The rebound of lipoproteins after LDL-apheresis. Kinetics and estimation of mean lipoprotein levels

Kroon, Abraham A.; Hof, M. A. Van't; Demacker, P.N.M.; Stalenhoef, Anton F. H.

doi:10.1016/s0021-9150(00)00371-3

Cited by 149 publications

(107 citation statements)

References 43 publications

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“…Therefore, the mean cholesterol value was b + 3.78* (a-b)/x, where a is the postapheresis cholesterol level, b is the preapheresis cholesterol level of subsequent procedures, and x is the treatment interval (days). [17][18][19] Coronary angiography: Coronary angiography (CAG) was performed before and after the combination therapy with intracoronary administration of 5 mg isosorbide dinitrate immediately before the injection of contrast medium. The degree of stenosis in 15 segments of the coronary artery for each patient was analyzed by 2 experienced cardiologists at different dates blinded to the clinical history of the patient.…”

Section: Methodsmentioning

confidence: 99%

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

Masaki

Tatami²,

Kumamoto³

et al. 2005

Int. Heart J.

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SUMMARYTo prevent coronary artery disease, it is necessary for patients with familial hypercholesterolemia (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 infarction 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. (Int Heart J 2005; 46: 833-843)

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Section: Methodsmentioning

confidence: 99%

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

Masaki

Tatami²,

Kumamoto³

et al. 2005

Int. Heart J.

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“…Time-averaged concentrations (C) for this interval can be estimated by using the empirical equation C interval mean =C min +K(C max −C min ), with C min for the concentration immediately after LA, C max for the concentration immediately before the next LA and K set as 0.73. 11,12 Time-averaged concentrations have been suggested as surrogate parameters for mean levels of LDL-C or Lp(a) during chronic LA. 11,12 Additional informed consent was obtained from patients to perform genetic analysis of the variants rs10455872 and rs3798220 of the LPA locus.…”

Section: Laboratory Measurementsmentioning

confidence: 99%

“…11,12 Time-averaged concentrations have been suggested as surrogate parameters for mean levels of LDL-C or Lp(a) during chronic LA. 11,12 Additional informed consent was obtained from patients to perform genetic analysis of the variants rs10455872 and rs3798220 of the LPA locus. 6,13 Genomic DNA was isolated from EDTA whole blood samples from patients with the QIAamp DNA Blood Mini Kit spin procedure (Qiagen, Germany).…”

Section: Laboratory Measurementsmentioning

confidence: 99%

Lipoprotein Apheresis in Patients With Maximally Tolerated Lipid-Lowering Therapy, Lipoprotein(a)-Hyperlipoproteinemia, and Progressive Cardiovascular Disease

Leebmann¹,

Roeseler²,

Julius³

et al. 2013

Circulation

288

151

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Background— Lipoprotein(a) (Lp(a)) hyperlipoproteinemia is a major risk factor for cardiovascular disease, which is not affected by treatment of other cardiovascular risk factors. This study sought to assess the effect of chronic lipoprotein apheresis (LA) on the incidence of cardiovascular events in patients with progressive cardiovascular disease receiving maximally tolerated lipid-lowering treatment. Methods and Results— In a prospective observational multicenter study, 170 patients were investigated who commenced LA because of Lp(a)-hyperlipoproteinemia and progressive cardiovascular disease. Patients were characterized regarding plasma lipid status, lipid-lowering drug treatment, and variants at the LPA gene locus. The incidence rates of cardiovascular events 2 years before (y-2 and y-1) and prospectively 2 years during LA treatment (y+1, y+2) were compared. The mean age of patients was 51 years at the first cardiovascular event and 57 years at the first LA. Before LA, mean low-density lipoprotein cholesterol and Lp(a) were 2.56±1.04 mmol·L −1 (99.0±40.1 mg·dL −1 ) and Lp(a) 3.74±1.63 µmol·L −1 (104.9±45.7 mg·dL −1 ), respectively. Mean annual rates for major adverse coronary events declined from 0.41 for 2 years before LA to 0.09 for 2 years during LA ( P <0.0001). Event rates including all vascular beds declined from 0.61 to 0.16 ( P <0.0001). Analysis of single years revealed increasing major adverse coronary event rates from 0.30 to 0.54 ( P =0.001) for y-2 to y-1 before LA, decline to 0.14 from y-1 to y+1 ( P <0.0001) and to 0.05 from y+1 to y+2 ( P =0.014). Conclusions— In patients with Lp(a)-hyperlipoproteinemia, progressive cardiovascular disease, and maximally tolerated lipid-lowering medication, LA effectively lowered the incidence rate of cardiovascular events. Clinical Trial Registration— URL: https://drks-neu.uniklinik-freiburg.de . Unique identifier: DRKS00003119.

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“…This decision was taken after consideration of the rebound kinetics of LDL-C. In this case, using the formula set out by Kroon et al, [16,17] it was estimated that the time averaged value of LDL-C could not reach target levels even if apheresis was intensified to twice weekly, and it was therefore probable that apheresis was making no meaningful contribution to the patient's treatment. The patient was advised that apheresis remains a viable treatment option depending on his clinical follow-up.…”

Section: Concluding Commentsmentioning

confidence: 99%

Clinical experience of lomitapide therapy in patients with homozygous familial hypercholesterolaemia

Cuchel

Blom

Averna

2014

Atherosclerosis Supplements

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The microsomal triglyceride transfer protein (MTP) inhibitor lomitapide is a licenced adjunct to a low-fat diet and other lipid-lowering medication, with or without low-density lipoprotein apheresis, for the treatment of adults with homozygous familial hypercholesterolaemia (HoFH). In a recently published phase 3 study, patients with HoFH received lomitapide in addition to maximally tolerated lipid-lowering therapy. Treatment with lomitapide resulted in a mean approximate 50% reduction in LDL-C levels after 26 weeks compared with baseline levels ( p < 0.0001). This decrease in LDL-C was maintained at Weeks 56 and 78 (44% [p < 0.0001] and 38% [p ¼ 0.0001], respectively). This paper offers clinical perspectives based on selected case histories of patients participating in the phase 3 lomitapide study. These cases provide illustrative examples of the efficacy of lomitapide, with or without apheresis, and show that the effective management of adverse effects can enable patients to remain on effective treatment.

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The rebound of lipoproteins after LDL-apheresis. Kinetics and estimation of mean lipoprotein levels

Cited by 149 publications

References 43 publications

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

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

Lipoprotein Apheresis in Patients With Maximally Tolerated Lipid-Lowering Therapy, Lipoprotein(a)-Hyperlipoproteinemia, and Progressive Cardiovascular Disease

Clinical experience of lomitapide therapy in patients with homozygous familial hypercholesterolaemia

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