First Steps Toward the Establishment of a German Low‐Density Lipoprotein‐Apheresis Registry: Recommendations for the Indication and for Quality Management

Abstract: New recommendations for the indication of treatment with selective extracorporeal plasma therapy low‐density lipoprotein apheresis (LDL‐apheresis) in the prevention of coronary heart disease are urgently needed. The following points are the first results of the ongoing discussion process for indications for LDL‐apheresis in Germany: all patients with homozygous familial hypercholesterolemia with functional or genetically determined lack or dysfunction of LDL receptors and plasma LDL cholesterol levels >13.0 mmol/L (>500 mg/dL); patients with coronary heart disease (CHD) documented by clinical symptoms and imaging procedures in which over a period of at least 3 months the plasma LDL cholesterol levels cannot be lowered below 3.3 mmol/L (130 mg/dL) by a generally accepted, maximal drug‐induced and documented therapy in combination with a cholesterol‐lowering diet; and patients with progression of their CHD documented by clinical symptoms and imaging procedures and repeated plasma Lp(a) levels >60 mg/dL, even if the plasma LDL cholesterol levels are lower than 3.3 mmol/L (130 mg/dL). Respective goals for LDL cholesterol concentrations for high‐risk patients have been recently defined by various international societies. To safely put into practice the recommendations for LDL‐apheresis previously mentioned, standardized treatment guidelines for LDL‐apheresis need to be established in Germany that should be supervised by an appropriate registry.     

Treatment of refractory familial hypercholesterolemia by low-density lipoprotein apheresis using an automated dextran sulfate cellulose adsorption system. The Liposorber Study Group.

A subgroup of patients with familial hypercholesterolemia (FH) respond inadequately to standard diet and drug therapy, and are therefore at high risk for the premature development or progression of coronary artery disease. This study evaluated low-density lipoprotein (LDL) cholesterol and lipoprotein (a) removal in a multicenter, controlled trial with a new LDL apheresis procedure (Liposorber LA-15 System). The study comprised patients with FH who had not responded adequately to diet and maximal drug therapy. There were 54 patients with heterozygous FH (45 randomized to treatment and 9 control subjects) and 10 with homozygous FH (all of whom received LDL apheresis). The study included three 6-week treatment phases and a 4-week rebound phase. Treatments were administered at 7- to 14-day intervals. Mean acute reductions in LDL cholesterol were 76% in heterozygous FH patients and 81% in homozygous ones. Time-averaged levels of LDL cholesterol were reduced 41% (243 to 143 mg/dl) in heterozygous FH patients and 53% (447 to 210 mg/dl) in homozygous ones. The substantial acute reduction of lipoprotein (a) (means: 65%, heterozygous FH; 68%, homozygous FH) has not been reported with other therapies. The Liposorber LA-15 System represents an important therapeutic option in FH patients who respond inadequately to diet and drug therapy.     

Long-term efficacy of low-density lipoprotein apheresis on coronary heart disease in familial hypercholesterolemia

Familial hypercholesterolemia (FH) is characterized by severe hypercholesterolemia and premature coronary heart disease (CHD). The lower the plasma cholesterol level, the more likely it is that CHD can be prevented or retarded; aggressive cholesterol-lowering therapies may be indicated for FH patients with CHD. This study describes the long-term (6 years) safety and efficacy of intensive cholesterol-lowering therapies with low-density lipoprotein (LDL) apheresis in heterozygous FH patients with CHD. One hundred thirty heterozygous FH patients with CHD documented by coronary angiography had been treated by cholesterol-lowering drug therapy alone (n = 87) or LDL apheresis combined with cholesterol-lowering drugs (n = 43). Serum lipid levels and outcomes in each treatment group were compared after approximately 6 years. Both treatment groups had significant reductions in serum cholesterol, LDL cholesterol, and high density lipoprotein cholesterol levels. LDL apheresis significantly reduced LDL cholesterol levels from 7.42 ± 1.73 to 3.13 ± 0.80 mmol/L (58%) compared with group taking drug therapy, from 6.03 ± 1.32 to 4.32 ± 1.53 mmol/L (28%). With Kaplan-Meier analyses of the coronary events including nonfatal myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, and death from CHD, the rate of total coronary events was 72% lower in the LDL-apheresis group (10%) than in drug therapy group (36%) (p = 0.0088). It is concluded that LDL-apheresis is effective as treatment of CHD in FH heterozygotes, and may become the therapy of choice in severe types of FH.     

