Hemodynamic consequences of stenosis remodeling during coronary angioplasty.
Quantitative hemodynamic assessment during various endovascular interventions including balloon angioplasty is lacking. Translesional pressure drops measured by angioplasty catheters can cause flow blockage and thus lead to inaccurate estimates of preintervention and postintervention flow rates. A new analytical model of the flow rate-pressure drop relation across vascular stenoses is utilized that is nonlinear yet relatively simple in principle, easily applicable in vivo, and compatible with the presence of catheters. The model incorporates in vitro experimental evidence, angiographic data on the dimensions and shapes of coronary arterial stenoses before and after balloon angioplasty, reported translesional pressure gradients, and measurements of coronary flow reserve. Reasonable estimates of mean coronary artery flow rates and translesional pressure drops in the absence of angioplasty catheters are obtained. Prior to angioplasty significant flow restriction across a 68% diameter stenosis exists during hyperemic flow conditions. Following successful balloon dilation, increased minimal cross-sectional area (residual 40% diameter stenosis) results in an improved flow rate-pressure drop relation. Despite minimal flow restriction during hyperemic conditions following angioplasty remodeling, residual luminal constriction leads to elevated wall shear stress levels within the entry region of the stenosis. The flow analysis described may be of clinical utility in evaluating the hemodynamic significance of the anatomic severity of stenoses in coronary and peripheral arteries before and after endovascular therapeutic interventions.
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Division of Vascular Surgery, Harbor-UCLA Medical Center, Torrance, USA.
White
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Kwack
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D015906:Angioplasty, Balloon, Coronary; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003251:Constriction, Pathologic; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology*; D012039:Regional Blood Flow