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)

The influence of the efficacy of triglyceride and cholesterol correction on cardiovascular complications and mortality was analysed in a follow-up study with 260 patients with primary HLP (triglycerides before entry greater than 2.9 mmol/l and/or cholesterol greater than 7.8 mmol/l). The follow-up time was 67.4 +/- 27 months. It was hypothesised that reduction of elevated levels of triglycerides and/or cholesterol influenced favourably the incidence of angina pectoris, MI, stroke and total mortality. For ethical reasons, it was not possible to carry out the investigations with a control group. Therefore, we performed an internal comparison of 3 categories of lipid correction achieved during the trial (effective, moderate, insufficient). A substantial improvement of the lipid disorder was obtained by individualizing the therapy. Triglycerides and cholesterol decreased on average by 50% and 20%, respectively. The incidence of MI was 10 times higher than in the general population. With respect to the type of HLP, hypertriglyceridemia revealed a significantly higher incidence of MI compared with hypercholesterolemia and mixed HLP. The therapy variant was only of importance with respect to gallstone diseases accumulating in the CPIB-treated subgroups. We found a majority of cases with newly manifested angina pectoris and stroke in the group with moderate correction of both triglycerides and cholesterol. Patients with effective triglyceride and cholesterol correction suffered less frequently from MI than those with insufficient correction. This was also the case with secondary prevention in cases with MI prior to entry. There was no significant difference in the distribution of lipid categories at entry between those with and without recurrent infarction. In the group without reinfarction, however, the percentage with insufficient control diminished significantly. Associated risk factors such as hypertension, diabetes, smoking and obesity were of minor or no significance. In subjects with effective triglyceride correction, the total mortality was 0.97/1000 treatment months vs. 3.63 in insufficiently treated patients. The figures for MI mortality were 0.36 and 1.91, respectively.
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PMID:Reduced incidence of cardiovascular complications and mortality in hyperlipoproteinemia (HLP) with effective lipid correction. The Dresden HLP study. 649 44

The serum lipoprotein profile was determined in 37 patients with chronic ischemic heart disease (IHD) and 100 practically healthy subjects, aged from 18 to 45. HLP was found in 59.5 per cent of the patients examined, 50 per cent in males and 100 per cent in females. Type IV has the highest incidence (54.5%), followed by type IIB(36.4%) and type IIa (9.1 per cent). In 27 per cent of the patients with no HLP determined, less significant changes in LDLP and VLDLP were found, admitted to be dyslipoproteinemia (DLP). HLP and DLP were confirmed in 86.5 per cent of the patients examined. In all patients serum concentration of HDLP-Chol was decreased (mostly in DLP and type IV HLP), whereas the level of HDLP-Tg was increased in most of the cases. As a result, the intralipoprotein index 1(2)(=HDLP-Chol/HDLP-Tg) was decreased, reaching the lowest values in IIa and type IV HLP. The only index of all studied, being changed (elevated) with a statistical significance in all groups of patients with IHD, in those with normolipoproteinemia (NLP) including, was the lipoprotein index II(=LDLP-Chol and VLDLP-Chol/HDLP-Chol). With the morbid process progressing, assessed by ECG data, the functional stage of stenocardia, the degree of the constriction and the number of the pathologically altered coronary arteries, the incidence of NLP, DLP and type IV HLP distinctly decreased, whereas IIa and IIB type HLP increased.
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PMID:[Changes in serum lipoproteins in patients with ischemic heart disease at an early age]. 710 95

Clinical symptoms, lipoprotein patterns, and apoE phenotypes were determined in 17 individuals with type III hyperlipoproteinemia (type III HLP) and in their relatives and spouses. The apoE phenotype E2/2 occurred in 15 type III HLP probands (88%) and the apoE phenotype E4/2 was found in 2 probands. In each of the families studied, the apoE phenotype inheritance was compatible with a model we previously proposed in which apoE is determined at a single genetic locus with three common alleles. The apoE phenotypes E4/4, E3/3, and E2/2 represent homozygosity for the apoE alleles epsilon4, epsilon3, and epsilon2, respectively, whereas the apoE phenotypes E4/3, E3/2, and E4/2 represent heterozygosity for the apoE alleles epsilon4/epsilon3, epsilon3/epsilon2, and epsilon4/epsilon2, respectively. Plasma lipids in 69 relatives of type III HLP probands were analyzed by apoE phenotype and revealed no significant differences between phenotypes in the levels of cholesterol, triglyceride, or HDL cholesterol. However, there were differences between the apoE phenotypes in LDL cholesterol levels (P = 0.01) and in the ratio of VLDL cholesterol/total triglyceride (ratio) (P < 0.01). Relatives with the apoE phenotype E2/2 had the lowest LDL cholesterol levels and the highest ratios. Of these eleven individuals with the apoE phenotype E2/2 who were not type III HLP probands, two males were taking lipid-lowering drugs, one male had mild angina at age 59, five individuals had ratios >0.25 and two had ratios >0.30 with the ratios for males (0.28 +/- 0.06) significantly greater than the ratios for females (0.17 +/- 0.06) (P < 0.01), and seven had evidence of floating betaVLDL on lipoprotein electrophoresis. In addition, when compared to a control group in the general population, the whole group of relatives had normal cholesterol and HDL cholesterol levels, slightly low LDL cholesterol levels, and almost twice elevated triglyceride levels. In summary, a) a very strong but not invariate association exists between type III HLP and the apoE phenotype E2/2 with some type III HLP individuals having the apoE phenotype E4/2; b) apoE phenotype inheritance is determined by three alleles at a single genetic locus; c) relatives of type III HLP probands, no matter what their apoE phenotype, have on the average nearly twofold elevated plasma triglyceride levels compared to a control population; and d) non-proband type III HLP individuals with the apoE phenotype E2/2 have been identified. As a group these individuals, particularly the males, show a tendency to express type III HLP, but clearly genetic or environmental factors other than the apoE phenotype E2/2 are required for the full phenotypic expression of this disease.-Breslow, J. L., V. I. Zannis, T. R. SanGiacomo, J. L. H. C. Third, T. Tracy, and C. J. Glueck. Studies of familial type III hyperlipoproteinemia using as a genetic marker the apoE phenotype E2/2.
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PMID:Studies of familial type III hyperlipoproteinemia using as a genetic marker the apoE phenotype E2/2. 717 79