Indication of low-density lipoprotein apheresis in severe hypercholesterolemia and its atherosclerotic vascular complications: dextran sulfate cellulose low-density lipoprotein apheresis

Homozygous familial hypercholesterolemia (FH) and heterozygous FH, with or without elevation of Lp(a), or isolated massive elevation of Lp(a) with clinically relevant coronary heart disease are indications for low-density lipoprotein (LDL) apheresis, as long as maximal conventional lipid lowering drug therapy does not lead to a LDL cholesterol level below 100 mg/dL. Reduction of lipoproteins and Lp(a), of oxidation of LDL, improvement of disturbed vasomotion, the procoagulatory state and disturbed hemorheology associated with atherosclerosis, as well as the stabilization of plaques and the decrease of cytokines and adhesion molecules have been induced by apheresis and are thought to favorably influence regression of artherosclerosis. Several intervention studies point in this direction.     

Long-term effect of low-density lipoprotein apheresis in patients with homozygous familial hypercholesterolemia

Patients that are homozygous for familial hypercholesterolemia (FH) exhibit severe hypercholesterolemia, cutaneous and tendon xanthomas and premature atherosclerosis beginning in childhood. They are resistant to drug therapy and low-density lipoprotein (LDL) apheresis is the practical treatment. Here we review the technique of LDL apheresis treatment, the long-term effects of LDL apheresis, the effect of apheresis on pregnancy, and the drugs that have proven beneficial in patients with homozygous FH. We also record our experiences of treating eight homozygous FH patients using the LDL apheresis treatment. Among the eight patients, one has been free from cardiovascular disease and two patients have each regressed once. In two patients, aortic valve stenosis developed and the other two patients died for acute myocardial infarction. Furthermore, two patients delivered healthy babies in spite of coronary artery disease. Thus, LDL apheresis therapy has the possibility of preventing the progression of atherosclerosis, but the prognosis assessed by long-term observation is still not satisfactory. A recent clinical trial showed some efficacy of the combination therapy of LDL apheresis and atorvastatin for reducing serum cholesterol levels in homozygous FH, suggesting that this combination therapy may be useful for prevention of atherosclerosis in patients homozygous for FH.     

Apheresis Technology for Prevention and Regression of Atherosclerosis

Abstract: Familial hypercholesterolemia (FH) is a congenital disorder of cholesterol metabolism, which is due to a deficiency in low‐density lipoprotein (LDL) receptors. The homozygous form of FH is especially liable to coronary artery disease (CAD) in youth because of the very high LDL‐cholesterol levels. It is resistant to drug therapy, and LDL‐apheresis is the only practical way of treatment for these patients. Some patients with heterozygous FH also have high LDL‐cholesterol levels that cannot be brought down into the optimum range by any combination drug therapy. We have treated or are treating 10 homozygous and 28 heterozygous FH patients in our hospital or in affiliated hospitals expert in blood purification. Among the 10 homozygous patients, 2 died of myocardial infarction. Only one young female patient is still free of symptoms, and the other patients have been suffering from regurgitation through the aortic valve although they have not experienced myocardial infarction. Rapid rebound of LDL‐cholesterol after each apheresis treatment limits the period during which LDL‐cholesterol is in the optimum range. The use of atorvastatin at a high dose (40 mg/day) was attempted to suppress this rebound. In contrast with good results in receptor‐defective‐type patients, receptor‐negative‐type patients did not show a response in LDL‐cholesterol levels to the statin therapy although there was a slight increase in high‐density lipoprotein (HDL)‐cholesterol with a decrease in very‐low‐density lipoprotein‐triglyceride and ‐cholesterol. Follow‐up study of the patients with heterozygous FH revealed that LDL‐apheresis was effective in lengthening the life expectancy of the patients with pre‐existing CAD, especially those who had received intervention coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA). It was also shown that the use of probucol in combination with LDL‐apheresis was effective in reducing coronary events as shown by the necessity of CABG or PTCA. Clinical data on the effect of LDL‐apheresis, recently reported from some other institutions in Japan, will also be reviewed.     

