Dr. Amir Ravandi
Cardiovascular Lipidomics, Institute of Cardiovascular Sciences
Staff Interventional Cardiologist
St. Boniface Hospital
Department of Cardiology and Physiology, University of Manitoba
The general focus of Dr. Ravandi’s laboratory is to study lipid oxidation products and their contribution to cardiovascular pathology. The laboratory uses LC/MS/MS Lipidomic platform for quantitation and identification of lipid oxidation products in both animal models and clinical conditions to determine the involvement of oxidized lipids in both cardiac and vascular lesions. The ultimate goal is to not only identify the contribution of bioactive lipids to cardiac muscle injury but also to determine new therapeutic approaches to prevent the pathological effects of oxidized lipids.
About Dr. Amir Ravandi
Dr. Amir Ravandi received his undergraduate degree, from University of Toronto and went on to complete a PhD at the Banting and Best Medical Research Institute at University of Toronto. He was at the Terrence Donnelly Vascular Research Labs at St. Michaels’s Hospital as postdoctoral fellow. After obtaining his MD at University of Toronto he went on to complete his internal medicine and cardiology training at McMaster University. He completed a fellowship in coronary and peripheral vascular interventions at University of California at San Diego.
He is currently on staff at St. Boniface Hospital as an interventional cardiologist. He is also an assistant professor of cardiology and physiology at University of Manitoba. He is a principal investigator at the Institute of Cardiovascular Sciences. His current focus is utilizing lipidomics to further our understanding of myocardial ischemia and plaque rupture.
For more information, please contact:
Dr. Amir Ravandi
Institute of Cardiovascular Sciences
St. Boniface Hospital Research
Rm 4026-351 Tache Avenue
Winnipeg, Manitoba, Canada
Clinical: (204) 237-2315
Role of Oxidized phospholipids in ischemia reperfusion injury:
Cardiovascular disease remains one of the leading causes of morbidity and mortality worldwide. One unifying mechanistic component is the role of inflammation in its initiation and progression. For many years lipids were considered to be only cellular building blocks with very little biological activity. Due to their susceptibility to oxidation they are modified in the presence of reactive oxygen species. Apart from impairment of their structural function, oxidation makes oxidized phospholipids (OxPL) acquire novel biological activities not characteristic of their unoxidized precursors. The effects of OxPLs described in vitro and in vivo suggest their potential relevance in different pathologies, including atherosclerosis, acute inflammation, lung injury, and many other conditions. The actions of OxPL can vary depending upon the specific species of phospholipid being oxidized. Recently, oxidized phosphatidylcholines (OxPC) have been recognized as not only products of oxidative damage but also mediators of its progression. These compounds exert their biological activity through multiple pathways. They have been shown to be potent stimulators of platelet activating factor receptor, prostaglandin receptors and PPAR receptors resulting in platelet aggregation, induction of the coagulation cascade and apoptosis and cell death. Recent advancements in softer methods of ionization, such as electrospray mass spectrometry, has allowed us to identify and quantitate OxPL’s in biological tissues. Our group has over the past decade developed mass spectrometric techniques that can identify and quantitate oxidized lipids within atherosclerotic plaques, oxidized Low Density Lipoprotein (OxLDL), and other biological tissues. As we move forward in trying to better understand the role of OxPL in cardiovascular pathology, it necessitates a detailed understanding of the oxidized lipidome within cardiac tissue such as ischemic myocardium or in plasma from patients with acute coronary syndromes. Using this knowledge as a platform, we are investigating the role of OxPL in cardiovascular pathology and will be able to tailor therapies to prevent OxPL induced injury.
1. Ravandi A, Boekholdt SM, Mallat Z, Talmud PJ, Kastelein JJ, Wareham NJ, Miller ER, Benessiano J, Tedgui A, Witztum JL, Khaw KT, Tsimikas S. Relationship of IgG and IgM autoantibodies and immune complexes to oxidized LDL with markers of oxidation and inflammation and cardiovascular events: Results from the Epic-Norfolk study. Journal of Lipid Research. 2011;52:1829-1836.
