Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In total, 30 patients suffering from familial hypercholesterolemia, resistant to diet and lipid-lowering drugs, were treated for up to 6 years (3.6 + or - 1.6; range, 0.2-6.8 years) with low-density lipoprotein (LDL) apheresis. Three different systems were used; the dextran sulfate adsorption system (Kaneka) for 27 of 30 patients, the immunoadsorption system from Baxter for 2 of 30 patients, and the immunoadsorption system with special lipoprotein(a) (Lp[a]) columns from Lipopak for one patient. Prior to the LDL apheresis, 23 of 30 patients suffered from coronary heart disease. Twenty of 23 patients suffered intermittently from symptoms of angina, excertional dyspnea, and claudication. With LDL apheresis, reductions of 47% for total cholesterol, 49% for LDL, 26% for Lp(a), and 40% for triglycerides were reached. Severe side effects such as shock or allergic reactions were very rare (0.55%). In the course of treatment with LDL apheresis, an improvement in general well-being and increased performance were experienced in 27 of 30 patients. A reduction of nitrate medication between 60 and 100% was observed in 17 of 23 patients. The present data clearly demonstrate that treatment with LDL apheresis in patients suffering from severe familial hyperlipidemia, resistant to maximum conservative therapy, is very effective and safe even over long periods of time.
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PMID:Treatment of severe hyperlipidemia: six years' experience with low-density lipoprotein apheresis. 913 20

Familial hypercholesterolemia was the first genetic disorder recognized to cause myocardial infarction. Patients with homozygous familial hypercholesterolemia have rapidly progressive coronary atherosclerosis with angina pectoris, myocardial infarction, or sudden death at a young age. Selective apheresis on dextran sulfate cellulose columns reduces mortality and may induce regression of coronary lesions. These patients have both increased levels and prolonged circulation residence time of low-density lipoprotein (LDL), which is not removed by cellular receptor. LDL oxidation may play a pivotal role in atherogenesis. LDL undergoes oxidation before being taken up by macrophages and then transformed into arterial wall foam cells. The aim of this study was to investigate LDL oxidation in eight homozygous patients with familial hypercholesterolemia during repeated LDL apheresis. LDL lipid peroxidation, estimated by conjugated-diene absorbance at 234 nm, lipid peroxides, and malondialdehyde showed an increased resistance against oxidation after repeated LDL apheresis. This phenomenon was also observed in the oxidative indexes of protein moiety of LDL (apolipoprotein-B100 fragmentation, trinitrobenzenesulfonic acid reactivity, and electrophoresis agarose mobility). Similarly, cholesteryl esterification was decreased after LDL apheresis. Thus selective LDL apheresis not only decreases the pool of LDL, but it also induces changes that render LDL less susceptible to oxidation. This phenomenon might contribute to reduce coronary atherosclerosis and thus mortality of these particular patients.
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PMID:Decreased low-density lipoprotein oxidation after repeated selective apheresis in homozygous familial hypercholesterolemia. 914 82

There are now several efficient and safe extracorporeal LDL eliminating procedures for the treatment of patients with familial hypercholesterolemia (FH) resistant to diet and combined drug therapy. In Germany, the most clinical experience is available from the heparin-induced extracorporeal LDL-precipitation (HELP) system. This procedure is additionally characterized by the effective elimination of not only LDL but also fibrinogen, a further independent risk factor of coronary heart disease CHD, which mainly influences blood flow characteristics. After 3-4 HELP treatments at weekly intervals, patients with CHD report markedly fewer episodes of angina pectoris, previously resistant to conventional therapy. This is probably related to a "functional regression" of CHD, which is due to the simultaneous lowering of LDL and fibrinogen, resulting in improved rheological properties followed by an increased oxygen supply to a previously insufficiently perfused myocardium. The restoration of endothelial function by maximal cholesterol lowering, as indirectly shown by changes in the cholesterol/phospholipid ratio in cellular membranes, obviously results in an improved vasomotoric response to endogenous vasodilatative substances, thus explaining the clinical improvement of our patients. As shown by a multicenter trial, regular long-term treatment with HELP is followed by an arrest of the atherosclerotic progression in 50% of the investigated segments. In 30% of the previously progressive segments, a significant regression was observed while only 20% of the segments progressed. The mean degree of stenosis decreased by 4.3%. Regular HELP-LDL-/Fibrinogen apheresis in patients with severe CHD and angina pectoris refractory to conventional therapy results within a relatively short period in an improved coronary perfusion and long-term treatment induces regression of atherosclerotic coronary lesions.
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PMID:[Heparin-induced extracorporeal LDL precipitation (HELP) in therapy refractory hypercholesterolemia and coronary heart disease: effect on clinical and morphological regression of coronary sclerosis]. 917 22