The Role of Low Density Lipoprotein Apheresis in the Treatment of Familial Hypercholesterolemia

Abstract: The chief indication for low density lipoprotein (LDL) apheresis is the treatment of homozygous familial hypercholesterolemia (FH), a potentially fatal condition that responds poorly to conventional therapy. Dextran sulfate/cellulose adsorption columns (Kaneka) and on-line heparin precipitation (HELP) are the most popular systems used in LDL apheresis. Weekly or biweekly procedures plus concomitant drug therapy enable LDL cholesterol to be maintained at 30–50% of its untreated level, with regression of xanthomas, arrest of progression of coronary atherosclerosis, and improved life expectancy. However, aortic stenosis may progress despite apheresis and necessitate valve replacement. Better control of hypercholesterolemia results from combining apheresis with a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, atorvastatin. LDL apheresis can also be useful in treating drug-resistant FH heterozygotes with coronary disease. However, the FH Regression Study showed no evidence that reduction by apheresis of both LDL and lipoprotein(a), was more advantageous than reduction by combination drug therapy of LDL alone.     

Low-density lipoprotein apheresis as a treatment option for hyperlipidemia

Opinion statement  Data support the relevance of blood cholesterol levels, particularly high levels of low-density lipoprotein (LDL), in the pathogenesis and progression of atherosclerosis. A strong and continuous relationship between dyslipidemia and vascular morbidity and mortality has been established. The initial approach to treating dyslipidemia consists of lifestyle modifications followed by pharmacologic therapy, usually beginning with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Some patients with familial hypercholesterolemia (FH) fail to achieve their LDL goal despite aggressive pharmacologic therapy. In certain cases, LDL apheresis may be an effective therapeutic option. In the United States, LDL apheresis is approved for homozygous FH patients with an LDL cholesterol level ≥ 500 mg/dL. For patients with heterozygous FH, LDL apheresis may be offered if their LDL is ≥ 300 mg/dL, or ≥ 200 mg/dL with known coronary artery disease, despite maximum medical treatment. This review focuses on the principles and methods of LDL apheresis, its potential benefit in clinical care, and its current indications.     

LDL apheresis

Low density lipoprotein (LDL) apheresis provides a safe and effective means of treating patients with homozygous familial hypercholesterolaemia (FH). It also has a role in preventing the progression of coronary artery disease in heterozygotes and others with severe dyslipidaemia who are refractory to or intolerant of high doses of lipid-lowering drugs. Established methods involve either adsorption of apolipoprotein B-containing lipoproteins by affinity columns containing anti-apolipoprotein B antibodies or dextran sulphate, or their precipitation at low pH by heparin, in each instance after first separating plasma from blood cells with a cell separator. The most recently developed method enables lipoproteins to be adsorbed directly from whole blood, using polyacrylate columns. All 4 methods have proved to be similarly efficient when used weekly or biweekly to lower LDL cholesterol and Lp(a) without unduly reducing HDL cholesterol. Economic constraints restrict the use of LDL apheresis to the treatment of potentially fatal disorders such as FH, where there is clear evidence of benefit compared with conventional therapy. Widening the indications to include the treatment of other dyslipidaemic disorders such as steroid-resistant nephrotic syndrome, post-transplant donor vessel disease, stroke and prevention of re-stenosis after coronary angioplasty requires evidence from controlled trials that is currently lacking.     

