Reduction in Mechanical Wall Strain Precedes Intimal Hyperplasia Formation in a Murine Model of Arterial Occlusive Disease

Coronary artery disease and peripheral artery disease remain a significant source of mortality and vascular morbidity in the United States; both affecting over 14 million Americans.[1] Although a number of both open and endovascular procedures are available for treating occlusive lesions, post-procedure intimal hyperplasia (IH) and pathological wall adaptation in treated arteries cause further need for treatment. As on average 50% of patients receiving these treatments must receive further vascular intervention to prevent the continued expansion of IH into the vessel lumen, there is a need to improve our understanding of the underlying causes of IH formation.[2]