We report a 46-year-old man with familial hypercholesterolemia who simultaneously developed angina pectoris and left hemiplegia. Angiography revealed complete tapering occlusion of the right internal carotid artery and a 75% stenosis of the right coronary artery. In addition to hypercholesterolemia, his serum Lp(a) levels were very high, with a mean (+/- SE) of 62 +/- 2 mg/dl.
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PMID:Concurrent development of hemiplegia and angina pectoris in a 46-year-old man with familial hypercholesterolemia and elevated serum Lp(a) concentrations. 922 81

Coronary heart disease (CHD) in familial hypercholesterolemia (FH) may be modified by genetic and/or environmental factors. We described the effect of the cholesteryl ester transfer protein (CETP) gene on CHD in heterozygous FH caused by low density lipoprotein receptor (LDL-R) gene mutation. In 288 unrelated Japanese subjects with heterozygous FH, the allele frequency of an intron 14 G(+1)-to-A mutation (Int14 A) and a missense mutation in exon 15 (Asp442 to Gly, D442G) was 0.3 and 3.0%, respectively. HDL-C levels (1.55 +/- 0.08 mmol/l) in FH patients with heterozygous CETP deficiency were higher than those (1.19 +/- 0.08 mmol/l) in FH without CETP deficiency (P < 0.03), while LDL-C levels in FH with CETP deficiency were moderately reduced. However, two FH patients with CETP deficiency suffered myocardial infarction, and six patients had effort angina pectoris and/or coronary atherosclerosis. No difference in the score of coronary stenosis index (CSI) was found in FH with/without CETP deficiency, although CSI was inversely correlated with HDL-C levels (P < 0.05). Thus, the effect of increased HDL-C levels caused by partial deficiency of CETP is insufficient to prevent CHD in FH.
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PMID:Clinical characteristics of double heterozygotes with familial hypercholesterolemia and cholesteryl ester transfer protein deficiency. 924 69

