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 relationship between high-density-lipoprotein (HDL) particle size subclasses and the levels of the major lipoprotein lipids was studied in 74 men consecutively referred to the lipid clinic. HDL (density 1.070-1.21 kg l-1) was separated by polyacrylamide gradient gel electrophoresis (GGE) into five size-defined subclasses, in order of decreasing size as follows: HDL2b, HDL2a, HDL3a, HDL3b and HDL3c. Cholesterol and triglyceride concentrations in very-low-density (VLDL), low-density (LDL) and high-density (HDL) lipoproteins were determined. The level of VLDL triglycerides was negatively correlated with HDL2b (r = -0.66, P less than 0.0001), and positively correlated with HDL3b concentrations (r = 0.65, P less than 0.0001). Both correlations were restricted to subjects with VLDL triglyceride concentrations of less than 1.80 mmol l-1, i.e. those with normotriglyceridaemia. Patients with a history of myocardial infarction and/or angina pectoris (n = 18) had significantly lower HDL2b levels than subjects with asymptomatic hyperlipidaemia (n = 50), i.e. 0.16 vs. 0.22 mg protein ml-1 (P less than 0.05), despite essentially similar cholesterol and triglyceride levels in the VLDL, LDL and HDL fractions, including HDL2 and HDL3 cholesterol.
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PMID:Close correlation between high-density lipoprotein and triglycerides in normotriglyceridaemia. 164 Jan 91

We examined the association of cholesterol levels in serum lipoprotein fractions, as well as of serum apolipoprotein-AI (apo-AI) and apo-AII levels, with coronary artery stenosis (CAS) and left ventricle function in a group of 43 patients with angina pectoris (33 men and 10 women) subjected to angiography. Cholesterol level in VLDL, LDL, HDL2, and HDL3 fractions was determined after separation of these fractions by density gradient ultracentrifugation. HDL-cholesterol is the sum of cholesterol in HDL2 and HDL3. Cineangiography yielded scores for CAS and for left ventricle ejection fraction (LVEF). On univariate regression CAS was correlated weakly with LDL-cholesterol (positive) and with HDL3-cholesterol and HDL-cholesterol (negative), and more strongly with LDL-cholesterol/HDL-cholesterol (positive), but not with HDL2-cholesterol. LVEF was correlated positively with HDL3-cholesterol, HDL-cholesterol, apo-AI, and apo-AII. Of other "risk factors," none was correlated with CAS, and a history of previous myocardial infarction (PMI) was the only one significantly correlated with LVEF. CAS itself was also correlated negatively with LVEF. In multiple regression analysis with two or three independent variables, the relation of HDL(3)-cholesterol with CAS remained significant when other risk factors were taken into account. LVEF remained related positively with HDL(3)-cholesterol, apo-AI, or apo-AII, when either of them was tested in combination with other risk factors; of these only PMI made a significant independent contribution. Conclusions for this patient group (with low HDL-cholesterol): HDL3-cholesterol, and not HDL2-cholesterol, is informative for CAS; HDL(3)-cholesterol, apo-AI, or apo-AII, as well as CAS and PMI, are associated with LVEF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of cholesterol concentrations in low-density lipoprotein, high-density lipoprotein, and high-density lipoprotein subfractions, and of apolipoproteins AI and AII, with coronary stenosis and left ventricular function. 309 80

In order to evaluate the long-term effects of propranolol and acebutolol on serum lipoprotein lipids, a double-blind clinical trial was carried out. Fifteen patients with stable angina pectoris, aged 32 to 79 years (mean = 53), were randomized to propranolol (80 to 160 mg/day) or acebutolol (400 mg/day) treatment groups, and followed for approximately 1 year (mean = 371 days). Blood was collected on the day treatment was begun, after approximately 5 months (mean = 158 days), and on completion of the trial. Very low-density lipoproteins (VLDL) (alpha less than 1.006), low-density lipoproteins (LDL) (1.006 to 1.063), and high-density lipoproteins (HDL) (1.063 to 1.125 [HDL2] and 1.125 to 1.21 [HDL3]) were isolated by sequential preparative ultracentrifugation, and their cholesterol and triglyceride quantified by enzymic procedures. After 1 year propranolol had raised the mean VLDL triglyceride concentration by 79% (p less than 0.005) and had lowered total HDL cholesterol by 24% (p less than 0.005). As LDL cholesterol was unchanged, the LDL cholesterol/HDL cholesterol ratio was increased by 26% (p less than 0.005). Mean values at 5 months were intermediate between those at baseline and those at 1 year. In contrast to these changes, acebutolol had no significant effect on any measured lipoprotein lipid.
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PMID:Double-blind trial of the long-term effects of acebutolol and propranolol on serum lipoproteins in patients with stable angina pectoris. 331 May 69

