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J.-M.M. "LDL, oui, mais HDL?" Revue Francophone des Laboratoires 2007, no. 392 (May 2007): 15. http://dx.doi.org/10.1016/s1773-035x(06)80621-0.
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Amrullah, Amran, Budi Handono, and Akhmad Yogi Pramatirta. "Rasio Low Density Lipoprotein dan High Density Lipoprotein pada Preeklamsi Berat dibandingkan dengan Kehamilan Normal di Rumah Sakit Dr. Hasan Sadikin Bandung." Indonesian Journal of Obstetrics & Gynecology Science 2, no. 1 (March 29, 2019): 67. http://dx.doi.org/10.24198/obgynia.v2i1.79.
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AbstractObjective: This study aims to distinguish level of (LDL/HDL) and Low Density Lipoprotein/High Density Lipoprotein ratio in severe preeclampsia patient compared to normal pregnancy.Method: The study design was comparative cross-sectional study with consecutive sampling method that compared the laboratory results of LDL, HDL and ratio LDL/HDL that met the inclusion criteria. Subjects of this study were severe preeclampsia and normal pregnancy patient that fulfilled the inclusion criteria (n=60) in Dr. Hasan Sadikin General Hospital Bandung during August-September 2017.Result: It is revealed that the differences in level of LDL and LDL/HDL ratios in both groups were significant with p value ≤ 0,05. But there were no differences in HDL level. Increased level of LDL/HDL ratio in pregnancy was related to increased risk of preeclampsia with cut-off point> 2,632. If the increased level of LDL/HDL above cut-off point then the insident of severe preeclampsia increased 21,36 times.Conclusion: It was concluded that level of LDL and LDL/HDL ratios in severe preeclampsia were higher than in normal pregnancy. The increased LDL/HDL ratio of > 2.632 increased the risk of severe preeclampsia by 21.36 times.Perbandingan Rasio Low Density Lipoprotein/High Density Lipoprotein antara Preeklamsi Berat dan Kehamilan Normal di RSUP Dr. Hasan Sadikin BandungAbstrakTujuan: Penelitian ini adalah untuk mencari perbedaan rasio Low Density Lipoprotein/High Density Lipoprotein (LDL/HDL) pada preeklamsi berat dibandingkan dengan kehamilan normal sebagai faktor risiko timbulnya preeklamsi.Metode: Rancangan penelitian kasus kontrol membandingkan LDL, HDL, dan rasio LDL/HDL penderita preeklamsi berat dan kehamilan normal (n=60) bulan Agustus-September 2017 di Rumah Sakit Dr. Hasan Sadikin Bandung.Hasil: Hasil penelitian didapatkan perbedaan kadar LDL dan rasio LDL/HDL pada kedua kelompok secara bermakna dengan nilai p ≤0,05. Namun tidak didapatkan perbedaan yang bermakna pada kadar HDL. Peningkatan kadar LDL dan rasio LDL/HDL berhubungan dengan peningkatan risiko terjadinya preeklamsi dengan nilai cut-off > 2,632. Bila terjadi peningkatan rasio LDL/HDL diatas nilai cut-off maka risiko tejadinya preeklamsi berat sebesar 21,36 kali.Simpulan: Kadar LDL yang tinggi dan nilai cut-off rasio LDL/HDL >2,632 meningkatkan risiko terjadinya preeklamsi berat 21,36 kaliKata kunci: Preeklamsi, LDL, HDL, Rasio LDL/HDL
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Fujihara, Kazuya, Hiroaki Suzuki, Akira Sato, Satoru Kodama, Yoriko Heianza, Kazumi Saito, Hitoshi Iwasaki, et al. "Circulating Malondialdehyde-Modified LDL-Related Variables and Coronary Artery Stenosis in Asymptomatic Patients with Type 2 Diabetes." Journal of Diabetes Research 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/507245.
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Aims. To elucidate the levels of malondialdehyde-modified LDL (MDA-LDL)-related variables for predicting coronary artery stenosis (CAS) by coronary CT angiography (CCTA) in asymptomatic patients with type 2 diabetes (T2DM).Methods. Enrolled were 36 Japanese patients with T2DM who underwent CCTA and in whom MDA-LDL levels were measured. Definition of CAS was luminal narrowing of ≥50%. Trends through tertiles of each MDA-LDL-related variable were analyzed with a general linear model. The ability of each MDA-LDL-related variable to predict CAS was compared to areas under the curve (AUCs) in receiver operating characteristic curve (ROC) analysis.Results. Seventeen patients had CAS. Each MDA-LDL-related variable was an independent predictor of CAS (P=0.039for MDALDL,P=0.013for MDA-LDL/LDL-C,P=0.047for MDA-LDL/HDL-C, andP=0.013for (MDA-LDL/LDL-C)/HDL-C). AUCs of MDA-LDL, MDA-LDL/LDL-C, MDA-LDL/HDL-C, and (MDA-LDL/LDL-C)/HDL-C were 0.675 (95% CI 0.496–0.854), 0.765 (0.602–0.927), 0.752 (0.592–0.913), and 0.799 (0.643–0.955), respectively, for predicting CAS. Trends throughout the tertiles showed significant associations between MDA-LDL/LDL-C, MDA-LDL/HDL-C, or (MDALDL/LDL-C)/HDL-C and CAS (P=0.003for MDA-LDL/LDL-C,P=0.042for MDA-LDL/HDL-C, andP=0.001for (MDA-LDL/LDL-C)/HDL-C).Conclusions. Data suggest that measurements of MDA-LDL/LDL-C, MDA-LDL/HDLC, and (MDA-LDL/LDL-C)/HDL-C are useful for predicting CAS.