Low-density lipoprotein (LDL) apheresis is a potent treatment for patients with coronary heart disease and severe hereditary forms of LDL hypercholesterolemia not adequately responsive to drug treatment. Until now, the beneficial effect of aggressive reduction of LDL cholesterol by LDL apheresis on the course of coronary heart disease has been demonstrated in one 3-year study and several studies lasting 2 years. We now report on the clinical course, lipoprotein concentrations, coronary angiograms, and side effects in patients undergoing LDL apheresis for as long as 8.6 years. Thirty-four patients (21 men and 13 women) with coronary heart disease and heterozygous familial hypercholesterolemia (FH) not adequately responsive to lipid-lowering drugs received weekly (four patients biweekly) LDL apheresis for 4.6 +/- 2.6 years under diet and lipid-lowering drug therapy; after 0.5 to 3 years, simvastatin in the maximal tolerable dose was added. The baseline LDL cholesterol concentration was 6.9 +/- 1.6 mmol/L. Combined treatment in the steady state yielded a pretreatment and posttreatment LDL cholesterol concentration of 4.8 +/- 0.9 and 1.8 +/- 0.4 mmol/L, respectively. The calculated interval mean LDL cholesterol was 3.3 +/- 0.6 mmol/L. Evaluation of the coronary angiographies revealed a definite regression of coronary lesions in four patients (11.8%); in 19 patients, there was a cessation of progression. Two patients developed atheromatous lesions in bypass grafts (L.H., 60% stenosis; S.M., occlusion). Of 23 patients eligible for the scoring of anginal symptoms, five (21.7%) reported a reduction of the frequency and severity of angina pectoris. The mean coronary symptom score in 23 patients changed from 1.65 +/- 0.83 at baseline to 1.39 +/- 0.66 at the end of the study. During the whole observation period, we observed three sudden deaths, one nonfatal myocardial infarction, and five patients requiring hospital admission because of unstable angina pectoris, one of which was followed by a transluminal coronary angioplasty. Aggressive reduction of LDL cholesterol with combined LDL apheresis and drugs induced regression of coronary lesions in four of 34 patients and prevented progression in 29 patients for as long as 8.6 years. The effect on LDL and high-density lipoprotein (HDL) cholesterol and lipoprotein(a) [Lp(a)] was comparable with all three apheresis techniques. Therefore, no obvious difference between the three techniques was found regarding changes in coronary lesions.
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PMID:Long-term effect of low-density lipoprotein apheresis on plasma lipoproteins and coronary heart disease in native vessels and coronary bypass in severe heterozygous familial hypercholesterolemia. 966 36

Thirty patients (13 males, 17 females) suffering from familial hypercholesterolemia resistant to diet and lipid-lowering drugs were treated for 48.7 +/- 19.2 months (range, 2-87 months) with low density lipoprotein (LDL) apheresis. Three different systems (dextran sulfate adsorption for 27 of 30 [Kaneka, Liposorber, Japan], immunoadsorption system for 2 of 30 [Baxter, Therasorb, Germany], immunoadsorption system with special lipoprotein a [Lp(a)] columns for 1 of 30 patients [Lipopak, Pocard, Russia]) were applied. Before LDL apheresis 24 of 30 patients suffered from coronary heart disease (CHD) with angina symptoms. With LDL apheresis, reductions of 46% for total cholesterol, 49% for LDL, 30% for Lp(a), and 38% for triglycerides were reached. Severe side effects such as shock or allergic reactions were very rare (0.5%). In the course of treatment, an improvement in general well-being and increased performance were experienced in 27 of 30 patients. A 60 to 100% reduction of nitrate medication was observed in 17 of 24 patients. Regarding the different apheresis systems used, at the end of the trial there were no significant differences with respect to the clinical outcome experienced by the patients and concerning total cholesterol, LDL, high density lipoprotein, and triglyceride concentrations. But to reduce high Lp(a) levels, the immunoadsorption method with special Lp(a) columns seems to be the most effective (-57% versus 25% [Kaneka] and 23% [Baxter]). The present data clearly demonstrate that treatment with LDL apheresis of patients suffering from familial hypercholesterolemia, resistant to maximum conservative therapy, is very effective and safe, even in long-term application.
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PMID:LDL apheresis in clinical practice: long-term treatment of severe hyperlipidemia. 1022 81

Familial hypercholesterolemia is characterized by a high plasma level of cholesterol and is frequently associated with rapidly progressing coronary heart disease. The internal thoracic artery is recognized as the conduit of choice for coronary artery bypass grafting. This study was performed to determine whether multiple arterial grafting was associated or not with additional benefits for patients with familial hypercholesterolemia. Between June 1980 and March 1998, 95 patients with familial hypercholesterolemia. underwent a total of 103 coronary artery bypass procedures with one hospital death. The patients were divided into 3 groups according to the type of bypass graft. Group 1 included 31 patients with only saphenous vein grafts; Group 2,48 patients with one arterial graft and supplemental vein grafts; and Group 3, 24 patients with multiple arterial grafts. The overall actuarial survival rate was 90.9% at 10 years and 81.8% at 18 years. The overall actuarial freedom from recurrent angina was 68.9% at 10 years and 55.8% at 16 years. The actuarial survival rate in group 2 was higher than that in Group 1 (p < 0.05). There was no difference in the actuarial survival or in the freedom from cardiac events between Group 2 and Group 3. Single arterial grafting improved the long-term survival in patients with familial hypercholesterolemia. However, no additional benefit from multiple arterial grafting was identified.
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PMID:Arterial revascularization. 18-year experience with coronary artery bypass grafting in familial hypercholesterolemia. 1048 91

