Volume 10, Issue 6 pp. 510-517

Improved Coronary Vasodilatatory Capacity by H.E.L.P. Apheresis: Comparing Initial and Chronic Treatment

Klaus P Mellwig

Corresponding Author

Klaus P Mellwig

Department of Cardiology,

Dr K.P. Mellwig, Heart Center North Rhine-Westphalia—Department of Cardiology, Georgstr. 11 Bad Oeynhausen 32545, Germany. Email: [email protected]Search for more papers by this author
Frank Van Buuren

Frank Van Buuren

Department of Cardiology,

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Henning K Schmidt

Henning K Schmidt

Department of Cardiology,

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Peter Wielepp

Peter Wielepp

Institute for Radiology, Nuclear Medicine and Molecular Imaging, Heart Center North Rhine-Westphalia, Bad Oeynhausen, Germany

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Wolfgang Burchert

Wolfgang Burchert

Institute for Radiology, Nuclear Medicine and Molecular Imaging, Heart Center North Rhine-Westphalia, Bad Oeynhausen, Germany

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Dieter Horstkotte

Dieter Horstkotte

Department of Cardiology,

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First published: 20 December 2006
Citations: 26

Abstract

Abstract: Hypercholesterolemia impairs endothelial function and subsequently decreases coronary vasodilatatory capacity. We examined the quantitative effects of one single LDL apheresis on vasodilatatory capacity. Using N-13 ammonia as a tracer for dynamic quantitative positron emission tomography (PET), mean myocardial perfusion measurements were carried out before and 20 h later after LDL apheresis, both under resting conditions and after pharmacological vasodilatation with dipyridamole. LDL apheresis was carried out using the heparin induced extracorporeal LDL precipitation (H.E.L.P.) procedure. We examined 47 patients (12 women and 35 men), with angiographically-proven coronary artery disease. All of them suffered from hypercholesterolemia. Of the patients, 35 received a chronic weekly H.E.L.P. procedure (group A), while H.E.L.P. procedure treatment was started for the first time in 12 patients, who were subsequently enrolled in a chronic apheresis program (group B). H.E.L.P. apheresis was combined with cholesterol lowering drugs in all patients. Both groups underwent positron emission tomography twice (prior to LDL apheresis and 20 h later). In group A, LDL cholesterol levels decreased from 175 ± 50 mg/dL to 60 ± 21 mg/dL immediately after H.E.L.P. (77 ± 25 mg/dL before the second PET). Corresponding values for fibrinogen levels were 287 ± 75 mg/dL to 102 ± 29 mg/dL (155 ± 52 mg/dL), minimal coronary resistance dropped from 0.56 ± 0.20 to 0.44 ± 0.17 mm Hg × 100 g × min/mL (P < 0.0001). Plasma viscosity decreased by 7.8%. In group B, LDL cholesterol decreased from 187 ± 45 mg/dL to 75 ± 27 mg/dL (85 ± 29 mg/dL) and fibrinogen from 348 ± 65 mg/dL to 126 ± 38 mg/dL (168 ± 45 mg/dL). Minimal coronary resistance was reduced from 0.61 ± 0.23 to 0.53 ± 0.19 mm Hg × 100 g × min/mL (P < 0.01). Plasma viscosity was observed to decrease by 7.6%. The strong LDL drop in patients under chronic H.E.L.P. treatment has a significant impact on coronary vasodilatatory capacity within 20 h leading to an improved overall cardiac perfusion. Nearly the same effect can be seen in patients after their first H.E.L.P. treatment. 

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