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Journal articles on the topic 'Lipoproteins and coronary heart disease'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Schaefer, Ernst J., and Margaret E. Brousseau. "DIET, LIPOPROTEINS, AND CORONARY HEART DISEASE." Endocrinology and Metabolism Clinics of North America 27, no. 3 (September 1998): 711–32. http://dx.doi.org/10.1016/s0889-8529(05)70035-9.

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2

Clifton, P. M. "Postprandial Lipoproteins and Coronary Heart Disease." European Journal of Cardiovascular Prevention & Rehabilitation 1, no. 3 (October 1, 1994): 197–201. http://dx.doi.org/10.1177/174182679400100302.

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3

Lamprea-Montealegre, Julio A., Robyn L. McClelland, Morgan Grams, Pamela Ouyang, Moyses Szklo, and Ian H. de Boer. "Coronary heart disease risk associated with the dyslipidaemia of chronic kidney disease." Heart 104, no. 17 (February 22, 2018): 1455–60. http://dx.doi.org/10.1136/heartjnl-2017-312794.

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ObjectiveThis study sought to characterise the main dyslipidaemic phenotypes present in chronic kidney disease (CKD) and their association with coronary heart disease (CHD) risk.MethodsAnalyses included 6612 individuals in the multiethnic study of atherosclerosis free of CHD at baseline. CKD was defined as an estimated glomerular filtration rate (eGFR) of 15 to <60 mL/min/1.73 m2 (stages 3–4). Principal component analyses were used to characterise the main dyslipidaemic phenotypes of CKD accounting for the correlation among different lipoproteins and lipoprotein particles. CHD was defined as incident myocardial infarction, angina followed by revascularisation, resuscitated cardiac arrest or CHD death.ResultsCHD developed in 303 individuals (5%) with eGFR ≥60 and in 72 individuals (12%) with CKD (p for difference <0.001). A dyslipidaemic phenotype (principal component 1 (PC1)) consisting of elevations in triglycerides, triglyceride-rich lipoproteins (VLDL particles), small LDL particles and reductions in HDL particles, was more common in those with CKD, compared with those without CKD (p for difference <0.001). This phenotype was also more strongly associated with CHD in those with CKD: adjusted HRs (95% CIs) per SD increase in PC1 1.13 (95% CI 1.00 to 1.27; P=0.05) and 1.51 (95% CI 1.17 to 1.94; P<0.001) in eGFR ≥60 and CKD, respectively (P for interaction=0.05).ConclusionIn individuals with mainly stage 3 CKD, a dominant lipid phenotype consisting of triglyceride-rich lipoproteins and other closely correlated lipoproteins is strongly associated with CHD risk. Future studies should investigate whether modification of the components of this phenotype leads to a reduction in the CHD burden in individuals with CKD.

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4

BARTER, P. J. "High density lipoproteins and coronary heart disease." Australian and New Zealand Journal of Medicine 21, no. 3 (June 1991): 299–301. http://dx.doi.org/10.1111/j.1445-5994.1991.tb04693.x.

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5

Barter, P. J., and K. A. Rye. "High-Density Lipoproteins and Coronary Heart Disease." European Journal of Cardiovascular Prevention & Rehabilitation 1, no. 3 (October 1, 1994): 217–21. http://dx.doi.org/10.1177/174182679400100306.

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6

Barter, P. J., and K. A. Rye. "High density lipoproteins and coronary heart disease." Atherosclerosis 121, no. 1 (March 1996): 1–12. http://dx.doi.org/10.1016/0021-9150(95)05675-0.

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7

Ahmed, Munir. "CORONARY HEART DISEASE;." Professional Medical Journal 21, no. 06 (December 10, 2014): 1171–73. http://dx.doi.org/10.29309/tpmj/2014.21.06.2250.

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Objective: This study was done to find any correlation among total cholesterol, triglycerides, low density lipoprotein cholesterol and high density lipoprotein cholesterol estimated in serum of offsprings of coronary heart disease patients. Study Design: A cross sectional comparative study. Patients and Methods: Two hundred and fifty (250) subjects having parents with coronary heart disease were selected from Punjab Institute of Cardiology Lahore. The serum total cholesterol, triglycerides, low density lipoprotein cholesterol, and high density lipoprotein cholesterol were estimated. Coefficient of variation was calculated to find whether observations in one series vary correspondingly with observations in another series. Results: Highly significant positive correlation was found between total cholesterol and triglycerides, and, total cholesterol and low density lipoprotein cholesterol. Highly significant negative correlation was found between low density lipoprotein cholesterol and high density lipoprotein cholesterol. Correlation between TG and LDL-c was also significant. Conclusions: Serum total cholesterol, triglycerides, low density lipoprotein cholesterol and high density lipoprotein cholesterol have strong association with one and other. For prediction, prevention and management of coronary heart disease it is important to estimate and observe the correlation among these parameters.

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8

Miller, N. E. "Plasma Lipoproteins, Antihypertensive Drugs and Coronary Heart Disease." Journal of Cardiovascular Pharmacology 7 (1985): S105—S109. http://dx.doi.org/10.1097/00005344-198507002-00020.

