Peter Kerr Henke, MD

Dr. Henke is the James C. Stanley Professor of Vascular Surgery, operating both at the University of Michigan and the Veteran’s Administration Hospital. He graduated from the University of Wisconsin with a Bachelor of Science in Biochemistry and Molecular Biology in 1988, and from the University of Wisconsin School of Medicine in 1992. He did his General Surgery residency at the University of Louisville, where he was honored with the Chairman’s Award for Personal Scholarship and the C. M. Edelen Award for best resident paper of the year in 1997. He joined the University of Michigan for his Vascular Surgery fellowship, and graduated to join the faculty in 2000. He is the past Chief of Surgery at the Ann Arbor VA, Co-director of the BCBSM Vascular Intervention Collaboration and the past President of the American Venous Forum

Clinical Specialization:

His clinical and research focus is on lower extremity arterial, venous and vascular medicine patient issues.

Vascular surgery, distal bypass and endovascular surgery

University of Michigan Health participates with most health insurance plans.

The focus of the Henke laboratory is to determine the basic mechanisms of deep vein thrombosis resolution as well as the effect of the vein wall. The clinical relevance of this is that DVT is a major, and until recently, neglected health problem. The acute sequlae may be pulmonary embolism which can be fatal and more commonly, post thrombotic syndrome with its significant morbidity. Using state of the art physiological, immunological and molecular biological techniques, mouse and rat models are used to define the process of venous thrombus resolution.

Over the last 5 years, much has been learned. First, the thrombus is biologically active with leukocytes directing the adjacent vein wall response. Secondly, the thrombi undergo neovascularization as a normal process to allow return of prograde blood flow. Third, the leukocyte is essential for thrombus resolution, and is directed by a class of signaling molecules termed chemokines. More specifically, neutrophils are essential for early DVT resolution while monocytes are critical for the later processes. Forth, matrix metalloproteinases play an integral role in both vein wall injury and remodeling as well as DVT resolution. Lastly, the mechanism of how a thrombus forms directs the vein wall response. For example, stasis derived DVT is more damaging to the vein wall than endothelial injury or an inert stretch injury. This latter data is clinically applicable because it suggests that methods to actively remove thrombus in a timely fashion, rather than passive anticoagulation, may decrease the long term risk of fibrotic injury.