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Baruch, Lawrence, Valerie J. Chiong, Sanjay Agarwal, and Bhanu Gupta. "Discordance of Non-HDL and Directly Measured LDL Cholesterol: Which Lipid Measure is Preferred When Calculated LDL Is Inaccurate?" Cholesterol 2013 (April 23, 2013): 1–6. http://dx.doi.org/10.1155/2013/502948.
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Objective. To determine if non-HDL cholesterol (N-HDL) and directly measured LDL cholesterol (D-LDL) are clinically equivalent measurements. Patients and Methods. Eighty-one subjects recruited for 2 cholesterol treatment studies had at least 1 complete fasting lipid panel and D-LDL performed simultaneously; 64 had a second assessment after 4 to 6 weeks, resulting in 145 triads of C-LDL, D-LDL, and N-HDL. To directly compare N-HDL to D-LDL and C-LDL, we normalized the N-HDL by subtracting 30 from the N-HDL (N-HDLA). Results. There was significant correlation between N-HDLA, D-LDL, and C-LDL. Correlation was significantly greater between N-HDLA and C-LDL than between N-HDLA and D-LDL. A greater than 20 mg/dL difference between measures was observed more commonly between N-HDLA and D-LDL, 29%, than between C-LDL and N-HDLA, 11% (P<0.001), and C-LDL and D-LDL, 17% (P=0.028). Clinical discordance was most common, and concordance was least common between N-HDL and D-LDL. Conclusions. Our findings suggest that N-HDL cholesterol and D-LDL cholesterol are not clinically equivalent and frequently discordant. As N-HDL may be superior to even C-LDL for predicting events in statin-treated patients, utilizing N-HDL to guide therapy would appear to be preferable to D-LDL when C-LDL is inaccurate.
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Garcia-Rios, Antonio, Dragana Nikolic, Pablo Perez-Martinez, Jose Lopez-Miranda, Manfredi Rizzo, and Ron Hoogeveen. "LDL and HDL Subfractions, Dysfunctional HDL: Treatment Options." Current Pharmaceutical Design 20, no. 40 (October 14, 2014): 6249–55. http://dx.doi.org/10.2174/1381612820666140620154014.
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Benitez, S., C. Bancells, J. Ordonez-Llanos, and J. L. Sanchez-Quesada. "HDL COUNTERACTS INFLAMMATORY PROPERTIES OF ELECTRONEGATIVE LDL (LDL(-))." Atherosclerosis Supplements 9, no. 1 (May 2008): 50. http://dx.doi.org/10.1016/s1567-5688(08)70195-8.
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Pian, M. S., and L. G. Dobbs. "Lipoprotein-stimulated surfactant secretion in alveolar type II cells: mediation by heterotrimeric G proteins." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 3 (September 1, 1997): L634—L639. http://dx.doi.org/10.1152/ajplung.1997.273.3.l634.
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Low- and high-density lipoproteins (LDL and HDL, respectively) stimulate alveolar type II cells to secrete surfactant. Increases in phosphoinositide hydrolysis, cytosolic Ca2+, and membrane-associated protein kinase C activity precede LDL- and HDL-stimulated secretion. We report three lines of evidence supporting the hypothesis that Gi mediates LDL- and HDL-stimulated surfactant secretion and signal transduction in type II cells. First, pertussis toxin (PTX) inhibited secretion stimulated by the apolipoprotein ligands for either the LDL receptor or the HDL binding protein. Second, PTX inhibited protein kinase C activity in cell membranes stimulated by LDL or HDL. Third, treatment of cell membranes with LDL or HDL inhibited PTX-catalyzed labeling of substrates corresponding in molecular mass to Gi alpha. These observations suggest that receptor-mediated activation of Gi is required for LDL- and HDL-stimulated secretion and that LDL and HDL activate Gi. These studies in type II cells are the first to support the hypothesis that Gi mediates the effects of LDL or HDL on important phenotype-specific functions of differentiated cells.
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Enomoto, Mika, Hisashi Adachi, Yuji Hirai, Ako Fukami, Akira Satoh, Maki Otsuka, Shun-Ichi Kumagae, et al. "LDL-C/HDL-C Ratio Predicts Carotid Intima-Media Thickness Progression Better Than HDL-C or LDL-C Alone." Journal of Lipids 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/549137.
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High-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) are strong predictors of atherosclerosis. Statin-induced changes in the ratio of LDL-C to HDL-C (LDL-C/HDL-C) predicted atherosclerosis progression better than LDL-C or HDL-C alone. However, the best predictor of subclinical atherosclerosis remains unknown. Our objective was to investigate this issue by measuring changes in carotid intima-media thickness (IMT). A total of 1,920 subjects received health examinations in 1999, and were followed up in 2007. Changes in IMT (follow-up IMT/baselineIMT×100) were measured by ultrasonography. Our results showed that changes in IMT after eight years were significantly related to HDL-C (inversely,P<0.05) and to LDL-C/HDL-C ratio (P<0.05). When the LDL-C/HDL-C ratios were divided into quartiles, analysis of covariance showed that increases in the ratio were related to IMT progression (P<0.05). This prospective study demonstrated the LDL-C/HDL-C ratio is a better predictor of IMT progression than HDL-C or LDL-C alone.
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Miida, Takashi, Yuichi Nakamura, Toru Mezaki, Osamu Hanyu, Seitaro Maruyama, Yoshinori Horikawa, Sachiko Izawa, Yukio Yamada, Hiroshi Matsui, and Masahiko Okada. "LDL-cholesterol and HDL-cholesterol concentrations decrease during the day." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 3 (May 1, 2002): 241–49. http://dx.doi.org/10.1258/0004563021901946.