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9

Katan, M. B., P. L. Zock, and R. P. Mensink. "Dietary oils, serum lipoproteins, and coronary heart disease." American Journal of Clinical Nutrition 61, no. 6 (June 1, 1995): 1368S—1373S. http://dx.doi.org/10.1093/ajcn/61.6.1368s.

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10

Bittner, Vera. "Atherogenicity of Postprandial Lipoproteins and Coronary Heart Disease." Endocrinologist 4, no. 5 (September 1994): 359–72. http://dx.doi.org/10.1097/00019616-199409000-00007.

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11

Manttari, M., J. K. Huttunen, P. Koskinen, V. Manninen, L. Tenkanen, O. P. Heinonen, and M. H. Frick. "Lipoproteins and coronary heart disease in the Helsinki Heart Study." European Heart Journal 11, suppl H (January 2, 1990): 26–31. http://dx.doi.org/10.1093/eurheartj/11.suppl_h.26.

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12

Muscella, Antonella, Erika Stefàno, and Santo Marsigliante. "The effects of exercise training on lipid metabolism and coronary heart disease." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 1 (July 1, 2020): H76—H88. http://dx.doi.org/10.1152/ajpheart.00708.2019.

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Blood lipoproteins are formed by various amounts of cholesterol (C), triglycerides (TGs), phospholipids, and apolipoproteins (Apos). ApoA1 is the major structural protein of high-density lipoprotein (HDL), accounting for ~70% of HDL protein, and mediates many of the antiatherogenic functions of HDL. Conversely, ApoB is the predominant low-density lipoprotein (LDL) Apo and is an indicator of circulating LDL, associated with higher coronary heart disease (CHD) risk. Thus, the ratio of ApoB to ApoA1 (ApoB/ApoA1) is used as a surrogate marker of the risk of CHD related to lipoproteins. Elevated or abnormal levels of lipids and/or lipoproteins in the blood are a significant CHD risk factor, and several studies support the idea that aerobic exercise decreases CHD risk by partially lowering serum TG and LDL-cholesterol (LDL-C) levels and increasing HDL-C levels. Exercise also exerts an effect on HDL-C maturation and composition and on reverse C transport from peripheral cells to the liver to favor its catabolism and excretion. This process prevents atherosclerosis, and several studies showed that exercise training increases heart lipid metabolism and protects against cardiovascular disease. In these and other ways, it more and more appears that regular exercise, nutrition, and strategies to modulate lipid profile should be viewed as an integrated whole. The purpose of this review is to assess the effects of endurance training on the nontraditional lipid biomarkers, including ApoB, ApoA1, and ApoB/ApoA1, in CHD risk.

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13

Lauderdale, Stacy A., and Amy Heck Sheehan. "Intensive Lipid-Lowering Therapy in Patients with Coronary Heart Disease." Annals of Pharmacotherapy 39, no. 2 (February 2005): 329–34. http://dx.doi.org/10.1345/aph.1e330.

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OBJECTIVE: To describe current data evaluating the use of intensive lipid-lowering therapy in patients with coronary heart disease. DATA SOURCES: A literature search using MEDLINE (1966–September 2004) was conducted using the search terms lipoproteins, low-density lipoprotein cholesterol (LDL-C), hydroxymethylglutaryl-coenzyme A reductase inhibitors, coronary arteriosclerosis, and coronary disease to identify published trials comparing the effects of intensive and conventional lipid-lowering therapy. DATA SYNTHESIS: Intensive lipid-lowering therapy reduces LDL-C levels significantly more than conventional treatment and appears to reduce cardiovascular morbidity and mortality in patients who have recently experienced acute coronary syndrome (ACS). However, evidence suggesting clinical benefits in patients with stable coronary heart disease is currently lacking. CONCLUSIONS: Although data are limited, patients with ACS may benefit from intensive lipid-lowering therapy. Several studies are underway to determine the appropriate role of intensive lipid-lowering therapy.

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14

Kuller, Lewis H., and Daniel Edmundowicz. "Imaging of Coronary Arteries Aid in Prevention of Atherosclerosis and Clinical Coronary Heart Disease." Open Epidemiology Journal 4, no. 1 (December 30, 2011): 152–64. http://dx.doi.org/10.2174/1874297101104010152.

