-Dean, Health Engagement, Faculty of Medicine, UBC

"Always to be right, always to trample forward, and never to doubt, are not these the great qualities with which dullness takes lead in the world?" - William Makepeace Thackeray

Biography

I am Professor of the Department of Pathology and Laboratory Medicine and Vice-Dean, Health Engagement of the Faculty of Medicine at the University of British Columbia (UBC) and a Cardiovascular Pathologist in the Department of Pathology and Laboratory and a Principal Investigator in the Centre for Heart Lung Innovation at St. Paul's Hospital.

I was born and raised in Vancouver and attended the University of British Columbia (UBC) where I obtained a BSc in Biology in 1978 and an MD in 1981. Following a Rotating Internship at St. Michael’s Hospital in Toronto, I returned to UBC for post-graduate clinical training in anatomic pathology that included training in renal pathology at St. Thomas’ Hospital in London, England and a pulmonary research fellowship with Dr. James Hogg in the UBC Pulmonary Research Laboratory from 1985 to 1987. Subsequently, I undertook cardiovascular research training at the University of Alabama at Birmingham in the United States with Drs. Sanford Bishop and Peter Anderson, returning to UBC and St.Paul's Hospital in 1990.

My research program focuses primarily on adaptation of the heart to physiological states, such as endurance exercise, and pathological processes, such as hypertension, that result in cardiac hypertrophy. I am particularly interested in how substrate use by the heart is altered under these conditions and how changes in substrate use influence heart function. A major recent focus of my research has been delineation of the cellular and molecular mechanisms that account for the alterations in substrate use by the hypertrophied heart.

Away from work, I am married with two children and used to have a dog. I commute to work on my bike whenever possible, am an avid year-round recreational hockey player and have a passion for travel.

Academic Background

  • BSc Biology, University of British Columbia 1974-1978
  • MD Medicine, University of British Columbia 1977-1981
  • Rotating Internship, St. Michael's Hospital, University of Toronto, 1981-1982
  • Anatomical Pathology, University of British Columbia 1983 -1988
  • Experimental Respiratory Pathology, University of British Columbia 1985-1987
  • Experimental Cardiovascular Pathology, University of Alabama at Birmingham, 1988-1990

Areas of Special Interests

  • Control of energy metabolism in the heart
  • Physiologic and Pathologic Cardiac hypertrophy
  • Cardiovascular Pathology
  • Academic Information Technology
  • Assessment of workload in academic pathology practice environments

Teaching Interests

Cardiovascular structure, physiology, pathophysiology and pathology

Selected Publications

  • Allard, M.F., Schonekess, B., Henning, S.L., English, D.R., Lopaschuk, GD. Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts. Am J Physiol 267:H742-H750, 1994.
     
  • Henning, S.L., Wambolt, R.B., Shonekess, B.O., Lopaschuk, G.D., Allard, M.F. Contribution of glycogen to aerobic myocardial glucose utliization. Circulation 93:1549-1555, 1996.
     
  • Shonekess, B.O., Allard, M.F., Lopaschuk, G.D. Recovery of glycolysis and oxidative metabolism during postischemic reperfusion of hypertrophied rat hearts. Am J Physiol 271(Heart Circ Physiol 40):H798-H805, 1996.
     
  • Allard, M.F., Henning, S.L., Wambolt, R.B., Gransleese, S.R., English, D.R., Lopaschuk, G.D. Glycogen metabolism in the aerobic hypertrophied heart. Circulation 96(2):676-682, 1997.
     
  • Wambolt, R.B., Lopaschuk, G.D., Brownsey, R.W., Allard, M.F. Dichloroacetate improves postischemic function of hypertrophied rat hearts. J Am Coll Cardiol 36:1378-1385, 2000.
     
  • Longnus, S.L., Wambolt, R.B., Barr, R.L., Lopaschuk, G.D., Allard, M.F. Regulation of myocardial fatty acid oxidation by substrate supply. Am J Physiol Heart Circ Physiol 281(4):H1561-7, 2001.
     
