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Intravascular ultrasound study in heart transplant recipients at proximal and distal branch points

      Arterial remodeling, or compensatory vessel enlargement, has been recognized to be an important mechanism in the development of atherosclerosis. The phenomenon, originally described by Glagov et al,
      • Glagov S.
      • Weisenberg E.
      • Zarins C.K.
      • Stankunavicius R.
      • Kolettis G.J.
      Compensatory enlargement of human atherosclerotic coronary arteries.
      resembles a potential response of the artery to plaque growth. To maintain the lumen, arteries enlarge and maintain an adequate lumen size until plaque area occupies approximately 30% to 40% of the lumen.
      • Glagov S.
      • Weisenberg E.
      • Zarins C.K.
      • Stankunavicius R.
      • Kolettis G.J.
      Compensatory enlargement of human atherosclerotic coronary arteries.
      ,
      • Losordo D.W.
      • Rosenfield K.
      • Kaufmann J.
      • Pieczek A.
      • Isner J.M.
      Focal compensatory enlargement of human coronary arteries in response to progressive atherosclerosis in vivo documentation using intravascular ultrasound.
      ,
      • Zarins C.K.
      • Weisenberg E.
      • Kolettis G.
      • Stankunavicius R.
      • Glagov S.
      Differential enlargement of artery segments in response to enlarging atherosclerotic plaques.
      ,
      • Hermiller J.B.
      • Tenaglia A.N.
      • Kisslo K.B.
      • Phillips H.R.
      • Bashore T.M.
      • Stack R.S.
      • Davidson C.J.
      In vivo validation of compensatory enlargement of atherosclerotic coronary arteries.
      With higher degrees of stenosis, the artery loses the ability to compensate for further plaque growth, allowing plaques to encroach the lumen and to diminish blood flow. Remodeling has also been described in transplant vasculopathy and seems to be of relevance for the development of transplant vasculopathy.
      • Lim T.T.
      • Liang D.H.
      • Botas J.
      • Schroeder J.S.
      • Oesterle S.N.
      • Yeung A.C.
      Role of compensatory enlargement and shrinkage in transplant coronary artery disease serial intravascular ultrasound study.
      Intravascular ultrasound (IVUS) and histologic studies have revealed higher degrees of stenoses at branch points and bifurcations, and it has been shown that these regions are prone to specific conditions, exposing the arterial wall to altered amounts of flow- and pressure-induced forces.
      • Thubrikar M.J.
      • Robicsek F.
      Pressure-induced arterial wall stress, and atherosclerosis.
      ,
      • Traub O.
      • Berk B.C.
      Laminar shear stress–mechanisms by which endothelial cells transduce an atheroprotective force.
      Although the mechanisms involved in remodeling are not clear, there is increasing evidence that flow, shear, and tensile stress play important roles in its development.
      • Thubrikar M.J.
      • Robicsek F.
      Pressure-induced arterial wall stress, and atherosclerosis.
      ,
      • Traub O.
      • Berk B.C.
      Laminar shear stress–mechanisms by which endothelial cells transduce an atheroprotective force.
      ,
      • Schwarzacher S.P.
      • Uren N.G.
      • Ward M.R.
      • Schwarzkopf A.
      • Gianetti N.
      • Hunt S.
      • Fitzgerald P.J.
      • Oesterle S.N.
      • Yeung A.C.
      Determinants of coronary remodeling in transplant coronary disease a simultaneous intravascular and Doppler flow study.
      ,
      • Kamiya A.
      • Togawa T.
      Adaptive regulation of wall shear stress to flow change in the canine carotid artery.
      ,
      • Zarins C.K.
      • Zatina M.A.
      • Giddens D.P.
      • Ku D.N.
      • Glagov S.
      Shear stress regulation of artery lumen diameter in experimental atherogenesis.
      ,
      • Buga G.M.
      • Gold M.E.
      • Fukuto J.M.
      • Ignarro L.J.
      Shear-stress-induced release of nitric oxide from endothelial cells grown on beads.
      The purpose of this study was to analyze the dimensions and the remodeling behavior of arterial branch points by comparing them with those of nonbranching segments. In this manner, we tried to characterize whether alterations in this area influence the remodeling of arteries at these specific sites.
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