Stretch-induced increased hemodynamic load adversely affects endothelial cell function and is an important contributor to thromboembolus formation in heart failure, valvular heart disease, atrial fibrillation, venous insufficiency, and pulmonary hypertension, and in thrombus occluded vein grafts. Local thrombus formation and thromboenbolic events can be reduced by inhibiting the TGF-beta signaling pathway or TGF-beta per se. Inhibitors can be administered to patients or veins (prior to interposition) at risk for thromboembolic events or local thrombus formation. Inhibitors can be applied to harvested veins to be used as arterial grafts.