Kristopher B. Deatrick

Bio: Kristopher B. Deatrick is an academic researcher from University of Michigan. The author has contributed to research in topics: Medicine & Extracorporeal membrane oxygenation. The author has an hindex of 10, co-authored 17 publications receiving 435 citations. Previous affiliations of Kristopher B. Deatrick include Columbia University Medical Center.

The vessel wall: A forgotten player in post thrombotic syndrome.

Abstract: Much research in venous thrombotic diseases focuses on the acute thrombotic process such as anticoagulation and risk factors. Deep-vein thrombosis directly leads to post thrombotic syndrome, and this can cause significant patient disability. Little research has focused on the vein wall injury response to the thrombotic inflammatory insult. Herein, we review what is currently known about this process with emphasis on the matrix, mediators, and vascular medial smooth muscle response after thrombotic injury. Translational therapies and potential future agents are reviewed.

Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives

Abstract: Vascular endothelial cells (ECs) are exposed to hemodynamic forces, which modulate EC functions and vascular biology/pathobiology in health and disease. The flow patterns and hemodynamic forces are not uniform in the vascular system. In straight parts of the arterial tree, blood flow is generally laminar and wall shear stress is high and directed; in branches and curvatures, blood flow is disturbed with nonuniform and irregular distribution of low wall shear stress. Sustained laminar flow with high shear stress upregulates expressions of EC genes and proteins that are protective against atherosclerosis, whereas disturbed flow with associated reciprocating, low shear stress generally upregulates the EC genes and proteins that promote atherogenesis. These findings have led to the concept that the disturbed flow pattern in branch points and curvatures causes the preferential localization of atherosclerotic lesions. Disturbed flow also results in postsurgical neointimal hyperplasia and contributes to pathophysiology of clinical conditions such as in-stent restenosis, vein bypass graft failure, and transplant vasculopathy, as well as aortic valve calcification. In the venous system, disturbed flow resulting from reflux, outflow obstruction, and/or stasis leads to venous inflammation and thrombosis, and hence the development of chronic venous diseases. Understanding of the effects of disturbed flow on ECs can provide mechanistic insights into the role of complex flow patterns in pathogenesis of vascular diseases and can help to elucidate the phenotypic and functional differences between quiescent (nonatherogenic/nonthrombogenic) and activated (atherogenic/thrombogenic) ECs. This review summarizes the current knowledge on the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. Such information can contribute to our understanding of the etiology of lesion development in vascular niches with disturbed flow and help to generate new approaches for therapeutic interventions.

Acute pulmonary embolism.

Abstract: Deep vein thrombosis (DVT) and, therefore, pulmonary embolism (PE) are often preventable. Because of the lack of specificity of symptoms and signs, DVT and PE are frequently clinically unsuspected, leading to substantial diagnostic and therapeutic delays and resulting in considerable morbidity and mortality. Furthermore, prophylaxis continues to be dramatically underused. The incidence of venous thromboembolism is high in hospitalized patients, and both surgical as well as medical patients are at risk.

Abdominal aortic aneurysm : Pathogenesis and implications for management

Abstract: Abdominal aortic aneurysm (AAA) affects approximately 5% of elderly men and is responsible for a significant number of deaths in Western Countries. At present surgery by open or endovascular means is the only widely used therapy for this condition. In this review we examine the risk factors, serum, and genetic associations of AAA. Epidemiology studies suggest that smoking cessation and control of cholesterol and blood pressure should reduce the number of patients developing AAA. Natural history studies suggest that smoking cessation should reduce the rate of progression of AAA. Clear level 1 evidence for drug treatments of AAA are presently lacking; however, animal and human in vitro studies suggest that medication targeted at reducing inflammation and proteolysis are most likely to be beneficial, with limited data to support the use of statins, Angiotensin II inhibitors, and macrolides. Work has commenced in understanding which patients, identified by clinical, serum, and genotype, are more at risk of AAA progression and thus should be selected out for aggressive treatment. Well designed large multicenter randomized controlled trials are required to examine the medical treatment of AAA.