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Prevention of progression of atherosclerosis is the best approach to reduce incidence of myocardial infarction, sudden coronary heart disease (CHD) death, stroke and peripheral vascular disease. Research over the past 40 years has identified the risk factors for atherosclerotic disease, noninvasive methods for measuring the extent of atherosclerosis in multiple vascular beds and very efficacious therapy to reduce the level of risk factors and prevent cardiovascular diseases. Cardiovascular incidence and death rates have declined. Nevertheless, rates of CHD and other vascular disease remain much higher in many countries and within select regions of certain countries than necessary. Prevention of atherosclerosis depends on 4 key steps: 1) a much more aggressive effort to lower modifiable risk factors, especially apolipoprotein-B (ApoB)-containing lipoproteins, low density lipoprotein (LDL) particles, LDL cholesterol, blood pressure, obesity, and smoking during adolescence and young adult years; 2) identify and treat elevated ApoB lipoproteins, diabetes and smoking cessation of very high risk young adults as early as possible; 3) use of imaging to identify atherosclerosis of coronary and other arteries for appropriate segments of the adult population and treatment of risk factors for those with identifiable atherosclerosis; and 4) improved approaches to deliver prevention of cardiovascular disease to large numbers of asymptomatic individuals identified by non invasive imaging to maximize adherence to therapies. The major missing piece is better methods to identify vulnerable coronary plaques on the verge of an atherothrombotic transition and better treatments to prevent “acute” events. However, the four steps above will still lead to very substantial reductions in CHD incidence and mortality.

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15

Sönmez, Hüseyin, Selma Süer, Turgut Ulutin, Emine Kökoglu, and Nergiz Uçişik. "The Relationship of Various Factors in the Pathogenesis of Atherosclerosis." Clinical and Applied Thrombosis/Hemostasis 4, no. 2 (April 1998): 105–10. http://dx.doi.org/10.1177/107602969800400205.

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In this study we investigated the levels of lipid parameters, fibronectin, tissue-type plasminogen activator and plasminogen activator inhibitor (t-PA-PAI-1) complex and si alidase in patients with coronary heart disease and a control group. Total cholesterol, triglyceride, low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) cholesterol and lipoprotein Lp(a), levels in patients with coronary heart disease were found to be significantly higher than in the control group (p < .001). High-density lipoprotein (HDL) cholesterol levels in patient group were significantly lower than control group (p < .001). Plasma fibronectin and t-PA-PAI-1 complex levels in patients with coronary heart disease were found to be significantly higher than control group (p < .05 and p < .001, respectively). In addition, we found that serum sialidase levels in patients with coronary heart disease were significantly higher than in the control group (p < .001). The electrophoretic mobility of lipoproteins from patients with coronary heart dis ease was found to be greater than those from the control group. As a result Lp(a) may play an important role in the pathogen esis of atherosclerosis by causing foam cell formation because of interacting with LDL or fibronectin and by interfering with the fibrinolytic system because of binding to plasminogen re ceptors. In addition, modifications of Lp(a) (including desi alylation) may effect these events. Key words: Coronary heart disease—tPA-PAI-1 complex-Fibronectin-sialidase-Lipid parameters.

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16

Hamsten, Anders. "9 Hypertriglyceridaemia, triglyceride-rich lipoproteins and coronary heart disease." Baillière's Clinical Endocrinology and Metabolism 4, no. 4 (December 1990): 895–922. http://dx.doi.org/10.1016/s0950-351x(05)80084-9.

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17

Harris-Hooker, Sandra, and Gary L. Sanford. "Lipids, lipoproteins and coronary heart disease in minority populations." Atherosclerosis 108 (August 1994): S83—S104. http://dx.doi.org/10.1016/0021-9150(94)90155-4.

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18

AHMED, MUNIR, and MOHAMMAD TAYYIB. "CORONARY HEART DISEASE." Professional Medical Journal 16, no. 01 (March 10, 2009): 87–93. http://dx.doi.org/10.29309/tpmj/2009.16.01.2988.

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O b j e c t i v e s : This study was conducted to perform serum lipid profile in off springs of premature coronary heart disease(CHD) patients and age and sex matched normal controls and compare the results of two groups. S t u d y d e s i g n : A cross sectional study.Patients a n d m e t h o d s : 250 off springs of diagnosed premature CHD patients were selected from Punjab institute of cardiology, Lahoreand Services hospital, Lahore. 50 age and sex matched normal controls were selected from different areas of Lahore. Serum totalcholesterol (TC), serum triglycerides (TG) serum low density lipoprotein-cholesterol (LDC-c) and serum high density lipoprotein cholesterol(HDL-c) was performed. Results: Serum TC, TG, LDL-c of off springs of premature CHD patients was increased as compared with normalcontrols. Serum HDL-c of all the subjects of off springs of premature CHD patients was decreased as compared with normal controls.C o n c l u s i o n : Off springs of premature CHD patients are more prone to develop lipid abnormalities as compared with normal controls.

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19

Seed, Mary. "Postmenopausal Hormone Replacement Therapy, Coronary Heart Disease and Plasma Lipoproteins." Drugs 47, Supplement 2 (1994): 25–34. http://dx.doi.org/10.2165/00003495-199400472-00006.

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20

Feher, M. D., and D. J. Betteridge. "Lipids, lipoproteins, and coronary heart disease: Implications for antihypertensive therapy." Cardiovascular Drugs and Therapy 3, S1 (June 1989): 333–40. http://dx.doi.org/10.1007/bf00148479.

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21

Pyörälä, Kalevi. "Diabetes and Coronary Heart Disease." Acta Endocrinologica 110, no. 4_Suppl (December 1985): S11—S19. http://dx.doi.org/10.1530/acta.0.110s011.