2. Ravandi A, Penny WF. Percutaneous intervention of an acute left main coronary occlusion due to dissection of the aortic root. JACC. Cardiovascular Interventions. 2011;4:713-715
3. K. Bin Thani, A. Ravandi W.E. Bennett, , S. Tsimikas. Successful treatment of in stent restenosis of a covered stent graft with a paclitaxel eluting stent. Journal Cardiology Cases. 2011; 4:13-1.
4. Prasad A, Ilapakurti M, Ravandi A. Successful retrieval of a frayed coronary stent using the peripheral crossover technique. The Journal of Invasive Cardiology. 2011;23:E69-71
5. Ravandi A, Teo KK. Blocking the renin-angiotensin system: Dual- versus mono-therapy. Expert Review of Cardiovascular Therapy. 2009;7:667-674
6. Ravandi A, Sun JC, Lamy A, Valettas N. Fluoroscopy of acutely thrombosed aortic valve. Circulation. 2008;118:e705
7. Hartvigsen K, Ravandi A, Harkewicz R, Kamido H, Bukhave K, Holmera G, Kuksis A. 1 -o-alkyl-2-(omega-oxo)acyl-sn-glycerols from shark oil and human milk fat are potential precursors of PAF mimics and ghb. Lipids. 2006;41:679-693
8. Williams DJ, Wharton S, Ravandi A, Achong M. Cutaneous myiasis of the eyelid masquerading as periorbital cellulitis. Emergency Medicine Journal: EMJ. 2006;23:737
9. Ahmed Z, Ravandi A, Kuksis A. Bioactive oxolipids and cardiovascular disease: antiatherogenic effect of High-Density Lipoprotein. Journal of Clinical Ligand Assay 2006; 29: 6-15.
10. Healey JS, Wharton S, Al-Kaabi S, Pai M, Ravandi A, Nair G, Morillo CA, Connolly SJ. Stroke prevention in patients with atrial fibrillation: The diagnosis and management of hypertension by specialists. The Canadian Journal of Cardiology. 2006;22:485-488
11. Kuksis A, Ravandi A, Schneider M. Covalent binding of acetone to aminophospholipids in vitro and in vivo. Annals of the New York Academy of Sciences. 2005;1043:417-439
12. Ravandi A, Babaei S, Leung R, Monge JC, Hoppe G, Hoff H, Kamido H, Kuksis A. Phospholipids and oxophospholipids in atherosclerotic plaques at different stages of plaque development. Lipids. 2004;39:97-109
13. Ahmed Z, Ravandi A, Maguire GF, Kuksis A, Connelly PW. Formation of apolipoprotein AI-phosphatidylcholine core aldehyde Schiff base adducts promotes uptake by thp-1 macrophages. Cardiovascular Research. 2003;58:712-720
Society for Cardiac Angiography and Interventions. C3 Summit Finalist, Baltimore,MD, USA
Gold Medal. Best Research Presentation McMaster University Internal Medicine Research Day.
Chief Cardiology Fellow. McMaster University.
Outstanding Chief Medical Resident. Department of Medicine. McMaster University
Outstanding PGY2. Department of Medicine. McMaster University
Pharmaceutical Manufacturers of Canada Research Fellowship
Pharmaceutical Manufacturers of Canada Research Fellowship
Stuart Allan Hoffman Award, Best Ph.D. thesis. Department of Laboratory Medicine & Pathobiology, University of Toronto
Best presentation, AOCS Annual meeting among 1500 presentations, Orlando
Young Investigator Award, Canadian Society for Atherosclerosis, Thrombosis and Vascular Biology
Ontario Graduate Scholarship
Dutkevich Foundation Award.
University of Toronto Doctoral Open Fellowship
Dr. Ravandi’s laboratory invites applications for Graduate Students. Please forward an application and academic CV to Dr. Amir Ravandi at firstname.lastname@example.org.