The objective of this study was to evaluate the incidence of pre-existing catheterization left pulmonary artery (LPA) gradients and correlation of these gradients with later LPA stenosis after successful patent ductus arteriosus (PDA) occlusion. We performed a single-center review of 130 patients with PDA closure from October 1993 to February 2005. We analyzed the pre-PDA closure LPA pressure gradients at catheterization to determine if these were predictive of late LPA stenosis. On follow-up, a V (max) >2 m/s by echocardiogram (transthoracic echocardiography; TTE) was considered indicative of possible LPA stenosis. Left lung perfusion of <35% was considered diagnostic of significant LPA stenosis. Post PDA closure, possible LPA stenosis by TTE was seen in 8 of 128 patients (6.25%). Seven of these eight had precatheter LPA gradients >7 mm Hg. Five of these had perfusion scans, three of the five had significant LPA stenosis, and two underwent LPA angioplasty. Patients with LPA catheter gradients >7 mm Hg were more likely to have possible LPA stenosis by TTE, significant LPA stenosis by lung scan, and intervention with LPA angioplasty. In conclusion, a preclosure main pulmonary artery-to-LPA pressure gradient >7 mm Hg was found in all patients who developed significant LPA stenosis on follow-up after transcatheter PDA closure. It appears likely that these patients have LPA abnormality rather than stenosis caused by the PDA occlusion device. Patients with preclosure LPA gradients >7 mm Hg should undergo follow-up evaluations for detection of significant stenosis and may require treatment if an important flow abnormality is documented.
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http://dx.doi.org/10.1007/s00246-009-9448-8 | DOI Listing |
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).
View Article and Find Full Text PDFInt J Cardiol Heart Vasc
December 2024
Department of Cardiology, University of Miami Miller School of Medicine/Jackson Memorial Hospital, Miami, FL, USA.
Lipoprotein(a) (Lp(a)) has garnered increasing attention as a significant contributor to the pathogenesis of aortic stenosis (AS), prompting a focused investigation into innovative pharmacological strategies to target this lipoprotein and its associated risks. Despite its recognized role in AS progression, Lp(a) often remains overlooked in clinical assessments, mirroring the broader challenges observed in holistic disease management. This review delves into the mechanistic intricacies of Lp(a) involvement in AS pathophysiology and its potential as a therapeutic target.
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