Long-term effects of LDL apheresis on carotid arterial atherosclerosis in familial hypercholesterolaemic patients

OBJECTIVES: To assess the long-term effect of LDL apheresis on carotid arterial atherosclerosis in severe familial hypercholesterolaemic (FH) patients. DESIGN: Changes in existing plaque, new plaque formation and annual progression rate of carotid early plaque were evaluated by B-mode ultrasonography. SUBJECTS: LDL apheresis group: two homozygous FH and nine heterozygous FH patients received a combination of LDL apheresis and cholesterol-lowering drug therapy for a mean of 7.8 years. Control group: 10 heterozygous FH patients were maintained by medication only for a mean of 5.5 years. RESULTS: As a result of LDL apheresis treatment, LDL cholesterol levels reduced from 16.0+/-3.60 to 6.43+/-0.07 mmol L(-1) in homozygous FH patients and from 11.5+/-2.46 to 4.32+/-1.2 mmol L(-1) in heterozygous FH patients. During the long-term treatment period, the existing plaque tended to progress and new plaque formation in carotid arteries was also observed in both groups. The annual progression rate of mean maximum intima-media thickness in the common carotid artery was a mean of -0.0023+/-0.0246 mm year(-1) in heterozygous FH patients in the LDL apheresis group, suggesting regression. This was significantly lower when compared with the control group, which had a mean of 0.0251+/-0.0265 mm year(-1) CONCLUSION: The results suggest that the long-term treatment with combined LDL apheresis and drugs may delay the progression of the atherosclerotic process and prompt the stabilization of atheromatous plaque in severe FH patients.     

Apheresis in coronary heart disease with elevated Lp (a): a review of Lp (a) as a risk factor and its management

Lipoprotein (a) (Lp (a)) increases global cardiovascular risk, especially when LDL cholesterol is concomitantly elevated. Epidemiologic data show that Lp (a) concentration in plasma can be used to predict the risk of early atherogenesis in a dose-dependent manner and late stages of atherosclerosis are accelerated by elevated Lp (a). Therapeutic means to lower Lp (a) are limited. The most effective method to reduce plasma Lp (a) concentration significantly is therapeutic apheresis. Because apheresis is laborious and expensive, patients considered for this procedure should suffer from high Lp (a) concentrations, well beyond 50 mg/dL, and have manifested and progressive coronary heart disease despite maximal drug therapy. Experimental data and therapeutic results will be discussed in the present paper.     

Low-density lipoprotein apheresis therapy with a direct hemoperfusion column: a Japanese multicenter clinical trial

Low-density lipoprotein (LDL) apheresis has been applied to patients with familial hypercholesterolemia (FH) with coronary artery disease (CAD). To examine the efficacy and safety of a new type of LDL adsorption column (KLD01, Kaneka, Osaka, Japan), which deals with whole blood without separating plasma, the new system was evaluated in a multicenter trial. The present study included 33 FH patients with CAD (24 males, 9 females, 57 +/- 13 years) who were treated five times with a mean interval of 2.12 +/- 0.60 weeks between treatments. We studied the removal efficacies for serum LDL cholesterol, Lipoprotein(a) (Lp(a)) and triglyceride, the times for the preparation of the system and for treatment, symptoms, and the biochemical data. The scheduled treatments were completed by 31 patients. Serum levels of LDL cholesterol, Lp(a) and triglycerides were all significantly reduced with KLD01; 61.5 +/- 6.2%, 72.4 +/- 5.9% and 69.5 +/- 9.7%, respectively. The times for both setting up the column system (26 +/- 7 min) and treatment (138 +/- 20 min) were shorter with KLD01 than conventional methods. Adverse reactions occurred in eight cases (17 episodes), but the patients fully recovered immediately after each apheresis therapy session. We conclude that the new type of LDL adsorption column, one that deals with whole blood, is a promising apheresis therapy for FH patients in view of its efficacy, reduced time for treatment, and safety.     

