John S. Ikonomidis, MD, PhD

John S. Ikonomidis is an Associate Professor of Cardiothoracic Surgery at the Medical University of South Carolina (MUSC) and Chief of the Cardiothoracic Surgery Section of the Ralph H. Johnson Veterans Affairs Medical Center.  Dr. Ikonomidis received his MD and PhD degrees from and completed General Surgery Training at The University of Toronto.  He completed his Cardiothoracic Surgery Residency at Stanford University before joining the faculty at MUSC in July 2000.

Dr. Ikonomidis’ research interests focus on the mechanisms of thoracic aortic aneurysm disease and the development of therapeutic strategies to reduce, halt, or reverse progression of this potentially lethal disorder.

Dr. Ikonomidis is a member of the American Association for Thoracic Surgery, Society of Thoracic Surgeons, Southern Thoracic Surgical Society and the Canadian Cardiovascular Society.  He holds fellowships from the Royal College of Physicians and Surgeons of Canada, American College of Surgeons, American Board of Thoracic Surgery and the American Heart Association.   He serves on several editorial boards including The Journal of Thoracic and Cardiovascular Surgery, Annals of Thoracic Surgery, Circulation and Cardiovascular Research.

Research Interests:

1) Myocardial Protection

• real time measurement of MMP/protease activity within the myocardium during cardiac surgery  

2) Thoracic Aortic Surgery

• outcomes of valve-sparing aortic root replacement
• outcomes/testing of endovascular stent graft devices

3) Etiology/Pathogenesis of Thoracic Aortic Aneurysms

• murine TAA model
• • histology
  • protease activity 
  • intervention using transgenic strains
  • upstream signaling
• clinical TAA bank
• • correlation to murine assesments

4) Methods of Obtaining Hemostasis in Cardiac Surgery

• results of use of factor VII
• potential novel uses/applications for aprotinin

Medial elastin breakdown contributes to thoracic aortic aneurysm disease.  Left:  normal structure of the thoracic aorta.  A: cross-section of aorta showing adventitial, medial and intimal layers.  B: normal medial architecture showing elastin layers interspersed with vascular smooth muscle cells. C: Infiltration of the media by inflammatory cells such as macrophages may result in release of specific activated protease systems such as the matrix metalloproteinases (MMPs) which degrade medial elastin and weaken the aortic wall. Right: Aortic wall weakening may cause aneurysm formation.

Recent Publications:

• Ikonomidis JS, Jones JA, Barbour JR, Stroud RE, Clark LL, Kaplan BS, Zeeshan A, Bavaria JE, Gorman JH 3rd, Spinale FG, Gorman RC. Expression of matrix metalloproteinases and endogenous inhibitors within ascending aortic aneurysms of patients with Marfan syndrome. Circulation. 2006 Jul 4;114(1 Suppl):I365-70.
• Ikonomidis JS, Jones JA, Barbour JR, Stroud RE, Clark LL, Kaplan BS, Zeeshan A, Bavaria JE, Gorman JH 3rd, Spinale FG, Gorman RC. Expression of matrix metalloproteinases and endogenous inhibitors within ascending aortic aneurysms of patients with bicuspid or tricuspid aortic valves. J Thorac Cardiovasc Surg. 2007 Apr;133(4):1028-36.
• Bowman LJ, Uber WE, Stroud MR, Christiansen LR, Lazarchick J, Crumbley AJ 3rd, Kratz JM, Toole JM, Crawford FA Jr, Ikonomidis JS. Use of recombinant activated factor VII concentrate to control postoperative hemorrhage in complex cardiovascular surgery.  Ann Thorac Surg. 2008 May;85(5):1669-76; discussion 1676-7.

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