  • Lydell, C.P., Chan, A., Wambolt, R.B., Sambandam, N., Parsons, H., Bondy, G.P., Rodrigues, B., Popov, K.M., Harris, R.A., Brownsey, R.W., Allard, M.F. Pyruvate dehydrogenase and the regulation of glucose oxidation in hypertrophied rat hearts. Cardiovasc Res 53: 841-851, 2002.
     
  • Burelle, Y., Wambolt, R.B., Grist, M., Parsons, H.L., Chow, J.C.F., Antler, C., Bonen, A., Keller, A., Dunaway, G.A., Popov, K.M., Hochachka, P.W., Allard, M.F. Regular exercise is associated with a protective metabolic phenotype in the rat heart. Am J Physiol Heart Circ Physiol 287(3): H1055-H1063, 2004.
     
  • Butany, J., Allard, M.F. Pathology of Prosthetic Heart Valves. In, Canadian Cardiovascular Society Consensus Conference on the Surgical Management of Valvular Heart Disease. Can J Cardiol 20 (Suppl E):74E-79E, 2004.
     
  • Saeedi, R., Grist, M., Wambolt, R.B., Bescond-Jacquet, A., Lucien, A., Allard, M.F. Trimetazidine normalizes postischemic function of hypertrophied rat hearts. J Pharmacol Exp Therap 314(1):446-454, 2005.
     
  • Allard, M.F., Parsons, H.L., Saeedi, R., Wambolt, R.B., Brownsey, R. AMPK and metabolic adaptation by the heart to pressure overload. Am J Physiol Heart Circ Physiol. 292:H140-H148, 2007.
     
  • Saeedi, R., Saran, V.V., Wu, S.S.Y., Kume, E.S., Paulson, K., Chan, A.P.K., Parsons, H.L., Wambolt, R.B., Dyck, J.R., Brownsey, R.W., Allard, M.F. AMP-activated protein kinase influences metabolic remodeling in H9c2 cells hypertrophied by arginine vasopressin. Am J Physiol 296(6):H1822-H1832, 2009.
     
  • Sharma, V., Sharma, A., Saran, V., Bernatchez, P.N., Allard, M.F., McNeill, J.H. β-receptor antagonist treatment prevents the activation of cell death signalling in the diabetic heart independent of its metabolic actions. Eur J Pharmacol, 657(1-3):117-125, 2011.
     
  • Folmes, K.D., Chan, A.Y.M., Koonen, D.P.Y., Pulinilkunnil, T.C., Baczk., I., Hunter, B.E., Thorn, S., Allard, M.F., Roberts, R., Gollob, M.H., Light, P.E., Dyck, J.R.B.  Distinct early signaling events resulting from the expression of the PRKAG2 R302Q mutant of AMPK contribute to increased myocardial glycogen. Circ Cardiovasc Genet 2:457-466, 2009.
     
  • Nietlispach, F., Webb, J.G., Ye, J., Cheung, A., Lichtenstein, S.V., Carere, R.G., Gurvitch, R., Thompson, C.R., Ostry, A.J., Matzke, L., Allard, M.F. Pathology of transcatheter valve therapy. JACC Cardiovasc Interv 5(5):582-590, 2012.
     
  • Bround, M.J., Allard, M.F., Wambolt, R., Kulpa, J., Brownsey, R.W. Rodrigues, B., Luciani, D, Johnson, J. Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo. J Biol Chem 28;288(26):18975-18986, 2013.
     
  • Saran, V., Sharma, V., Wambolt, R., Yuen, V.G., Allard, M., McNeill, JH. Combined metroprolol and ascorbic acid treatment prevents intrinsic damage to the heart during diabetic cardiomyopathy. Can J Physiol Pharmacol 92(10):827-837, 2014.
     
  • Maung, R.L. et al. CAP-ACP Workload Model odel insic damage to Pathol 7(2): 13-18, 2015.

Contact

Department of Pathology and Laboratory Medicine
University of British Columbia
Vancouver, BC V6T 2B5
604-827-0673
mike.allard@ubc.ca

External Links / Resources

  • Twitter Account: @AllardMike
  • UBC Department of Pathology and Laboratory Medicine: www.pathology.ubc.ca



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