Effects of Low‐Density Lipoprotein Apheresis on Coronary and Carotid Atherosclerosis and Diabetic Scleredema in Patients with Severe Hypercholesterolemia

Abstract: Correlations between serum cholesterol levels and progression of coronary and peripheral atherosclerosis have been found in many recent studies. It has also been demonstrated that aggressive cholesterol‐lowering therapy with low‐density lipoprotein (LDL) apheresis, a method of LDL elimination by extracorporeal circulation, is effective not only for coronary artery disease, but also for systemic circulatory disturbance in severe hypercholesterolemic patients with familial hypercholesterolemia (FH) in particular. We found that LDL apheresis treatment with medical therapy improved coronary atherosclerotic lesions, based on coronary angiography evaluation and histopathological observation, suppressed progression of early carotid atherosclerotic lesions on annual B‐mode ultrasonography, and improved diabetic scleredema in FH patients. This effectiveness of LDL apheresis appears to be due to recovery of vascular endothelial function and improvement of blood rheology. For diseases that are possibly due to circulation disturbance and that are intractable with drugs alone, LDL apheresis may be worth trying, particularly for patients complicated by hyperlipemia.     

The scientific basis and future of lipoprotein apheresis

Lipoprotein apheresis plays a vital role in the management of the severe hyperlipidemias that predispose to atherosclerosis. Determinants of efficacy are the acute reduction in lipoproteins achieved by each apheresis procedure, their frequency, and the fractional catabolic rates and hence pool sizes of low-density lipoprotein (LDL) or lipoprotein (a) (Lp(a)) of the patient being treated. A useful criterion of the efficacy of apheresis plus lipid-lowering drug therapy is the decrease in the interval (time-averaged) mean of serum total or LDL cholesterol or Lp(a) between procedures, expressed as the percent decrease in the interval means below the maximal levels of these lipoproteins when off all treatment. Recent advances in lipid-lowering drug therapy may diminish the use of lipoprotein apheresis but will not abolish its unique role as a therapeutic “last chance saloon,” especially for children and pregnant women with homozygous familial hypercholesterolemia.     

The Retardation of Progression,Stabilization, and Regression of Coronary and Carotid Atherosclerosis by Low-Density Lipoprotein Apheresis in Patients with Familial Hypercholesterolemia

Abstract: The long-term effects of low-density lipoprotein (LDL) apheresis (LA) on the progression and regression of atherosclerosis were evaluated by angiographic and pathological findings as well as ultrasonography based studies, and the clinical significance of the treatment was evaluated. We studied 11 patients with familial hypercholesterolemia (FH), 2 with homozygous FH and 9 with severe heterozygous FH who received combined LA and drug therapy for a mean of 7.7 years. During the treatment period, the mean time-averaged level of LDL cholesterol was 181 ± 52 mg/dl. According to the coronary angiographic results, 3 patients showed regression, 6 patients showed progression, and 2 patients showed no change. Cardiac events occurred in 6 patients. We pathologically examined at autopsy the coronary arteries of 1 FH patient who had received long-term LA therapy before death. The results revealed the process of scarring of atheromatous plaque, suggesting pathological regression correlated with the angiographic regression shown in serial angiograms taken during LA treatment. It was further suggested that the formation of an eccentric thick end wall lesion rich in collagen fiber prevented atheromatous plaque from tearing off. However, the annual progression rate of the mean maximal intima-media thickness in the common carotid artery was 0.0002 mm/year in the LA group, which was significantly lower than the mean of 0.251 mm/year seen in the control group (drug therapy only group). In the patients with heterozygous FH (9 patients), the annual progression rate was lowered to 0.0023 mm/year, suggesting regression. The findings of the present study indicate that patients with severe FH refractory to drug treatment may benefit from more aggressive cholesterol lowering treatments such as LA combined with cholesterol lowering drug therapy. The progression of atherosclerosis may be prevented, plaque may be stabilized (regressed), and clinical events may be reduced as seen with patients with non-FH hypercholesterolemia.     

