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The failure of vein bypass grafting in the coronary or lower extremity circulation is a common clinical occurrence that incurs significant morbidity, mortality, and cost.
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Although the pathophysiology of vein graft failure is incompletely understood, numerous relevant molecular targets have been elucidated.
The pathophysiology of vein graft failure involves a complex interplay between an acute vascular injury response and the hemodynamic adaptation of the vein to arterial forces.
Vein graft stenosis is believed to be the pathophysiologic response of vascular tissue to injury and is the major cause of vein graft failure.
Genetic therapy in the cardiovascular system has been proposed for a variety of diseases ranging from prevention of vein graft failure to hypertension.
In summary, diabetes has been associated with increased prevalence of vein graft failure.
Taken together, these data may help explain why diabetes is associated with an increased risk of vein graft failure.
The present strategy may also be combined with molecular/biologically based contrast agents to provide a better understanding of vascular wall remodeling mechanisms and improve our understanding of vein graft failure.
Intimal hyperplasia is the main cause of vein graft failure after the first month [2] making it important to understand the mechanisms that regulate vascular smooth muscle cell (VSMC) proliferation.
VSMC proliferation and hyperplasia is a key feature of a variety of cardiovascular diseases including atherosclerosis, hypertension, pulmonary arterial hypertension (PAH), and its existence contributes to the failure of coronary artery bypass vein grafts and to the restenosis following percutaneous coronary intervention.
Emerging data supports a role for negative wall remodeling in the failure of vascular interventions such as vein grafts, yet clinicians/researchers currently lack the ability to temporally/efficiently investigate adventitial surface topography/total vascular wall anatomy in vivo.
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