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Background Homogenous assays for LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) are highly accurate, with little interference from triglyceride. Using these methods, we measured postprandial LDL-C and HDL-C. Earlier studies suggested a postprandial decrease in LDL-C. Methods To elucidate whether LDL-C and HDL-C decrease significantly during the day, we determined daily profiles of LDL-C and HDL-C using homogeneous assays in subjects with normal coronary arteries (N; n = 10), and subjects with coronary artery disease (CAD; n = 23). Results In both groups, LDL-C and HDL-C were significantly lower from after breakfast until midnight than they were before breakfast. The next morning, they returned to baseline levels. The mean reduction in LDL-C was 0·09--0·13 mmol/L in N and 0·05--0·20 mmol/L in CAD, while that in HDL-C was 0·02--0·06 mmol/L in N and 0·00--0·05 mmol/L in CAD. Conclusion LDL-C and HDL-C decrease significantly over the course of the day.
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Karádi, I., L. Romics, P. Kempler, I. Balogh, I. Szilvási, and L. Littmann. "HDL protection against atherogenic LDL?" Basic Research in Cardiology 82, no. 6 (November 1987): 596–97. http://dx.doi.org/10.1007/bf01907230.
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Aumiller, Jochen. "DEFINE: HDL verdoppelt, LDL halbiert." CardioVasc 10, no. 6 (December 2010): 16. http://dx.doi.org/10.1007/bf03358836.
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Nurhani, Mazdalina Rahmawandari, Kusworini, and Bambang Rahardjo. "Correlation between LDL, HDL, LDL/HDL Ratio and Preeclampsia incidence at RSUD Pamekasan, indonesia." Indian Journal of Public Health Research & Development 10, no. 9 (2019): 1139. http://dx.doi.org/10.5958/0976-5506.2019.02596.8.
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Giorgi Gogishvili, Giorgi Gogishvili, Shalva Petriashvili Shalva Petriashvili, Nino Nanobashvili Nino Nanobashvili, Nino Megrelishvili Nino Megrelishvili, and Iamze Taboridze Iamze Taboridze. "CHARACTERISTICS OF THE LIPID PROFIL YOUNG ADULTS WITH ISCHEMIC HEART DISEASE IN GEORGIAN POPULATION." PIRETC-Proceeding of The International Research Education & Training Centre 11, no. 01 (February 28, 2021): 47–52. http://dx.doi.org/10.36962/1101202147.
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Objective: Impaired lipoprotein metabolism is a significant and modifiable risk factor for atherosclerotic cardiovascular disease. Aim: The aim of our study was to determine the diagnostic accuracy of lipid profile indices in young adults in Georgian population. Methods: Under our observation were 107 patients with ischemic heart disease, aged 18-45 years, From the St. John The Merciful Private Clinic contingent. Examination: anamnesis, cardiography, echocardiography, coronography, blood lipid metabolism. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), Triglycerides (TG), mmol/L) and lipid indices -TC-HDL/HDL, TG /HDL, and LDL/HDL Results: With IHD for young adults, TC-HDL/HDL distinguished by good sensitivity and sufficient specificity, TG /HDL - bad sensitivity and very excellent specificity, LDL/HDL - sufficient sensitivity and good specificity, With IHD, for TC-HDL/HDL Cut off=2.29, for TG /HDL, cut off=2.76 and for LDL/HDL - 2.17 High lipid indices on these data indicate a high risk of ischemic heart disease. Conclusion: lipid indices TC-HDL/HDL, TG /HDL, and LDL/HDL can be used for the primary diagnosis of ischemic heart disease in young adults. Keywords: risk factors IHD, dyslipidemia.
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Mascarenhas-Melo, Filipa, José Sereno, Edite Teixeira-Lemos, Daniela Marado, Filipe Palavra, Rui Pinto, Petronila Rocha-Pereira, Frederico Teixeira, and Flávio Reis. "Implication of Low HDL-c Levels in Patients with Average LDL-c Levels: A Focus on Oxidized LDL, Large HDL Subpopulation, and Adiponectin." Mediators of Inflammation 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/612038.
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To evaluate the impact of low levels of high density lipoprotein cholesterol (HDL-c) on patients with LDL-c average levels, focusing on oxidative, lipidic, and inflammatory profiles. Patients with cardiovascular risk factors (n=169) and control subjects (n=73) were divided into 2 subgroups, one of normal HDL-c and the other of low HDL-c levels. The following data was analyzed: BP, BMI, waist circumference and serum glucose Total-c, TGs, LDL-c, oxidized LDL, total HDL-c and subpopulations (small, intermediate, and large), paraoxonase-1 (PON1) activity, hsCRP, uric acid, TNF-α, adiponectin, VEGF, and iCAM1. In the control subgroup with low HDL-c levels, significantly higher values of BP and TGs and lower values of PON1 activity and adiponectin were found, versus control normal HDL-c subgroup. However, differences in patients’ subgroups were clearly more pronounced. Indeed, low HDL-c subgroup presented increased HbA1c, TGs, non-HDL-c, Ox-LDL, hsCRP, VEGF, and small HDL-c and reduced adiponectin and large HDL. In addition, Ox-LDL, large-HDL-c, and adiponectin presented interesting correlations with classical and nonclassical markers, mainly in the normal HDL-c patients’ subgroup. In conclusion, despite LDL-c average levels, low HDL-c concentrations seem to be associated with a poor cardiometabolic profile in a population with cardiovascular risk factors, which is better evidenced by traditional and nontraditional CV biomarkers, including Ox-LDL, large HDL-c, and adiponectin.
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Merdiana, Novita, and Hesti Murwani Rahayuningsih. "PENGARUH PEMBERIAN ESTER STANOL TERHADAP KADAR KOLESTEROL LDL DAN HDL WANITA DISLIPIDEMIA." Journal of Nutrition College 3, no. 1 (January 27, 2014): 243–50. http://dx.doi.org/10.14710/jnc.v3i1.4603.