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Abstract. Clinically manifest coronary heart disease (CHD) is not uncommon in diabetics with insulin-dependent type of the disease below the age of 40, particularly when the duration of diabetes is long. Clinically manifest CHD is very common in diabetics with maturity-onset, non-insulin-dependent type of the disease, and in this type of diabetes the frequency of CHD shows little or no relation to the duration of diabetes. Premenopausal female diabetics have a clinically manifest CHD almost as often as male diabetics of the same age - a situation in sharp contrast to that in non-diabetics with large excess of CHD in males. The incidence of all manifestations of CHD (sudden and non-sudden CHD death, non-fatal myocardial infarction, »silent« myocardial infarction, and angina pectoris) is increased in diabetics as compared to non-diabetics, but the excess of CHD mortality in diabetics is especially marked, being 3 to 4 times higher than in non-diabetics. The incidence of congestive heart failure is markedly increased in diabetics and this is in part independent of increased occurrence of CHD and hypertension among diabetics. Subclinical abnormalities of left ventricular function are common in diabetics and these abnormalities appear to show some relationship to the metabolic control of diabetes and in insulin-dependent diabetics also to the presence of microangiopathy. Diabetes is associated with changes in general CHD risk factors to atherogenic direction. These changes include abnormalities in the levels and composition of plasma lipids and lipoproteins and increased frequency of hypertension. The impact of general risk factors on CHD risk appears to be similar in diabetics and non-diabetics. The major part of the excess CHD in diabetics, however, is not explained by the effect of diabetes on general cardiovascular risk factors, but is due to an independent effect of diabetes itself through mechanisms which are far from solved.

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22

JANKOWSKI, J., J. R. NOFER, M. TEPEL, B. GRIEWEL, H. SCHLÜTER, G. ASSMANN, and W. ZIDEK. "Identification of oxidized low-density lipoprotein in human serum by NMR spectroscopy." Clinical Science 95, no. 4 (October 1, 1998): 489–95. http://dx.doi.org/10.1042/cs0950489.

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1.In this study we compared the 500 MHz 1H-NMRs from native and oxidized low-density lipoproteins. 2.The measurements revealed a characteristic pattern of three resonances in spectra from oxidized, but not from native low-density liprotein at 1.17 p.p.m., 1.18 p.p.m. and 1.20 p.p.m. (relative to 3-trimethylsilyl-[2,2,3,3-2H4]-propionate). 3.A quantitative comparison between these resonances in sera from patients with coronary heart disease and healthy control subjects revealed that the intensity was significantly higher in patients with coronary heart disease (1.17 p.p.m.: 0.026±0.014 versus 0.015±0.019; 1.18 p.p.m.: 0.032±0.011 versus 0.017±0.021; 1.20 p.p.m.: 0.030±0.066 versus 0.010±0.005; P< 0.05 compared with healthy control subjects for each resonance). 4.Fractionation of sera from patients with coronary heart disease revealed that the resonances equal to those obtained from experimentally oxidized low-density lipoprotein are indeed caused by the low-density lipoprotein fraction of the sera. 5.When the NMRs from sera were calibrated with oxidized low-density lipoprotein prepared by Cu2+ oxidation, a concentration of 66.5±28.6 ;μg/ml and 36.3±23.7 ;μg/ml (P< 0.05) was estimated in patients with coronary heart disease and healthy subjects respectively. Elevated levels of oxidized low-density lipoprotein also occurred in those patients with normal serum concentrations of total low-density lipoprotein. 6.The study shows a simple method to measure oxidized low-density lipoprotein in human serum and may gain interest to assess the cardiovascular risk factor profiles more completely.

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23

Hristich, T. M., and D. O. Gontsariuk. "Chronic pancreatitis in patients with coronary heart disease: a lipid spectrum of blood, a possibility of correction." Bulletin of the Club of Pancreatologists 41, no. 3 (September 6, 2018): 31–39. http://dx.doi.org/10.33149/vkp.2018.03.05.

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Aim of research is to evaluate significance of changes in the lipid spectrum of blood in patients with chronic pancreatitis with coronary heart disease in the pathogenesis of the comorbidity of these diseases and in the dynamics of treatment with polycosanol. Materials and methods. The study was conducted in 22 patients (10 patients with chronic pancreatitis and dyslipidemia, 12 patients with comorbidity of chronic pancreatitis and coronary heart disease in CHD II-II A-B syndrome of stage II-III functional class) and in 10 almost healthy individuals. There were 13 men, 9 women, 31–69 years old. Patients of two groups in addition to protocol treatment were prescribed polycosanol 10 mg 1 time in the evening during dinner, up to 3 months. To study the characteristics of the lipid spectrum of the blood, the level of total cholesterol, high-density lipoprotein cholesterol, triglycerols was determined (using the Zlatix-Zack-based Lachema reagents (Czech Republic)). The level of low-density lipoprotein cholesterol was determined using the Friedewald calculation method, taking into account that the triglycerol concentration did not exceed 4.5 mmol/l. In addition, very low density lipoprotein cholesterol and an atherogenicity index were determined using conventional calculation methods. Results. In patients with a combined course of chronic pancreatitis with coronary heart disease, in most cases there is a significant (p<0.05) increase in total cholesterol, low and very low-density lipoproteins and triglycerols. When analyzing the types of dyslipidemia, it was found that ІІа and ІІв types were more common (22 і 25%, respectively), but with comorbidity ІІ and ІV type of dyslipidemia was more often detected. In the dynamics of a three-month treatment with polycosanol in patients with chronic pancreatitis, the cholesterol levels of high-density lipoproteins increased significantly and the triglycerol values significantly decreased, indicating a hypolipidemic effect of the drug and the possibility of using it in combination with statins in order to reduce the risk of cardiovascular events. Conclusion. The comorbidity of chronic pancreatitis with ischemic heart disease increases the risk of progression of dyslipidemia and atherosclerosis. This is confirmed by an increased atherogenic index in this group of patients, along with the severity of lipid spectrum disorders. The addition of polycosanol to patients with chronic pancreatitis and dyslipidemia, as well as in combination with coronary heart disease, contributes to the reduction and normalization of certain parameters of the lipid spectrum of the blood. This allows us to recommend a drug for long-term treatment of these groups of patients, including in combination with statin therapy.

