PMID- 15186959
OWN - NLM
STAT- MEDLINE
DCOM- 20041122
LR  - 20171116
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 175
IP  - 1
DP  - 2004 Jul
TI  - Effects of heparin-mediated extracorporeal low-density lipoprotein precipitation 
      beyond lowering proatherogenic lipoproteins--reduction of circulating 
      proinflammatory and procoagulatory markers.
PG  - 145-50
AB  - In addition to hypercholesterolemia, proinflammatory and prothrombotic markers 
      have been suggested to play an important role in atherogenesis. We examined 
      whether heparin-mediated extracorporeal low-density lipoprotein precipitation 
      (HELP) therapy modulates the circulating levels of proinflammatory and 
      prothrombotic markers. Twenty-two coronary heart disease (CHD) patients 
      undergoing regular HELP-apheresis (18 males, 4 females, mean age 57.3 +/- 10.9 
      years) were enrolled in this study. A single HELP therapy treatment significantly 
      decreased the circulating levels of high sensitivity C-reactive protein (hs-CRP), 
      soluble vascular adhesion molecule-1 (sVCAM-1), soluble E-selectin, 
      lipopolysaccharide binding protein (LBP), endothelin-1 (ET-1), and monocyte 
      chemoattractant protein-1 (MCP-1) on average by 67, 37, 24, 27, 24, and 15%, 
      respectively. Prothrombotic factors including fibrinogen, tissue factor (TF), 
      soluble CD40 ligand (sCD40L), and homocysteine were decreased by 66, 27, 16, and 
      22%, respectively. In accordance with previous studies HELP therapy reduced total 
      cholesterol, low density lipoprotein (LDL) cholesterol, and Lp(a) mass by 50, 61, 
      and 62%, respectively. Our data suggest that simultaneous reduction of 
      proinflammatory and prothrombotic factors together with atherogenic lipoproteins 
      by HELP-apheresis may contribute to improvement of endothelial dysfunction and 
      thereby inhibit progression of atherosclerotic lesions and stabilize the existing 
      plaque.
FAU - Wang, Ying
AU  - Wang Y
AD  - Institute of Clinical Chemistry, University Hospital Grosshadern, 
      Marchioninistrasse 15, 81377 Munich, Germany.
FAU - Blessing, Frithjof
AU  - Blessing F
FAU - Walli, Autar K
AU  - Walli AK
FAU - Uberfuhr, Peter
AU  - Uberfuhr P
FAU - Fraunberger, Peter
AU  - Fraunberger P
FAU - Seidel, Dietrich
AU  - Seidel D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Blood Coagulation Factors)
RN  - 0 (CD40 Antigens)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipoproteins, LDL)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Arteriosclerosis/blood/prevention & control
MH  - Blood Coagulation Factors/*analysis
MH  - *Blood Component Removal
MH  - C-Reactive Protein/analysis
MH  - CD40 Antigens/blood
MH  - Cell Adhesion Molecules/blood
MH  - Female
MH  - Homocysteine/blood
MH  - Humans
MH  - Hyperlipoproteinemia Type II/blood/complications/*therapy
MH  - Inflammation Mediators/*blood
MH  - Lipoproteins, LDL/*blood
MH  - Male
MH  - Middle Aged
EDAT- 2004/06/10 05:00
MHDA- 2004/12/16 09:00
CRDT- 2004/06/10 05:00
PHST- 2003/10/09 00:00 [received]
PHST- 2004/03/01 00:00 [revised]
PHST- 2004/03/17 00:00 [accepted]
PHST- 2004/06/10 05:00 [pubmed]
PHST- 2004/12/16 09:00 [medline]
PHST- 2004/06/10 05:00 [entrez]
AID - S0021-9150(04)00157-1 [pii]
AID - 10.1016/j.atherosclerosis.2004.03.011 [doi]
PST - ppublish
SO  - Atherosclerosis. 2004 Jul;175(1):145-50. doi: 
      10.1016/j.atherosclerosis.2004.03.011.