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Latar belakang : Dislipidemia merupakan salah satu faktor risiko terjadinya penyakit jantung dan pembuluh darah. Ester stanol merupakan pangan fungsional yang dapat menurunkan kadar kolesterol LDL dengan cara menghambat penyerapan kolesterol di usus halus dan mengaktifkan reseptor LDL di permukaan sel.Metode : Jenis penelitian ini adalah quasi experimental. Subyek wanita dislipidemia dengan kadar kolesterol LDL ≥ 130 mg/dl dan HDL < 50 mg/dl. Subyek dibagi menjadi 2 kelompok, yaitu kelompok perlakuan yang diberikan ester stanol 3,4 g dalam susu rendah lemak dan kelompok kontrol yang diberikan susu rendah lemak saja selama 2 minggu. Metode pengukuran kadar kolesterol LDL menggunakan perhitungan Friedewald dan kadar kolesterol HDL menggunakan phosphotungstic precipitation.Hasil : Ester stanol 3,4 g terbukti menurunkan kolesterol LDL sebesar 7,68% dan terjadi penurunan kolesterol HDL sebesar 1,57%, namun tidak bermakna secara statistik. Rerata kadar kolesterol LDL dan HDL sebelum penelitian kelompok perlakuan berturut-turut yaitu 161,86 mg/dl dan 44,38 mg/dl. Rerata kadar kolesterol LDL dan HDL sesudah penelitian kelompok perlakuan berturut-turut yaitu 148,63 mg/dl dan 43,54 mg/dl. Konsumsi ester stanol 3,4 g tidak berpengaruh secara bermakna terhadap kadar kolesterol LDL dan HDL (p > 0,05). Kesimpulan : Konsumsi ester stanol 3,4 g/hari selama 2 minggu tidak memiliki pengaruh yang bermakna terhadap kadar kolesterol LDL dan HDL wanita dislipidemia. Tidak ada perbedaan yang bermakna kadar kolesterol LDL dan HDL antara kelompok perlakuan dan kontrol.
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Kalahasthi, Ravibabu, Vinaykumar Adepu, Rakesh Balachandar, and Raju Nagaraju. "Association between non-high density lipoprotein-cholesterol fractions and presence of allostatic load among industrial workers." Indian Journal of Physiology and Pharmacology 66 (December 29, 2022): 268–75. http://dx.doi.org/10.25259/ijpp_164_2022.
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Objectives: Non-high density lipoprotein-cholesterol (non-HDL-C) fraction is the total cholesterol (TC) minus HDL-C. It is not a routinely reported component of lipid profile and is used in lipoprotein lowering therapy and prediction of coronary artery disease, target organ damage and atherosclerosis. Allostatic load (AL) is an imbalance between repetitive chronic exposure to stress and adaptive response. The present study investigates the association between non-HDL-C and its fractions (non-HDL-C/HDL-C, non-HDL-C/TC, non-HDL-C/ triglyceride [TG] and non-HDL-C/low-density lipoprotein-cholesterol [LDL-C]) and the presence of AL to determine, which fractions of non-HDL-C predict the diagnostic accuracy and optimal cut points. Materials and Methods: The study design is cross-sectional and data were collected from 169 male industrial workers. AL was measured using neuroendocrine (cortisol and dehydroepiandrosterone sulphate), cardiovascular (systolic blood pressure, diastolic blood pressure and heart rate), metabolic (TC, TG, HDL-C and LDL-C) and anthropometric (waist-hip ratio and body mass index) factors. The fractions of non-HDL-C/HDL-C, nonHDL-C/TC, non-HDL-C/TG and non-HDL-C/LDL-C were calculated using non-HDL-C, HDL-C, TC, TG and LDL-C values. Results: About 43.2% and 56.8% of workers had low and high AL, respectively. The non-HDL-C and its fractions such as non-HDL-C/HDL-C, non-HDL-C/TC and non-HDL-C/LDL-C were significantly increased in the high AL group. Stepwise regression analysis was used to examine the association between non-HDL-C fractions and AL. The fractions of non-HDL-C (b = 0.785, P = 0.001), non-HDL-C/TC (b = −0.336, P = 0.001) and nonHDL-C/LDL-C (b = 0.295, P = 0.001) influenced AL by 38.6%. The AUC with 95% CI in the high AL group was as follows: non-HDL-C 0.766 (0.696–0.837, P = 0.001); non-HDL-C/HDL-C 0.638 (0.555–0.721, P = 0.002); nonHDL-C/TC 0.635 (0.552–0.712, P = 0.003) and non-HDL-C/LDL-C 0.520 (0.433–0.607, P = 0.657). Non-HDL-C and its fractions were more precisely predicted in the high AL category of workers than in the low AL category. Non-HDL-C predicted the most precisely, followed by non-HDL-C/HDL-C, non-HDL-C/TC, non-HDL-C/ LDL-C and non-HDL-C/TG. Conclusion: According to the present study, non-HDL-C and its fractions such as non-HDL-C/HDL-C, nonHDL-C/TC and non-HDL-C/LDL-C should be considered regular lipid profiles and could be used as biomarkers to reduce the risk of AL.
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García-Heredia, Anabel, Judit Marsillach, Anna Rull, Iris Triguero, Isabel Fort, Bharti Mackness, Michael Mackness, Diana M. Shih, Jorge Joven, and Jordi Camps. "Paraoxonase-1 Inhibits Oxidized Low-Density Lipoprotein-Induced Metabolic Alterations and Apoptosis in Endothelial Cells: A Nondirected Metabolomic Study." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/156053.
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We studied the influence of PON1 on metabolic alterations induced by oxidized LDL when incubated with endothelial cells. HUVEC cells were incubated with native LDL, oxidized LDL, oxidized LDL plus HDL from wild type mice, and oxidized LDL plus HDL from PON1-deficient mice. Results showed alterations in carbohydrate and phospholipid metabolism and increased apoptosis in cells incubated with oxidized LDL. These changes were partially prevented by wild type mouse HDL, but the effects were less effective with HDL from PON1-deficient mice. Our results suggest that PON1 may play a significant role in endothelial cell survival by protecting cells from alterations in the respiratory chain induced by oxidized LDL. These results extend current knowledge on the protective role of HDL and PON1 against oxidation and apoptosis in endothelial cells.