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24

Abbasi, Fahim, Tracey McLaughlin, Cindy Lamendola, Hee Sun Kim, Akira Tanaka, Tao Wang, Katsuyuki Nakajima, and Gerald M. Reaven. "High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk." American Journal of Cardiology 85, no. 1 (January 2000): 45–48. http://dx.doi.org/10.1016/s0002-9149(99)00604-9.

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25

Ito, Y., S. Koba, T. Hirano, Y. Yokota, F. Tsunoda, Y. Ban, T. Sato, et al. "SIGNIFICANCE OF SMALL DENSE LOW-DENSITY LIPOPROTEINS IN CORONARY HEART DISEASE." Atherosclerosis Supplements 9, no. 1 (May 2008): 242–43. http://dx.doi.org/10.1016/s1567-5688(08)70971-1.

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26

Seed, Mary, and David Crook. "Post-menopausal hormone replacement therapy, coronary heart disease and plasma lipoproteins." Current Opinion in Lipidology 5, no. 1 (February 1994): 48–58. http://dx.doi.org/10.1097/00041433-199402000-00009.

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27

Savolainen, Markku J., and Y. Antero Kesäniemi. "Effects of alcohol on lipoproteins in relation to coronary heart disease." Current Opinion in Lipidology 6 (August 1995): 243–50. http://dx.doi.org/10.1097/00041433-199508000-00009.

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28

Otvos, J. D., E. J. Jeyarajah, and D. W. Bennett. "Quantification of plasma lipoproteins by proton nuclear magnetic resonance spectroscopy." Clinical Chemistry 37, no. 3 (March 1, 1991): 377–86. http://dx.doi.org/10.1093/clinchem/37.3.377.

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Abstract A new analytical procedure for quantifying plasma lipoproteins by proton nuclear magnetic resonance (NMR) spectroscopy has been developed that potentially offers significant advantages over existing clinical methods used for assessing risk of coronary heart disease. Analysis of a single spectrum of a nonfasting plasma sample, acquired simply and rapidly at moderate magnetic field strength (250 MHz), yields a complete profile of lipoprotein concentrations: chylomicrons and very-low-, low-, and high-density lipoproteins. The method is based on curve-fitting (spectral deconvolution) of the plasma methyl lipid resonance envelope, the amplitude and shape of which depend directly on the amplitudes of the superimposed methyl resonances of the lipoprotein components. A linear least-squares curve-fitting algorithm was developed to efficiently extract the signal amplitudes (concentrations) of the lipoproteins from the plasma spectrum. These signal amplitudes correlate well with lipoprotein concentrations determined by triglyceride and cholesterol measurements.

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29

Yagensky, A. V. "Is there life after acute coronary syndrome?" Medicine of Ukraine, no. 4(250) (June 16, 2021): 30–32. http://dx.doi.org/10.37987/1997-9894.2021.4(250).238121.

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The role of coronary heart disease and acute coronary syndrome in the structure of morbidity and mortality of the population of Ukraine cannot be overestimated. The main pathogenetic mechanism of corticosteroids is atherothrombosis, the influence of which is the basis of treatment of patients with coronary heart disease with or without corticosteroids. The effect on the progression of atherothrombosis is possible due to statins, due to slowing the growth of atherosclerotic plaques in blood vessels by reducing the level of low-density lipoproteins in the blood.

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30

Cullen, P. "Smoking, lipoproteins and coronary heart disease risk Data from the Münster Heart Study (PROCAM)." European Heart Journal 19, no. 11 (November 1998): 1632–41. http://dx.doi.org/10.1053/euhj.1998.1086.

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31

Gorshunskaya., M. Yu. "Paraoxonase activity and lipid peroxidation in female patients with type 2 diabetes mellitus and without coronary heart disease." Problems of Endocrinology 49, no. 1 (February 15, 2003): 17–20. http://dx.doi.org/10.14341/probl11394.