Ten-year follow-up of familial hypercholesterolemia patients after intensive cholesterol-lowering therapy

To prevent coronary artery disease, it is necessary for patients with familial hyper-cholesterolemia (FH) to maintain a low cholesterol level. Recently a combination therapy of low-density lipoprotein (LDL) apheresis and statins has been used for FH patients, but their long-term prognosis over 10 years is unknown. In this single center prospective report, 18 FH patients with severe coronary stenosis received LDL apheresis every 2 or 4 weeks and statin therapy for 9.8 +/- 3.0 years. Probucol was given to 17 of the 18 patients. We observed their clinical events as well as coronary stenosis findings and ejection fractions for 10.7 +/- 2.6 years. Total and LDL cholesterol levels before therapy were 345 +/- 46 and 277 +/- 48 mg/dL, respectively. Immediately following LDL-apheresis, these levels decreased to 104 +/- 7.5 and 66 +/- 16 mg/dL, respectively. There were no cardiac deaths and 4 patients were free from any coronary events. There was one noncardiac death. Nonfatal myocardial in-farction occurred in 2 patients and coronary bypass surgery was required in one patient. Twelve patients received additional coronary angioplasty. There was little change in coronary stenosis and ejection fraction following 10 years of the combination therapy. Univariate Cox regression analysis revealed that the calculated mean LDL cholesterol level was the predictive value of treatment efficacy (mean LDL cholesterol < 140 mg/dL, hazard ratio 0.23, P = 0.028). The combination therapy of LDL-apheresis and antilipid drugs delayed the progression of coronary atherosclerosis and prevented a major cardiac event, although complete inhibition was limited to a small group. Additional coronary angioplasty is likely to be required for a favorable clinical outcome in FH patients.     

The Familial Hypercholesterolemia Regression Study: A Randomized Comparison of Therapeutic Reduction of Both Low-Density Lipoprotein and Lipoprotein(a) Versus Low-Density Lipoprotein Alone

Abstract: Lipoprotein (a) [Lp (a)] is a risk factor for coronary heart disease (CHD), especially in the presence of a raised low-density lipoprotein (LDL)-cholesterol (LDL-C). To ascertain whether reduction of both LDL and Lp(a) is more advantageous than reduction of LDL alone, patients with heterozygous FH and CHD were selected randomly to receive either LDL apheresis fortnightly plus simvastatin 40 mg/day or colestipol 20 g plus simvastatin 40 mg/day. Quantitative coronary angiography was undertaken before and after 2.1 years. Changes in serum lipids were similar in both groups except for the greater reduction of LDL-C and Lp(a) by apheresis. There were no significant differences in primary angiographic endpoints, and none of the angiographic changes correlated with Lp(a). Although LDL apheresis plus simvastatin was more effective than colestipol plus simvastatin in reducing LDL-C and Lp(a), it was not more beneficial in influencing coronary atherosclerosis. Decreasing Lp(a) seems unnecessary if LDL-C is reduced below 130 mg/dl.—     

The association of LDL receptor activity, LDL cholesterol level, and clinical course in homozygous familial hypercholesterolemia

Patients with homozygous familial hypercholesterolemia (FH), reveal a marked heterogeneity in plasma cholesterol levels, response to diet as well as drug treatment, and clinical course. Low-density lipoprotein (LDL) receptor activities were assessed by the rate of 14C-oleate cholesteryl ester biosynthesis in fibroblasts from 13 FH homozygotes in tissue culture. The receptor activity of the individual patients was highly correlated with initial pretreatment plasma cholesterol and LDL cholesterol levels (P less than .001, r = -0.89). In addition, the LDL receptor activity was positively correlated with the age of onset of angina based on the Cox model (P less than .035, likelihood ratio = 6.71). An association was also noted between LDL receptor activity and cholesterol reduction with drugs. These data provide direct evidence for the correlation between the heterogeneity of the LDL receptor and the expression of the clinical manifestations of homozygous FH. The determination of pretreatment plasma cholesterol level and LDL receptor activity in patients with homozygous FH provide useful parameters on which to base predictions of the clinical progression of cardiovascular disease. These parameters may also influence the selection of a program for diet and drug therapy. Patients with markedly elevated plasma cholesterol levels and very low LDL receptor activity should be considered to be candidates for multiple drug therapy, and portacaval shunt, and/or periodic plasma exchanges.     