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Saputro, Zanuar Bagus, Tjitra Wardani, and Purwo Sri Rejeki. "The Effect of Moderate Intensity Fun Aerobic Gym on HDL-C and LDL- C on Overweight Women." Folia Medica Indonesiana 55, no. 2 (January 14, 2021): 89. http://dx.doi.org/10.20473/fmi.v55i2.24511.
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Overweight and obesity is a major health problem in throughout the world. Hyperlipidemia and obesity are risk factor the occurrence of cardiovascular disease. Exercise is recommended as a therapeutic lifestyle changes because it leads to a variety of health benefits. Fun Aerobic gymnastics aerobics one which is quite popular in the community and a gym. Describe the gymnastics fun aerobic workout's effectiveness against related to prevention of cardiovascular disease with seeing the results before and after doing gymnastics with the result of increasing levels of HDL-c and LDL/HDL Ratios as well as lowering LDL-c levels. Using design research one group pretest and posttest design with the subject as many as 19 people and given gymnastics moderate fun aerobic intensity for 45 minutes 3 day a week for 6 weeks. Gymnastics moderate fun aerobic intensity can increase HDL-c and LDL/HDL ratio and LDL-c. The paired t test results HDL-c pre test and post test (p = 0.000), LDL-c pre test and post test (p = 0,015), HDL/LDL Ratio (p = 0.000). Mean there are meaningful difference between the before and after of gymnastics. The effect of moderate intensity fun aerobic gym on the increase of HDL-c and LDL/HDL Ratio and a decrease in LDL-c in overweight women.
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Saputro, Zanuar Bagus, Tjitra Wardani, and Purwo Sri Rejeki. "The Effect of Moderate Intensity Fun Aerobic Gym on HDL-C and LDL- C on Overweight Women." Folia Medica Indonesiana 55, no. 2 (July 12, 2019): 89. http://dx.doi.org/10.20473/fmi.v55i2.14331.
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Overweight and obesity is a major health problem in throughout the world. Hyperlipidemia and obesity are risk factor the occurrence of cardiovascular disease. Exercise is recommended as a therapeutic lifestyle changes because it leads to a variety of health benefits. Fun Aerobic gymnastics aerobics one which is quite popular in the community and a gym. Describe the gymnastics fun aerobic workout's effectiveness against related to prevention of cardiovascular disease with seeing the results before and after doing gymnastics with the result of increasing levels of HDL-c and LDL/HDL Ratios as well as lowering LDL-c levels. Using design research one group pretest and posttest design with the subject as many as 19 people and given gymnastics moderate fun aerobic intensity for 45 minutes 3 day a week for 6 weeks. Gymnastics moderate fun aerobic intensity can increase HDL-c and LDL/HDL ratio and LDL-c. The paired t test results HDL-c pre test and post test (p = 0.000), LDL-c pre test and post test (p = 0,015), HDL/LDL Ratio (p = 0.000). Mean there are meaningful difference between the before and after of gymnastics. The effect of moderate intensity fun aerobic gym on the increase of HDL-c and LDL/HDL Ratio and a decrease in LDL-c in overweight women.
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Kurniawan, Liong Boy, Uleng Bahrun, and Darmawaty ER. "ANGKA BANDING LIPID DI INFARK MIOKARD." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 20, no. 1 (October 16, 2016): 1. http://dx.doi.org/10.24293/ijcpml.v20i1.437.
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Lipid profiles are used as the regular tests which performed to predict and evaluate the risk of coronary heart disease. The routine lipid tests include total cholesterol, LDL, HDL and triglyceride level. The total cholesterol/HDL and LDL/HDL ratio are often used as predictors of coronary heart disease. This study was performed to know the lipid level and ratio by comparing the condition in myocardial infarction patients and young adult controls and to observe the percentage of their lipid level and ratio exceeding the recommended optimal value. A retrospective study was performed using secondary data of 73 myocardial infarction patients, whom hospitalized in the Intensive Cardiac Care Unit Dr. Wahidin Sudirohusodo Hospital Makassar from June 2010 to July 2011 and 21 healthy young adult as controls. The mean level of the total cholesterol, LDL, HDL, triglyceride, ratio of total cholesterol/HDL and LDL/HDL of myocardial infarction patients are compared with the control subjects were 209.99±51.70 vs 151.42±27.90 mg/dL (p=0.000), 141.18±41.92 vs 76.76±20.45 mg/dL (p=0.000), 36.96±10.47 vs 47.05±8.24 mg/dL (p=0.000), 132.27±65.67 vs 142.14±54.93 mg/dL (p=0.155), 5.99±1.71 vs 3.26±0.59 (p=0.000) and 4.06±1.45 vs 1.66±0.44 (p=0.000), respectively. It was shown that the percentage of myocardial infarction patients with total cholesterol, LDL level, total cholesterol/HDL and LDL/HDL ratio exceeding recommended optimal value were 57.53%, 63.01%, 73.97% and 86.30%, respectively. The level of total cholesterol and LDL, ratio of total cholesterol/HDL and LDL/HDL in myocardial infarction patients were significantly higher, but the HDL level was lower compared to the control subjects. The percentage of myocardial infarction patients with LDL/HDL ratio exceeding recommended optimal value was higher than the other lipid levels and ratio. Therefore, it is concluded that the LDL/HDL ratio is better in predicting coronary heart disease than other routine lipid markers.
