Objective: Currently, no quantitative guidelines have been established for treatment of left pulmonary artery (LPA) stenosis. This study aims to quantify the effects of LPA stenosis on postoperative hemodynamics for single-ventricle patients undergoing stage II superior cavopulmonary connection (SCPC) surgery, using a multiscale computational approach.
Methods: Image data from 6 patients were segmented to produce 3-dimensional models of the pulmonary arteries before stage II surgery. Pressure and flow measurements were used to tune a 0-dimensional model of the entire circulation. Postoperative geometries were generated through stage II virtual surgery; varying degrees of LPA stenosis were applied using mesh morphing and hemodynamics assessed through coupled 0-3-dimensional simulations. To relate metrics of stenosis to clinical classifications, pediatric cardiologists and surgeons ranked the degrees of stenosis in the models. The effects of LPA stenosis were assessed based on left-to-right pulmonary artery flow split ratios, mean pressure drop across the stenosis, cardiac pressure-volume loops, and other clinically relevant parameters.
Results: Stenosis of >65% of the vessel diameter was required to produce a right pulmonary artery:LPA flow split <30%, and/or a mean pressure drop of >3.0 mm Hg, defined as clinically significant changes.
Conclusions: The effects of <65% stenosis on SCPC hemodynamics and physiology were minor and may not justify the increased complexity of adding LPA arterioplasty to the SCPC operation. However, in the longer term, pulmonary augmentation may affect outcomes of the Fontan completion surgery, as pulmonary artery distortion is a risk factor that may influence stage III physiology.
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http://dx.doi.org/10.1016/j.jtcvs.2014.12.040 | DOI Listing |
Am Heart J
January 2025
Department of Cardiology, Gødstrup Regional Hospital, Hospitalsparken 15, 7400 Herning, Denmark; Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark. Electronic address:
Background: The role of lipoprotein(a) (Lp(a)) in the risk-assessment of patients with de-novo stable chest pain is sparsely investigated. We assessed the association between Lp(a) concentration and the presence of coronary stenosis on coronary computed tomography (CT) angiography in a broad population of patients referred with stable chest pain.
Methods: Lp(a) measurements and coronary CT angiography were performed in 4,346 patients with stable chest pain and no previous history of coronary artery disease.
J Clin Med
November 2024
Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland.
Increased lipoprotein(a) [Lp(a)] level is associated with elevated possibility of atherosclerosis progression. SYNTAX score enables to grade the anatomy of coronary arteries. To identify the impact of increased Lp(a) level on SYNTAX score in individuals with acute myocardial infarction (AMI).
View Article and Find Full Text PDFClin Res Cardiol
December 2024
Clinic for General and Interventional Cardiology/Angiology, Herz- und Diabeteszentrum Nordrhein-Westfalen, Ruhr-Universität Bochum, Georgstraße 11, 32545, Bad Oeynhausen, Germany.
Background: Elevated levels of lipoprotein(a) (Lp[a]) have been recognized as substantial risk factors for cardiovascular disease and aortic stenosis (AS). However, the specific role of Lp(a) in promoting aortic valve calcification (AVC) and influencing mortality in elderly, multimorbid patients undergoing transcatheter aortic valve replacement (TAVR) remains unclear and warrants further investigation.
Methods: A retrospective analysis was conducted on all consecutive patients who underwent TAVR between August 2019 and June 2020 at our clinic.
Front Cardiovasc Med
November 2024
Cardiac Catheterization Laboratories, Department of Pediatric Cardiology, German Pediatric Heart Centre, University Hospital Bonn, Bonn, Germany.
Curr Atheroscler Rep
November 2024
McGill University Health Centre and Research Institute, Montréal, Québec, Canada.
Purpose Of Review: Elevated lipoprotein(a) (Lp[a]) is a genetically determined cardiovascular risk factor, causally linked to both atherosclerotic coronary artery disease and aortic stenosis. Elevated Lp(a) is widely prevalent, and several cardiovascular societies now recommend performing Lp(a) screening at least once in all adults. However, there are currently no approved drugs aimed specifically at lowering Lp(a).
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