Pathological and angiographic regression of coronary atherosclerosis by LDL-apheresis in a patient with familial hypercholesterolemia

Koga, Nobuhiko; Iwata, Y.

doi:10.1016/0021-9150(91)90239-y

Cited by 48 publications

(32 citation statements)

References 16 publications

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“…A pathology report showed scarring of atheromatous plaque and formation of a thick fibrous cap after 7 years of LDL apheresis in a FH patient. 18) Combination therapy may lead to stable postangioplasty plaque. Angiographic and intravascular ultrasound investigations revealed the regression of coronary atherosclerosis after LDL-apheresis.…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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: Discussionmentioning

confidence: 99%

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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“…This number would greatly strain our resources in terms of health budgets and treatment facilities with extracorporeal LDL elimination. 24 ' 25 The use of extracorporeal LDL-removal techniques remains controversial in subjects with heterozygous FH. LDL apheresis or filtration techniques are not widely available, and the cost of LDL filtration in our institution is currently approximately $12 300 Canadian per year.…”

Section: -23mentioning

confidence: 99%

Response to HMG CoA reductase inhibitors in heterozygous familial hypercholesterolemia due to the 10-kb deletion ("French Canadian mutation") of the LDL receptor gene.

Karayan¹,

Qiu²,

Bétard³

et al. 1994

Arterioscler Thromb

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The 10-kb deletion ("French Canadian mutation") of the low-density lipoprotein (LDL) receptor gene is the most common mutation causing familial hypercholesterolemia among subjects of French Canadian descent. In affected subjects, it results in a null allele of the LDL receptor gene and provides a unique opportunity to examine single-allele regulation of this gene in humans. We sought to ascertain the response of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase in subjects with the French Canadian mutation of the LDL receptor gene and to correlate this response with biochemical variables and the haplotype of the nondeletion LDL receptor allele. The prevalence of nonresponders to high doses of HMG CoA reductase inhibitors (denned as <15% decrease in LDL cholesterol [LDL-C] from baseline values after dietary intervention) was ascertained in 105 patients heterozygous for the 10-kb deletion after excluding first-degree relatives and those on combined lipid-lowering therapy or other lipid-lowering agents. Lipoprotein cholesterol levels were examined after a diet period (30% calories as fat) and after receiving HMG CoA reductase inhibitors as monotherapy for a minimum of 3 months. The mean reduction in total cholesterol was 45±23%, in LDL-C 33±15%, and in F amilial hypercholesterolemia (FH) is a genetic disorder characterized by elevated plasma levels of total cholesterol due to elevated low-density lipoprotein (LDL) cholesterol (LDL-C) and cutaneous lipid deposits (xanthelasmas, xanthomas, and corneal arcus) as well as the presence of premature coronary artery disease in probands and family members.1 ' 2 Mutations within the gene coding for the LDL receptor have been identified as the cause of FH.3 Multiple mutations have been described, 4 and five classes of phenotypes at the cellular level have been established. Class 1 defects do not produce LDL receptor protein (null allele); class 2 defects encode proteins that are blocked between the endoplasmic reticulum and the Golgi complex; class 3 defects encode proteins that do triglycerides 32±49% (all P<.005). There was a slight increase in high-density lipoprotein cholesterol of 8.5±18% (P>.05). Overall, 68.4% of patients had more than a 30% decrease in LDL-C levels and 23% had a decrease ranging from 15% to 30%; 8.6% of patients failed to respond, and some even showed an increase in their LDL-C levels (mean change, 1.2±11.9%). This response was independent of age, gender, triglycerides, or high-density lipoprotein cholesterol levels. There was no significant overall effect of the apolipoprotein E phenotype in predicting the degree of total cholesterol or LDL-C reduction. Haplotypes of the LDL receptor gene were determined with the use of five polymorphic markers. The 10-kb deletion is known to be present on a single haplotype, thus allowing the haplotype determination of the nondeletion allele. Analysis of the nondeletion allele of the LDL receptor did not reveal a difference between responders and nonresponders, suggesting that a defec...

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“…Reinforcement of drug therapy and the combined use of drug therapy and LDLapheresis are considered to be desirable for poorly controlled TC patients (14,15).…”

Section: Resultsmentioning

confidence: 99%

Secondary Prevention with Lipid Lowering Therapy in Familial Hypercholesterolemia: A Correlation between New Evolution of Stenotic Lesion and Achieved Cholesterol Levels after Revascularization Procedures.

et al. 1999

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Object: T o assess the value of secondary prevention with lipid lowering therapy following either balloon angioplasty (PTCA) or bypass surgery (CABG) in familial hypercholesterolemia patients, the correlation of the new evolution of stenotic lesions and therapeutically achieved cholesterol levels was studied in 50 patients.Methods: All surviving patients were followed angiographically after 5 years, and findings were correlated with the annually determined total serum cholesterol (TC) levels.Results: Newcoronary atherosclerotic plaques were not observed in 18 patients in whomthe TC was controlled to <220 mg/dl but in 19 of32 patients in whomthe TC was >220 mg/dl, a new evolution of stenotic lesions was observed angiographically.Conclusion: The new evolution of stenotic lesions following revascularization in patients with FH can be controlled significantly by lipid lowering therapy to maintain a TC level of <220 mg/dl, and if diet alone can not achieve it, aggressive medication and even LDLapheresis might be justified. (Internal Medicine 38: 330-335, 1999)

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Pathological and angiographic regression of coronary atherosclerosis by LDL-apheresis in a patient with familial hypercholesterolemia

Cited by 48 publications

References 16 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

Response to HMG CoA reductase inhibitors in heterozygous familial hypercholesterolemia due to the 10-kb deletion ("French Canadian mutation") of the LDL receptor gene.

Secondary Prevention with Lipid Lowering Therapy in Familial Hypercholesterolemia: A Correlation between New Evolution of Stenotic Lesion and Achieved Cholesterol Levels after Revascularization Procedures.

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