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LeCheminant, James D., Larry A. Tucker, Bruce W. Bailey, and Travis Peterson. "The Relationship Between Intensity of Physical Activity and HDL Cholesterol in 272 Women." Journal of Physical Activity and Health 2, no. 3 (July 2005): 333–44. http://dx.doi.org/10.1123/jpah.2.3.333.
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Purpose:To determine objectively measured intensity of physical activity (iPA) and its relationship to high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and the LDL/HDL ratio in women.Methods:Two hundred seventy-two women (40.1 y) wore CSA-MTI model 7164 accelerometers to index intensity and volume of physical activity for 7 d. Blood lipids were measured at a certified laboratory.Results:HDL-C was 52.1 ± 10.1, 52.2 ± 9.7, and 56.1 ± 11.1 mg/dL for the low, medium, and high intensity groups (P = 0.040), LDL-C differences were not significant (P = 0.23). LDL/HDL differences were observed (P = 0.030) with specific differences between the low and high iPA groups (P = 0.006). For HDL-C and LDL/HDL, significant relationships remained with control of dietary fat and age but not body fat percentage or volume of activity.Conclusions:High iPA had higher HDL-C levels and lower LDL/HDL ratios than low and medium iPA. The iPA was predictive of HDL-C partly due to its strong association with volume of activity and body fat percentage.
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Mascarenhas-Melo, Filipa, Filipe Palavra, Daniela Marado, José Sereno, Edite Teixeira-Lemos, Isabel Freitas, Maria Isabel-Mendonça, Rui Pinto, Frederico Teixeira, and Flávio Reis. "Emergent Biomarkers of Residual Cardiovascular Risk in Patients with Low HDL-c and/or High Triglycerides and Average LDL-c Concentrations: Focus on HDL Subpopulations, Oxidized LDL, Adiponectin, and Uric Acid." Scientific World Journal 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/387849.
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This study intended to determine the impact of HDL-c and/or TGs levels on patients with average LDL-c concentration, focusing on lipidic, oxidative, inflammatory, and angiogenic profiles. Patients with cardiovascular risk factors (n=169) were divided into 4 subgroups, combining normal and low HDL-c with normal and high TGs patients. The following data was analyzed: BP, BMI, waist circumference and serum glucose, Total-c, TGs, LDL-c, oxidized-LDL, total HDL-c and HDL subpopulations, paraoxonase-1 (PON1) activity, hsCRP, uric acid, TNF-α, adiponectin, VEGF, and iCAM1. The two populations with increased TGs levels, regardless of the normal or low HDL-c, presented obesity and higher waist circumference, Total-c, LDL-c, Ox-LDL, and uric acid. Adiponectin concentration was significantly lower and VEGF was higher in the population with cumulative low values of HDL-c and high values of TGs, while HDL quality was reduced in the populations with impaired values of HDL-c and/or TGs, viewed by reduced large and increased small HDL subfractions. In conclusion, in a population with cardiovascular risk factors, low HDL-c and/or high TGs concentrations seem to be associated with a poor cardiometabolic profile, despite average LDL-c levels. This condition, often called residual risk, is better evidenced by using both traditional and nontraditional CV biomarkers, including large and small HDL subfractions, Ox-LDL, adiponectin, VEGF, and uric acid.
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Liu, Kan-Zhi, R. Anthony Shaw, Angela Man, Thomas C. Dembinski, and Henry H. Mantsch. "Reagent-free, Simultaneous Determination of Serum Cholesterol in HDL and LDL by Infrared Spectroscopy." Clinical Chemistry 48, no. 3 (March 1, 2002): 499–506. http://dx.doi.org/10.1093/clinchem/48.3.499.
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Abstract Background: The purpose of this study was to assess the feasibility of infrared (IR) spectroscopy for the simultaneous quantification of serum LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) concentrations. Methods: Serum samples (n = 90) were obtained. Duplicate aliquots (5 μL) of the serum specimens were dried onto IR-transparent barium fluoride substrates, and transmission IR spectra were measured for the dry films. In parallel, the HDL-C and LDL-C concentrations were determined separately for each specimen by standard methods (the Friedewald formula for LDL-C and an automated homogeneous HDL-C assay). The proposed IR method was then developed with a partial least-squares (PLS) regression analysis to quantitatively correlate IR spectral features with the clinical analytical results for 60 randomly chosen specimens. The resulting quantification methods were then validated with the remaining 30 specimens. The PLS model for LDL-C used two spectral ranges (1700–1800 and 2800–3000 cm−1) and eight PLS factors, whereas the PLS model for HDL-C used three spectral ranges (800–1500, 1700–1800, and 2800–3500 cm−1) with six factors. Results: For the 60 specimens used to train the IR-based method, the SE between IR-predicted values and the clinical laboratory assays was 0.22 mmol/L for LDL-C and 0.15 mmol/L for HDL-C (r = 0.98 for LDL-C; r = 0.91 for HDL-C). The corresponding SEs for the test spectra were 0.34 mmol/L (r = 0.96) and 0.26 mmol/L (r = 0.82) for LDL-C and HDL-C, respectively. The precision for the IR-based assays was estimated by the SD of duplicate measurements to be 0.11 mmol/L (LDL-C) and 0.09 mmol/L (HDL-C). Conclusions: IR spectroscopy has the potential to become the clinical method of choice for quick and simultaneous determinations of LDL-C and HDL-C.
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Feng, Yingmei. "LDL and HDL Counteract Hematopoietic Stem/Progenitor Cells in Regulation of Inflammation and Atherosclerosis." Blood 118, no. 21 (November 18, 2011): 1288. http://dx.doi.org/10.1182/blood.v118.21.1288.1288.