The purpose of the present report is to demonstrate the long-term efficacy and safety of heparin-induced extracorporeal lipoprotein precipitation (HELP) of LDL-c and fibrinogen in the management of familial hypercholesterolemia. From June 1992 to June 1998 a 22-year-old young male patient with familial hypercholesterolemia (double heterozygote for C660X and S305C) resistant to medication and diet and with symptomatic coronary artery disease (angina) was treated weekly with 90-min sessions of the HELP system. The patient had also been previously submitted to right coronary artery angioplasty. The efficacy of the method was evaluated by comparing the reduction of total cholesterol, LDL-c and fibrinogen before and after the sessions and before and after initiation of the study (data are reported as averages for each year). During the study, angina episodes disappeared and there were no detectable adverse effects of the treatment. Total cholesterol (TC), fibrinogen, and LDL-c decreased significantly after each session by 59.6, 66.1 and 64%, respectively. HDL-c showed a nonsignificant reduction of 20.4%. Comparative mean values pre- and post-treatment values in the study showed significant differences: TC (488 vs 188 mg/dl), LDL-c (416.4 vs 145 mg/dl), and fibrinogen (144.2 vs 57.4 mg/dl). There was no significant change in HDL-c level: 29.4 vs 23 mg/dl. These data show that the HELP system, even for a long period of time, is a safe and efficient mode of treatment of familial hypercholesterolemia and is associated with disappearance of angina symptoms.
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PMID:Six years of treatment with the HELP system of a patient with familial hypercholesterolemia. 1213 16

There is clear clinical evidence that a drastic lowering of plasma LDL-Cholesterol (LDL) concentrations significantly reduces the rate of total and coronary mortality as well as the incidence of cardiovascular events in high risk hypercholesterolemic patients. We describe the case of a 51-year-old woman with coronary heart disease (CHD) who presented with increasing angina on exertion in 1995, at the age of 45. She suffered from a heterozygous familial hypercholesterolemia and in 1985 her total cholesterol (TCHO) was 328 +/- 62 mg/dl (mean value of ten analysis). After ten years of statins her mean values (20 analysis, 2 per year) were: TCHO 259 +/- 71, LDL 209 +/- 47, HDL 35 +/- 7 mg/dl. Coronary angiography (CA) performed in 1995 disclosed three vessel coronary heart disease with significant stenoses of the distal right coronary artery, multiple calcifications of the interventricularis artery and multiple plaques with significant stenoses in the ramus circumflexus. The woman underwent coronary by-pass surgery. Thereafter the patient was treated for six years with HELP in biweekly intervals, in combination with statins. TCHO, LDL, HDL and fibrinogen (fb) levels were measured before and after each treatment. Their mean values for an amount of 120 sessions were: TCHO pre 216 +/- 23, post 111 +/- 18 LDL pre 152 +/- 16 post 67 +/- 18, HDL pre 42 +/- 5 post 35 +/- 4 fb pre 306 +/- 48 post 125 +/- 31. In 2001 a new CA was performed. Calcifications disappeared and stenoses were identical to the previous CA or reduced. There were no further clinical manifestations of CHD. We trust that the clinical benefit of the HELP procedure will be substantial for those patients who have problems in clearing LDL from their plasma pool and who are at the same time sensitive to elevated LDL levels by the development of premature coronary sclerosis.
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PMID:Effectiveness of long-term heparin-induced extracorporeal LDL precipitation (HELP) in improving coronary calcifications. 1270 93


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