Imperial College London

ProfessorDudleyPennell

Faculty of MedicineNational Heart & Lung Institute

Professor of Cardiology
 
 
 
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Contact

 

+44 (0)20 7351 8810d.pennell

 
 
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Location

 

CMR UnitRoyal BromptonRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Khan:2019:10.1016/j.jacl.2019.06.009,
author = {Khan, TZ and Gorog, DA and Arachchillage, DJ and Ahnström, J and Rhodes, S and Donovan, J and Banya, W and Pottle, A and Barbir, M and Pennell, DJ},
doi = {10.1016/j.jacl.2019.06.009},
journal = {Journal of Clinical Lipidology},
pages = {788--796},
title = {Impact of lipoprotein apheresis on thrombotic parameters in patients with refractory angina and raised lipoprotein(a): Findings from a randomized controlled cross-over trial},
url = {http://dx.doi.org/10.1016/j.jacl.2019.06.009},
volume = {13},
year = {2019}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: Raised lipoprotein(a) [Lp(a)] is a cardiovascular risk factor common in patients with refractory angina. The apolipoprotein(a) component of Lp(a) exhibits structural homology with plasminogen and can enhance thrombosis and impair fibrinolysis. OBJECTIVES: The objective of the study was to assess the effect of lipoprotein apheresis on markers of thrombosis and fibrinolysis in patients with high Lp(a). METHODS: In a prospective, single-blind, crossover trial, 20 patients with refractory angina and raised Lp(a) > 50 mg/dL were randomized to three months of weekly lipoprotein apheresis or sham. Blood taken before and after apheresis/sham was assessed using the Global Thrombosis Test, to assess time taken for in vitro thrombus formation (occlusion time) and endogenous fibrinolysis (lysis time), as well as von Willebrand Factor, fibrinogen, D-dimer, thrombin/anti-thrombin III complex, prothrombin fragments 1 + 2, and thrombin generation assays. RESULTS: Lp(a) was significantly reduced by apheresis (100.2 [interquartile range {IQR}, 69.6143.0] vs 24.8 [17.2,34.0] mg/dL, P = .0001) but not by sham (P = .0001 between treatment arms). Apheresis prolonged occlusion time (576 ± 116 s vs 723 ± 142 s, P < .0001) reflecting reduced platelet reactivity and reduced lysis time (1340 [1128, 1682] s vs 847 [685,1302] s, P = .0006) reflecting enhanced fibrinolysis, without corresponding changes with sham. Apheresis, but not sham, reduced von Willebrand Factor (149 [89.0, 164] vs 64.2 [48.5, 89.8] IU/dL, P = .0001), and fibrinogen (3.12 ± 0.68 vs 2.20 ± 0.53 g/L, P < .0001), and increased prothrombin fragments 1 + 2 (158.16 [128.77, 232.09] vs 795.12 [272.55, 1201.00] pmol/L, P = .0006). There was no change in D-dimer, thrombin/anti-thrombin III complex, or thrombin generation assay with
AU - Khan,TZ
AU - Gorog,DA
AU - Arachchillage,DJ
AU - Ahnström,J
AU - Rhodes,S
AU - Donovan,J
AU - Banya,W
AU - Pottle,A
AU - Barbir,M
AU - Pennell,DJ
DO - 10.1016/j.jacl.2019.06.009
EP - 796
PY - 2019///
SN - 1876-4789
SP - 788
TI - Impact of lipoprotein apheresis on thrombotic parameters in patients with refractory angina and raised lipoprotein(a): Findings from a randomized controlled cross-over trial
T2 - Journal of Clinical Lipidology
UR - http://dx.doi.org/10.1016/j.jacl.2019.06.009
UR - https://www.ncbi.nlm.nih.gov/pubmed/31353231
UR - https://www.sciencedirect.com/science/article/pii/S1933287419302296?via%3Dihub
UR - http://hdl.handle.net/10044/1/73466
VL - 13
ER -