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The rate of lipid peroxidation and the parameters of antioxida- tive defense, including the activity of paraoxonase that is essential for the prevention of low-density lipoprotein oxidation, was studied in 229female patients with type 2 diabetes mellitus with and without coronary heart disease (CHD) under varying glycemic control. Carbohydrate and lipid metabolisms were explored by unified biochemical studies, blood insulin levels were measured by radioimmunological assay. The activity of paraoxonase associated with high-density lipoproteins of ester hydrolase was spectrophotometrically determined by using paraoxan as a substrate. Along with dyslipoproteinemia and insulin resistance, there was a drastically reduced paraoxonase activity that was associated with the high-density lipoproteins of the antioxidant enzyme and more pronounced in diabetics with CHD. A highly significant inverse correlation of the activity of the enzyme with the rate of lipid peroxidation and a less close relationship to basal glycemia have been verified, which substantiates the polygenic nature of decreased paraoxonase activity in diabetes mellitus.

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32

Plushner, Susyn L. "Lipoprotein Disorders in Women: Which Women are the Best Candidates for Hormone Replacement Therapy?" Annals of Pharmacotherapy 31, no. 1 (January 1997): 98–107. http://dx.doi.org/10.1177/106002809703100116.

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OBJECTIVE: To review the data examining hormone replacement therapy (HRT) in the treatment of lipoprotein disorders in women. DATA SOURCE: A MEDLINE search (1975–1995) of the English-language literature was performed to identify pertinent primary literature and review articles. Articles were also identified through bibliographies of selected articles. DATA EXTRACTION: Controlled and uncontrolled studies evaluating the effects of lipoprotein concentrations on coronary risk and the effects of estrogen and HRT on coronary heart disease and lipoprotein concentrations in women were evaluated. Trials pertaining to adverse effects of therapy were also examined. Emphasis was placed on recent clinical trials. DATA SYNTHESIS: The National Cholesterol Education Program's (NCEP's) 1993 report recommends estrogen replacement therapy as a treatment option in postmenopausal women with hyperlipidemia. Recent trials suggesting that triglycerides and high-density lipoproteins are more closely related to coronary risks in women necessitate an improved understanding of estrogen and progestin's effects on lipoprotein concentrations. A recent trial has clarified the lipoprotein effects of HRT in women with normal lipid concentrations and suggests that beneficial effects on low-density lipoproteins are maintained, although progestins attenuate beneficial changes in high-density lipoproteins and triglyceride elevations persist. The few trials evaluating estrogen use in women with hyperlipidemia suggest a beneficial effect as well. CONCLUSIONS: In the absence of contraindications, postmenopausal women with hyperlipidemia should be offered estrogen replacement therapy as conjugated equine estrogen 0.625 mg/d. Pending further information, NCEP's recommendations should be followed regarding goals of therapy.

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33

Gurewich, Victor. "Lipoprotein(a) in Coronary Heart Disease." JAMA 271, no. 13 (April 6, 1994): 1025. http://dx.doi.org/10.1001/jama.1994.03510370077037.

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34

Seed, M., and J. Loscalzo. "Lipoprotein(a) and coronary heart disease." BMJ 305, no. 6851 (August 22, 1992): 472–73. http://dx.doi.org/10.1136/bmj.305.6851.472-a.

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35

Danesh, John, Rory Collins, and Richard Peto. "Lipoprotein(a) and Coronary Heart Disease." Circulation 102, no. 10 (September 5, 2000): 1082–85. http://dx.doi.org/10.1161/01.cir.102.10.1082.

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36

Maher, Vincent M. G., and B. Greg Brown. "Lipoprotein (a) and coronary heart disease." Current Opinion in Lipidology 6 (August 1995): 229–35. http://dx.doi.org/10.1097/00041433-199508000-00007.

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37

Rodriguez, Carmen R., Leo J. Seman, Jose M. Ordovas, Jennifer Jenner, M. S. Jacques Genest, Peter W. F. Wilson, and Ernst J. Schaefer. "Lipoprotein(a) and coronary heart disease." Chemistry and Physics of Lipids 67-68 (January 1994): 389–98. http://dx.doi.org/10.1016/0009-3084(94)90161-9.

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38

Mahajan, Hemant, Maryam Zaid, Rachel Mackey, Aya Kadota, Abhishek Vishnu, Akira Fujiyoshi, Ahuja Vasudha, et al. "Lipoprotein particles and coronary artery calcium in middle-aged US-White and Japanese men." Open Heart 6, no. 2 (December 2019): e001119. http://dx.doi.org/10.1136/openhrt-2019-001119.

