Hemodynamic changes in the peripheral circulation after repeat low density lipoprotein apheresis in familial hypercholesterolemia.

Abstract

Repeat low density lipoprotein (LDL) apheresis and blood flow determinations in the forearm and leg were performed in 10 patients (age range, 13-49 years; four male, six female) with familial hypercholesterolemia (eight homozygous, two heterozygous). To perform LDL apheresis, plasma was first separated by a polysulphone hollow fiber filter; then, LDL was selectively removed from plasma by dextran sulphate cellulose beads packed in columns. Blood flows in the forearm and leg were determined at rest and during a reactive hyperemia test (peak flow). This test was performed noninvasively by a strain-gauge plethysmograph with semicontinuous registration of arterial blood flow variables before the first apheresis and 3 weeks after the last of six procedures for apheresis. Resting arterial blood flows in the forearm and leg were slightly increased after repeat LDL apheresis (p<0.05). Peak blood flow in the leg significantly increased (+34%, p<0.01). No change in peak blood flow in the forearm was observed. Systolic blood pressures were slightly but significantly reduced (p<0.05); forearm peripheral resistances were also reduced (p<0.05). Flow response was not related to LDL receptor status. Blood and plasma viscosities were determined before and 7 days after the last apheresis. Blood viscosity was significantly reduced after LDL apheresis at shear rates of 11.25-450 sec`.Plasma viscosity did not change. (Circulation 1990;81:610-616) F amilial hypercholesterolemia is an inherited disorder of metabolism characterized by hypercholesterolemia that is due to a marked increase of low density lipoproteins (LDL). This type of hyperlipidemia, in the homozygous form, is refractory to the conventional lipid-lowering treatments and leads to premature development of atherosclerotic cardiovascular disease.1 Nonpharmacologic treatments that have been proposed for the management of patients with familial hypercholesterolemia include plasma exchange2 and LDL apheresis.3-7The aim of these treatments is to produce a marked and sustained cholesterol-lowering effect to retard progression or induce regression of atheromatous plaques.8 There is evidence that blood flow to the

Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

“…Apheresis also ameliorated blood rheology and the endothelial function of coronary arteries, 25,26 and improved the prognosis of atherogenic patients. This may explain the beneficial effect of LDL apheresis in preventing fatal and nonfatal cardiovascular events from occurring in patients with hyperlipidemia and uremia.…”

Efficacy of Low-Density Lipoprotein Apheresis in Patients with Peripheral Arterial Occlusive Disease Undergoing Hemodialysis Treatment

“…The efficacy of LDL apheresis for patients with PAOD has been suggested by several lines of evidence [8,9,10,11,12,13,14,15,16,17,18,19]. Clinical evidence has suggested the following as mechanisms of the improvement of clinical symptoms in PAOD patients.…”

Ten-year Follow-up of Familial Hypercholesterolemia Patients After Intensive Cholesterol-lowering Therapy

“…4) These effects result from an improvement in endothelial nitric oxide (NO) production, [7][8][9][10] endothelial adhesiveness, 11,12) and blood rheology. [13][14][15] With the dramatic pharmacological development of hydroxymethylglutarylcoenzyme A (HMG-Co A) reductase inhibitors, or statins, further data are needed to determine if a combination therapy consisting of LDL-apheresis and statin can decrease coronary stenosis and prevent coronary events in FH patients.…”