Beta-Adrenoceptor blocker therapy is known to cause disturbances of the lipoprotein profile. The long-term effects of beta-adrenoceptor blockers and the influence of intrinsic sympathomimetic activity (ISA) has not been clearly defined. We measured serum lipoproteins during chronic beta-adrenoceptor blockade in patients with stable angina pectoris treated with propranolol (without ISA) (n = 21) or pindolol (with ISA) (n = 19). No significant changes occurred in the lipoprotein profile of the patients taking pindolol. In those taking propranolol, very low density lipoprotein (VLDL) increased at 52 weeks (P less than 0.05) and total high density lipoprotein (HDL) decreased at 26 weeks (P less than 0.01) and at 52 weeks (P less than 0.05). However, HDL2 rose significantly at 52 weeks (P less than 0.05). There was a corresponding increase in HDL2/HDL3 ratio. We conclude that pindolol is less likely to exert a harmful effect on plasma lipoproteins than beta-adrenoceptor blockers without ISA.
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PMID:Beta-adrenoceptor blockade and plasma lipoproteins. Comparison of the effects of propranolol and pindolol on plasma lipoproteins including high-density lipoprotein subfractions. 358 81

The concentrations of cholesterol (C) and phospholipid (PL) levels in the high density lipoprotein (HDL) fraction and the HDL2 and HDL3 subfractions were determined in 74 men with incapacitating angina pectoris and coronary artery disease (CAD) verified by angiography. An equal number of randomly sampled healthy men matched for age, occupation and place of living constituted the control group. The HDL2 and HDL3 fractions were separated by a combination of ultracentrifugation and precipitation. The levels of HDL-C and HDL-PL were reduced in the CAD patients. The reduction of HDL lipids was attributed to both the HDL2 and HDL3 fractions. Proportionally there was a greater reduction of C and PL in HDL2 than in HDL3. The decrease of HDL2-C and HDL3-PL were significant also after allowance for the influences of obesity and triglyceride level. The reductions of HDL2 and HDL3 were significant as well in smoking as in nonsmoking CAD patients and both in patients with and without beta-adrenoceptor blocking drugs.
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PMID:HDL2 and HDL3 lipid levels in coronary artery disease. 396 40

Since several beta-blocking agents increase the atherogenic VLDL-triglycerides and decrease the atheroprotective HDL-cholesterol we studied if verapamil also affects these lipoproteins or the most atherogenic LDL-cholesterol. Twelve patients (three females), mean age 56 years, with angina pectoris or hypertension/tachyarrhythmias were treated with verapamil 240-320 mg/day. Serum lipoproteins were measured before and after 6 and 24 weeks of therapy. Initial total serum cholesterol averaged 7.27 mmol/l. After 6 weeks of treatment it decreased by 9%, p less than 0.02. These results remained significant, p less than 0.01 after 24 weeks. The decrease was due to a fall in LDL-cholesterol by 12%, p less than 0.01. The reduction in LDL-cholesterol was correlated to initial LDL-cholesterol concentration, r = -0.73, p less than 0.01. Within LDL there was a parallel decrease in phospholipids, p less than 0.05. There were no changes in total or VLDL-triglycerides or total HDL-cholesterol. In the HDL fraction HDL2 decreased insignificantly but HDL3 cholesterol increased by 12%, p less than 0.05. We conclude that verapamil has a beneficial effect on serum lipoproteins in that it lowers the atherogenic LDL-cholesterol and does not affect the other lipoproteins in an undesirable way.
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PMID:Effect of verapamil on serum lipoproteins in patients with angina pectoris. 658 55

The effects of beta adrenoceptor blockade with propranolol or pindolol on serum total cholesterol, low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL), and its subfractions HDL2 and HDL3, serum triglyceride, and Intralipid clearance were studied in 17 normolipidaemic, non-diabetic patients with hypertension or angina pectoris. Both pindolol and propranolol had similar effects on fasting serum total and lipoprotein cholesterol concentrations. HDL2 cholesterol concentrations were reduced by 9 +/- 29% and HDL3 cholesterol increased by 11 +/- 16%, but there were no significant changes in total or LDL cholesterol in the combined groups after six weeks' treatment. After 12 weeks' treatment total cholesterol concentrations were reduced by 7 +/- 10% mainly owing to a reduction in the LDL fraction of 9 +/- 15%. Concentrations of HDL2 remained low, 8% less than control values. Serum triglyceride concentrations were increased by both drugs at six weeks but had returned to base values in the pindolol group by the twelfth week. Pindolol, but not propranolol, enhanced the rate of clearance of intravenous Intralipid.
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PMID:Effects of short term beta adrenoreceptor blockade on serum lipids and lipoproteins in patients with hypertension or coronary artery disease. 673 88