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ObjectiveThis cross-sectional study examined whether contrasting distributions of nuclear magnetic resonance (NMR)-measured lipoproteins contribute to differences in the prevalence of subclinical atherosclerosis measured using coronary artery calcium (CAC) between the two groups of middle-aged males: the US-residing Caucasian (US-White) and Japan-residing Japanese (Japanese).MethodsIn a population-based study of 570 randomly selected asymptomatic men aged 40–49 years (270 US-White and 300 Japanese), we examined the relationship between race/ethnicity, NMR-measured lipoproteins and CAC (measured by Electron Beam CT and quantified using the Agatston method) using multivariable robust Poisson regression adjusting for traditional and novel risk factors for coronary heart disease (CHD).ResultsThe US-White compared with the Japanese had significantly different NMR-measured lipoprotein particle distributions. The US-White had a significantly higher prevalence of CAC≥10 (CAC-prevalence) compared with the Japanese adjusting for CHD risk factors (prevalence ratio (PR)=2.10; 95% CI=1.24 to 3.48), and this difference was partially attenuated (~18%) with further adjustment for lipoprotein levels (PR=1.73; 95% CI=1.02 to 3.08). There was no reclassification improvement with further addition of lipoproteins particle concentrations/size to a model that already included traditionally measured lipids (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides), cardiovascular risk factors, and inflammatory markers (net reclassification improvement index=−2% to 3%).ConclusionsVariations in the distribution of NMR-measured lipoprotein particles partially accounted for the difference in the CAC-prevalence between middle-aged US-White and Japanese men.

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Churashova, Irina A., Alexey V. Sokolov, Valeria A. Kostevich, Nikolay P. Gorbunov, Olga L. Runova, Elvira M. Firova, and Vadim B. Vasilyev. "Myeloperoxidase/high-density lipoprotein cholesterol ratio in patients with arterial hypertension and chronic coronary heart disease." Medical academic journal 21, no. 2 (September 24, 2021): 75–86. http://dx.doi.org/10.17816/maj71486.

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BACKGROUND: Myeloperoxidase (MPO), the enzyme of leukocytes, catalyzes the production of reactive halogen species, which can modify the structure of lipoproteins. Chlorination and nitration of tyrosine residues in apolipoprotein A-1 lead to the formation of dysfunctional high-density lipoproteins (HDL-p), thus blocking the reverse cholesterol transport. Low level of high-density lipoprotein cholesterol (HDL-C) is associated with exacerbation of coronary heart disease, but the prognostic value of this index is not fully assessed. AIM: The aim of this study was to examine a possible contribution of MPO to the atherosclerotic plaque development (the stable growth or the erosion and rupture) via the modification of HDL-p. That is to say we investigated the diagnostic values of measuring the total MPO (MPO-T), the active MPO (MPO-A) and the MPO/HDL-С relation in patients with hypertension and various forms of chronic coronary heart disease. MATERIALS AND METHODS: The cohort under study included 44 patients with arterial hypertension and chronic coronary heart disease. All patients were divided into three groups according to the diagnosis: arterial hypertension without coronary heart disease (Group I, n = 20); arterial hypertension and the initially stable chronic coronary heart disease without acute complications in the anamnesis (Group II, n = 14); arterial hypertension and myocardial infarction (acute coronary syndrome) in the anamnesis (Group III, n = 10). The enzyme-linked immunosorbent assay (ELISA) for MPO-T and specific immuno-extraction followed by enzymatic detection (SIEFED) by fluorogenic substrate for MPO-A were applied. After that the ratio MPO-T/HDL-C or MPO-A/HDL-C was calculated. RESULTS: The MPO-A and MPO-A/HDL-C ratio were significantly increased in the group III of patients with old myocardial infarction as compared with the patients of group II who had the initially stable coronary heart disease (p = 0.009 and p = 0.003, respectively). Besides, the level of HDL-C in the group III was significantly reduced (p = 0.013). Our measurements revealed the negative correlation between MPO-A and HDL-C concentrations (r = 0.31; p 0.05), which is in line with the presumption of the study accomplished. Surprisingly, the correlation between MPO-T/HDL-C ratio and that MPO-A/HDL-C was stronger (r = 0.72; p 0.05), than between MPO-T and MPO-A (r = 0.36; p 0.05). CONCLUSIONS: Our study demonstrates the importance of assessing MPO-T and MPO-A plasma concentrations and of calculating the ratio MPO/HDL-C as promising biomarkers in the complicated cases of chronic coronary heart disease. MPO-A and MPO-A/HDL-C values were elevated in the patients with old myocardial infarction, while the concentration of HDL-C remained decreased upon the transition from the acute to chronic phase of the disease.

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Fruchart, J. C., and P. Duriez. "High density lipoproteins and coronary heart disease. Future prospects in gene therapy." Biochimie 80, no. 2 (February 1998): 167–72. http://dx.doi.org/10.1016/s0300-9084(98)80023-0.

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Mendivil, C., E. Rimm, J. Furtado, S. Chiuve, and F. Sacks. "Abstract: 1472 APOC-III CONTAINING LIPOPROTEINS AND RISK OF CORONARY HEART DISEASE." Atherosclerosis Supplements 10, no. 2 (June 2009): e447. http://dx.doi.org/10.1016/s1567-5688(09)70438-6.

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Grundy, Scott M., Gloria Lena Vega, and Y. Antero Kesäniemi. "Abnormalities in Metabolism of Low Density Lipoproteins Associated with Coronary Heart Disease." Acta Medica Scandinavica 218, S701 (April 24, 2009): 23–37. http://dx.doi.org/10.1111/j.0954-6820.1985.tb08887.x.