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Abstract Abstract 1288 Low-density lipoprotein (LDL) is an independent risk factor in cardiovascular disease. Hypercholesterolemia-associated monocytosis and transformation of monocytes into macrophages are the main features underlying the proatherogenic property of LDL. Different from LDL, high-density lipoprotein (HDL) and its major apolipoprotein, apoA-I, counteract atherosclerosis by reversing cholesterol transport, inhibiting inflammatory cell adhesion to plaques, maintaining endothelial integrity, inhibiting oxidation, and as has recently been shown, suppressing hematopoietic stem cell (HSC) proliferation. As inflammatory cells in atherosclerotic plaques are exclusively derived from hematopoietic stem/progenitor cells (HSPC) in bone marrow (BM), we hypothesized that differential effects of LDL and HDL on HSPC proliferation and differentiation may play a role in atherosclerotic plaque development. We explored the effect of HDL and LDL on HSPC number and function using LDL receptor knockout (LDLr ko) mice, fed with high fat diet, and C57BL/6 mice infused with purified apoA-I and or reconstituted (r)HDL. Compared to mice on normal diet, the number of lineage−/cKit+Sca-1+ (KLS) cells was 5-fold higher in LDLr ko mice on high-fat diet. By contrast, infusion of either 8 mg/kg apoA-I or 8, 12 and 16 mg/kg rHDL decreased the KLS cell frequency in BM. Using BrdU incorporation, we demonstrated that LDL induced but HDL inhibited KLS cell proliferation. When lineage negative cells, exposed to LDL or rHDL were used in competitive repopulation studies, HDL-treated cells supported greater chimerism than untreated controls, whereas LDL-treated cells competed less well. In addition, for HDL-treated Lin− cells, skewing of reconstitution to the B-lymphoid lineage at the expense of the granulocyte/monocyte lineage was seen. In vitro, LDL promoted KLS cell differentiation towards the monocytic lineage, which was abrogated by addition of HDL. In conclusion, LDL and HDL have opposing effects on HSPC number and function. These differential effects may contribute to the opposing effects of HDL and LDL on atherosclerosis development. Disclosures: No relevant conflicts of interest to declare.
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Nadhira, Aulia Ninggar, Ida Nurwati, and Dyah Ratna Budiani. "Efek Ekstrak Etanolik Daun Kelor Terhadap Kadar HDL, Kadar LDL, serta Ketebalan Aorta Tikus Wistar Model Sindrom Metabolik." Plexus Medical Journal 2, no. 1 (March 5, 2023): 1–8. http://dx.doi.org/10.20961/plexus.v2i1.219.
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Pendahuluan: Daun kelor diketahui memiliki potensi menurunkan gejala sindrom metabolik. Kriteria sindrom metabolik antara lain yait terdapat penurunan HDL, peningkatan LDL, dan penebalan dinding aorta. Tujuan penelitian ini adalah mengetahui pengaruh pemberian ekstrak etanolik daun kelor terhadap kadar HDL, kadar LDL, dan ketebalan aorta tikus wistar jantan model sindrom metabolik. Metode: Penelitian bersifat eksperimental laboratorik menggunakan lima kelompok, yaitu KKN diberi pakan standar; KKP, KP1, KP2, dan KP3 diberi pakan tinggi lemak selama 28 hari dan injeksi STZ-NA pada hari ke-25. Kelompok perlakuan (KP) diberikan dosis ekstrak etanolik daun kelor masing-masing 150; 250; dan 350 mg/kgBB/hari. Kadar HDL dan LDL diukur pada hari ke-0, 25, 28, dan 57. Terminasi pada hari ke-57, aorta pars thoracica diberi pengecatan HE. Kadar HDL dan LDL dianalisis menggunakan paired t-test. Kadar HDL, LDL, dan ketebalan aorta dianalisis menggunakan one-way ANOVA dilanjutkan post hoc Tukey HSD. Hasil: Hasil paired t-test terdapat perbedaan bermakna antara kadar HDL dan LDL sebelum dan setelah pemberian ekstrak. Hasil one-way ANOVA dan post hoc Tukey HSD, kadar HDL dan LDL terdapat perbedaan bermakna antar kelompok sedangkan ketebalan aorta tidak terdapat perbedaan bermakna antar kelompok. Kesimpulan: Ekstrak etanolik daun kelor dosis 150; 250; dan 350 mg/kgBB/hari dapat meningkatkan kadar HDL dan menurunkan kadar LDL, tetapi tidak berpengaruh terhadap ketebalan aorta tikus wistar jantan model sindrom metabolik.
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Sarjana, Guruh, and Deny Yudi Fitranti. "PENGARUH PEMBERIAN JUS KULIT DELIMA MERAH (Punica granatum) TERHADAP KADAR LDL DAN HDL WANITA DISLIPIDEMIA." Journal of Nutrition College 3, no. 4 (October 27, 2014): 538–46. http://dx.doi.org/10.14710/jnc.v3i4.6848.