Treatment of Familial Hypercholesterolemia: Is There a Need Beyond Statin Therapy?

Familial hypercholesterolemia (FH) is a genetic lipid disorder that is characterized by severely elevated cholesterol levels and premature cardiovascular disease. Both the heterozygous and homozygous forms of FH require aggressive cholesterol-lowering therapy. Statins alone frequently do not lower these patients’ cholesterol to therapeutic levels, and some patients are intolerant to statins. Combination or monotherapy with other current pharmacotherapies are options, but even with these some FH patients do not meet their low-density lipoprotein (LDL) cholesterol goals. In the cases of statin intolerance, LDL apheresis may be another treatment option. There are currently several novel therapies in development for LDL lowering that target either production or catabolism of LDL, plaque regression, and potentially gene transfer. We conclude that there is a need beyond statins for patients with FH, especially in cases of statin intolerance, and when even the highest doses of statin do not get patients to goal cholesterol levels.     

Influence of Atorvastatin Versus Simvastatin on Fibrinogen and Other Hemorheological Parameters in Patients with Severe Hypercholesterolemia Treated with Regular Low‐Density Lipoprotein Immunoadsorption Apheresis

Abstract: Low‐density lipoprotein (LDL) apheresis is a treatment option in patients with coronary artery disease and elevated LDL cholesterol concentrations if maximal drug therapy fails to achieve adequate LDL cholesterol reduction. This therapy is more effective when combined with strong lipid‐lowering drugs, such as atorvastatin. However, conflicting data have been published concerning the effect of atorvastatin on fibrinogen concentration. Therefore, we investigated the effect of atorvastatin compared to simvastatin on fibrinogen concentration and other hemorheological parameters in patients treated by weekly LDL apheresis. Hemorheological parameters were, studied twice in 9 patients (4 female, 5 male, 54.0 ± 8.9 years) with coronary artery disease treated by weekly LDL immunoadsorption, once during concomitant simvastatin therapy (40 mg daily) and once during atorvastatin therapy (40 mg daily). Fibrinogen concentration, plasma and blood viscosity at different shear rates, parameters of red cell aggregation at stasis and shear rate 3/s, and erythrocyte filterability were determined 7 days after the last LDL apheresis after each drug had been given for a minimum for 8 weeks. Fibrinogen concentration did not show any statistically significant difference during therapy with atorvastatin (3.09 ± 0.36 g/L) compared to simvastatin (3.13 ± 0.77 g/L). Plasma and blood viscosity as well as erythrocyte filterability were also unchanged. The increase in red cell aggregation at stasis during atorvastatin treatment (5.82 ± 1.00 U versus 4.89±0.48 U during simvastatin; p < 0.05) was inversely correlated with a lower high‐density liprotein (HDL) cholesterol concentration (1.17 ± 0.21 mmol/L versus 1.31 ± 0.30 mmol/L during simvastatin; p < 0.05). LDL cholesterol showed a strong trend to lower concentrations during atorvastatin (4.14 ± 0.61 mmol/L versus 4.56 ± 0.66 mmol/L during simvastatin; p = 0.07), despite a reduced plasma volume treated (3,547 ± 1,239 ml during atorvastatin versus 3,888 ± 1,206 mL during simvastatin; p < 0.05). In conclusion, fibrinogen concentration and other hemorheological parameters were unchanged during atorvastatin compared to simvastatin therapy with the exception of a higher red cell aggregation at stasis. Therefore, with respect to hemorheology, we conclude that atorvastatin should not be withheld from hypercholesterolemic patients regularly treated with LDL immunoadsorption.