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43

Simons, L. A., Y. Friedlander, J. Simons, and J. D. Kark. "Familial aggregation of coronary heart disease: partial mediation by high density lipoproteins?" Atherosclerosis 69, no. 2-3 (February 1988): 139–44. http://dx.doi.org/10.1016/0021-9150(88)90007-x.

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Grundy, S. M. "Role of low-density lipoproteins in atherogenesis and development of coronary heart disease." Clinical Chemistry 41, no. 1 (January 1, 1995): 139–46. http://dx.doi.org/10.1093/clinchem/41.1.139.

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Abstract There is a strong association between increased blood concentrations of low-density lipoprotein (LDL) and severity of coronary atherosclerosis. Multiple mechanisms affect hypercholesterolemia, e.g., diet, aging, hormones, and genetics. LDL receptors apparently are also important--through down-regulation, defects in structure, or decreased numbers--as are changes in LDL binding characteristics caused by alterations in apolipoprotein B content or structure. Current concepts of LDL metabolism are extensively reviewed, including the role of modified or oxidized LDL in atherogenesis.

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Kromhout, Daan. "Epidemiology of cardiovascular diseases in Europe." Public Health Nutrition 4, no. 2b (April 2001): 441–57. http://dx.doi.org/10.1079/phn2001133.

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AbstractWithin Europe large differences exist in mortality from coronary heart disease and stroke. These diseases show a clear West-East gradient with high rates in Eastern Europe. In spite the decreasing trend in age-adjusted cardiovascular disease mortality in Western European countries an increase in the number of cardiovascular patients is expected because of the ageing of the population. Consequently the health care cost for these diseases will increase.Total and HDL cholesterol are major determinants of coronary heart disease. Saturated and trans fatty acids have a total and LDL cholesterol elevating effect and unsaturated fatty acids a lowering effect. N-3 polyunsaturated fatty acids seem to have a protective effect on coronary heart disease occurrence independent of their effect on cholesterol.Dietary antioxidants could be of importance because they may prevent oxidation of the atherogenic cholesterol rich LDL lipoproteins. There is however no convincing evidence that either vitamin E, carotenoids or vitamin C protect against coronary heart disease. Observational research has shown that flavonols, polyphenols with strong antioxidant properties present in plant foods, may protect against coronary heart disease.Blood pressure is a major determinant of coronary heart disease and stroke. Historically salt is viewed as the most important dietary determinant of blood pressure. Recent research shows that also a low-fat diet rich in potassium, calcium and magnesium lowers blood pressure substantially. This suggests a multifactorial influence of different nutrients on blood pressure.It can be concluded that a diet low in saturated and trans fatty acids and rich in plant foods in combination with regular fish consumption is associated with a low risk of cardiovascular mortality.

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Djeric, Mirjana. "Pathophysiology and clinical significance of atherogenic lipoprotein phenotype and small dense LDL particles." Jugoslovenska medicinska biohemija 22, no. 2 (2003): 101–7. http://dx.doi.org/10.2298/jmh0302101d.

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In spite of strong proofs supporting cholesterol hypothesis, serum cholesterol concentration is not a good discriminative factor in assessing the risk of coronary heart disease. The degree of reduction of coronary risk depends also on the level of serum triglycerides. Namely, within metabolic disturbance of triglyceride rich lipoproteins, a reciprocal lipid transfer takes place in the course of delipidation cascade, yielding the remodelling of all the classes of lipoproteins and establishing the so-called atherogenic lipoprotein phenotype (increase in triglycerides, small dense LDL, and apolipoprotein B, and decrease in HDL cholesterol and apolipoprotein A-I). A major part of the atherogenic potential of this phenotype is related to the increase in the number of small dense LDL particles (phenotype B), and not because of the contribution to the serum cholesterol, but due to their lower affinity to LDL receptors, easier penetration to arterial intima, longer retention in subendothelium accelerated oxidation, prompt takeover by macrophages and establishing of endothelial dysfunction.

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Ramsay, Sarah. "Linking lipoprotein (a) and coronary heart disease." Lancet 356, no. 9233 (September 2000): 917. http://dx.doi.org/10.1016/s0140-6736(05)73905-2.

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Betteridge, D. J. "High density lipoprotein and coronary heart disease." BMJ 298, no. 6679 (April 15, 1989): 974–75. http://dx.doi.org/10.1136/bmj.298.6679.974.

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Natarajan, Pradeep, Kausik K. Ray, and Christopher P. Cannon. "High-Density Lipoprotein and Coronary Heart Disease." Journal of the American College of Cardiology 55, no. 13 (March 2010): 1283–99. http://dx.doi.org/10.1016/j.jacc.2010.01.008.

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Marcovina, Santica M., Robert A. Hegele, and Marlys L. Koschinsky. "Lipoprotein(a) and coronary heart disease risk." Current Cardiology Reports 1, no. 2 (July 1999): 105–11. http://dx.doi.org/10.1007/s11886-999-0067-z.

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