Treatment of hypertension with beta-adrenergic blockers (BB) slightly increases plasma triglycerides and decreases high density lipoprotein (HDL) cholesterol levels. However, only little is known about BB-related lipid changes in patients with coronary artery disease (CAD), who usually a priori have decreased HDL cholesterol levels; and even less data exist on HDL subfraction cholesterol in these patients. We therefore quantified levels of lipids, lipoprotein lipids including HDL2 and HDL3 cholesterol, and apolipoproteins in 107 consecutive men undergoing elective coronary angiography. Of the 107 patients, 84 had angiographically established coronary atherosclerosis (>or=1 lesion with >or=50% narrowing, CAD+), and 23 had no major lesion (CAD-); 67 were taking ss1-selective BB (metoprolol or atenolol) for treatment of angina and/or hypertension and 40 were not. Patients using BB had significantly higher cholesterol levels than patients not using BB (5.99 +/- 0.93 vs. 5.63 +/- 1.07 mmol/l, mean +/- SD, p = 0.029). Their HDL cholesterol and HDL2 cholesterol levels were significantly lower (1.19 +/- 0.27 vs. 1.28 +/- 0.33 mmol/l, p = 0.048, and 0.22 +/- 0.12 vs. 0.27 +/- 0.18 mmol/l, p = 0.038, respectively). Accordingly, the total cholesterol/HDL cholesterol ratio was significantly higher in patients taking BB than in those not taking BB (5.23 +/- 1.27 vs. 4.68 +/- 1.63, p = 0.010). Considering CAD+ and CAD- patients separately, there was a trend towards lower HDL cholesterol and its subfractions with significantly lower HDL2 cholesterol in patients with BB in the CAD- group, suggesting a stronger dyslipidemic effect of BB in these patients with a priori normal or near normal baseline lipid levels.
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PMID:High density-lipoprotein subfractions of patients using cardio-selective beta-blockers. 1209 Sep 5

Several parameters and risk factors were compared between Korean male myocardial infarction (MI) patients (n=10) and angina pectoris (AP) patients (n=17) to search unique biomarkers for myocardial infarction (MI) in lipoprotein level. Individual serum and lipoprotein fractions (VLDL, LDL, HDL2, HDL3) were isolated and analyzed by lipid and protein determination and enzyme assay. The MI group was found to have a 25 and 30% higher serum cholesterol and triacylglycerol (TG) level than the AP group, respectively, however, their body mass index (BMI), LDL-cholesterol (C), HDL-C, and glucose levels fell within the normal range. MI patients were found to have an approximately two-fold higher level of serum IL-6 and an 18% lower serum apoA-I level than that of the AP group. LDL and HDL2 fraction of the MI group were more enriched with TG than those of AP group. The increased TG was correlated well with the increased level of apoC-III in the same fraction. Cholesteryl ester transfer protein (CETP) activity and protein level were greatly increased in MI patients in the LDL and HDL3 fractions. MI patients showed more severely oxidized LDL fraction than patients in the AP group, as well as the weakest antioxidant ability of serum. Conclusively, MI patients were found to have unique serum and lipoprotein characteristics including increased IL-6 and TG in serum, with CETP and apoC-III in the LDL and HDL fractions, as well as severely impaired antioxidant ability of HDL.
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PMID:Myocardial infarction patients show altered lipoprotein properties and functions when compared with stable angina pectoris patients. 1928 87

In order to investigate non-invasive biomarkers for angina pectoris (AP), we analyzed the lipid and protein composition in individual lipoproteins from females with angina pectoris (n=22) and age- and gender-matched controls (n=20). In the low-density lipoprotein (LDL) fraction, the triglycerides (TG) and protein content increased in the AP group compared to the control group. The AP group had lower total cholesterol (TC) and elevated TG in the high-density lipoprotein (HDL) fraction. In the AP group, cholesteryl ester transfer protein (CETP) activity was enhanced in HDL and LDL, while lecithin:cholesterol acyltransferase (LCAT) activity in HDL3 was almost depleted. Antioxidant activity was significantly decreased in the HDL3 fraction, with a decrease in the HDL2 particle size. In the HDL3 fraction, paraoxonase and platelet activating factor-acetylhydrolase (PAF-AH) activity were much lower and the levels of CETP and apoC-III were elevated in the AP group. The LDL from the AP group was more sensitive to cupric ion-mediated oxidation with faster mobility. In conclusion, the lipoprotein fractions in the AP group had impaired antioxidant activity and increased TG and apoC-III with structural and functional changes.
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PMID:Females with angina pectoris have altered lipoprotein metabolism with elevated cholesteryl ester transfer protein activity and impaired high-density lipoproteins-associated antioxidant enzymes. 2221 Dec 42


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