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Latar Belakang : Dislipidemia merupakan salah satu faktor risiko terjadinya penyakit jantung dan pembuluh darah. Kulit delima mengandung anthocyanin yang dapat meningkatkan kadar HDL dan menurunkan kadar LDL. Penelitian ini bertujuan untuk mengetahui perbedaan kadar LDL dan HDL wanita usia 30-49 tahun yang diberi dan tidak diberi jus kulit delima (Punica granatum). Metode : Penelitian ini merupakan penelitian quasi experimental dengan rancangan pre-post control group design. Subjek adalah wanita dislipidemia dengan kadar kolesterol LDL > 130 mg/dl dan kadar kolesterol HDL < 40 mg/dl, Kelompok perlakuan mendapat 25 g/hari jus kulit delima dan kelompok kontrol mendapat plasebo. Perlakuan dilakukan selama 14 hari. Metode phosphotungstic precipilation digunakan untuk menganalisis kadar kolesterol HDL dan LDL sebelum dan setelah perlakuan, darah diambil setelah subjek berpuasa selama 10 jam. Uji beda kadar LDL dan HDL sebelum dan setelah perlakuan pada kelompok perlakuan menggunakan uji dependent t-test dan uji beda kadar kolesterol LDL dan HDL sebelum dan setelah perlakuan pada kelompok kontrol menggunakan uji non parametric Wilcoxon. Uji regresi linier berganda dilakukan untuk memprediksi besar pengaruh asupan zat gizi dan aktifitas fisik terhadap kadar LDL dan HDL.Hasil : : Dislipidemia sebagian besar terdapat pada wanita usia 40-49 tahun dan status gizi overweight sebesar 24,7% dan obesitas 25,55%. Aktivitas fisik subjek pada kelompok perlakuan 100% dalam kategori sedang, sedangkan pada kelompok kontrol 37,5% dalam kategori rendah dan 62,5% dalam kategori sedang. Rerata penurunan kadar kolesterol LDL pada kelompok perlakuan sebesar 2,52+31,86 mg/dl dan kelompok kontrol sebesar 4,56+25,23 mg/dl. Rerata penurunan kadar kolesterol LDL antara kelompok perlakuan dan kontrol tidak terdapat perbedaan (p>0,05).Rerata perubahan kadar kolesterol HDL pada kelompok perlakuan sebesar 0,00+6,80 mg/dl dan kelompok kontrol sebesar 2,25+3,80 mg/dl. Rerata perubahan kadar kolesterol HDL antara kelompok perlakuan dan kontrol tidak terdapat perbedaan (p>0,05). Perubahan kadar LDL 61,5% dipengaruhi oleh asupan protein. Perubahan kadar HDL 26,1% dipengaruhi oleh asupan serat.Kesimpulan : Pemberian jus kulit buah delima selama 14 hari dengan dosis 25 gram/hari pada wanita dislipidemia tidak berpengaruh terhadap kadar LDL dan HDL. Namun terjadi penurunan kadar LDL sebesar 2,52 mg/dl sedangkan kadar HDL tidak terjadi perubahan.
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., Adi Priyana. "PETANDA KEBAHAYAAN (RISIKO) PENYAKIT JANTUNG KORONER TERKAIT LDL." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 14, no. 3 (March 16, 2018): 102. http://dx.doi.org/10.24293/ijcpml.v14i3.931.
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Atherosclerosis is the most common cause of coronary heart disease (CHD), and it is still the primary cause of death in Indonesia and most industrialized countries. The conventional risk factor for atherosclerosis and CHD are diabetes mellitus, hypertension, dyslipidemiaand smoking. On the other hand, Lp (a), homocystein and small dense LDL (sd-LDL) have been considered as novel risk factors for CHDLow of high density lipoprotein (HDL), high of low density cholesterol (LDL-c) and high homocystein as part of dyslipidemia, has beenconsidered as independent risk factor for CHD.The principal objective of the present study was to compare between HDL-c, Lp (a), andsd-LDL and homocystein as a risk marker of CHD. The study subject were divided into two groups, risk group consist of 94 subjects whohad > 2 CHD risk factors and control group recruited 49 subject who had no CHD risk factors. Both groups had fasted for 10-12 hourbefore their sera were collected. The sera were examined for HDL-c, Lp (a), sd-LDL and homocystein. Four alternative multivariate modelwere compared: sd-LDL, sd-LDL + HDL-c, sd-LDL, HDL-c + Lp (a) and sd-LDL, HDL-c + sd-LDL + Lp (a) + homocystein. Result of thistudy showed that the sd-LDL had the most significant and accurate as risk marker for CHD. Lp (a), HDL-c and homocystein were lessaccurate if used as risk marker for CHD compare with sd-LDL. Small dense LDL is an accurate risk marker for CHD. Further study musbe done using larger sample size of CHD subjects with similar age between risk and control groups.
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Mackness, M. I., C. Abbott, S. Arrol, and P. N. Durrington. "The role of high-density lipoprotein and lipid-soluble antioxidant vitamins in inhibiting low-density lipoprotein oxidation." Biochemical Journal 294, no. 3 (September 15, 1993): 829–34. http://dx.doi.org/10.1042/bj2940829.
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1. The oxidation of low-density lipoprotein (LDL) is believed to play a central role in atherogenesis. We have compared the effect of antioxidant vitamins and high-density lipoprotein (HDL) on the Cu(2+)-catalysed oxidation of LDL. 2. Antioxidant vitamin supplementation significantly reduced conjugated diene formation but did not affect the formation of lipid peroxides. 3. Conversely, HDL did not affect conjugated diene formation but inhibited the formation of lipid peroxides by up to 90%. 4. The inhibition by HDL of lipid peroxide formation in oxidized LDL was dependent on the concentration of HDL and was not due to HDL chelating Cu2+. 5. Large interindividual variations in the inhibition of lipid peroxide formation by autologous HDL were evident, which were related to the rate of lipid peroxide generation in the LDL. 6. We conclude that HDL is a powerful antioxidant or more probably inhibitor of LDL oxidation in vitro and may play an important role in vivo in preventing atherosclerosis by inhibiting LDL oxidation in the artery wall.
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Ciplak, Sibel, Ahmet Adiguzel, Yusuf Ziya Deniz, Melike Aba, and Unal Ozturk. "The Role of the Low-Density Lipoprotein/High-Density Lipoprotein Cholesterol Ratio as an Atherogenic Risk Factor in Young Adults with Ischemic Stroke: A Case—Control Study." Brain Sciences 13, no. 8 (August 9, 2023): 1180. http://dx.doi.org/10.3390/brainsci13081180.
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Dyslipidemia is a major atherogenic risk factor for ischemic stroke. Stroke patients tend to have high levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C). Therefore, it is noteworthy that there has been an increase in ischemic stroke cases in young and elderly individuals in recent years. This study investigated the TC/HDL-C ratio and the LDL-C/HDL-C ratio, which may be more specific and common lipid parameters in young patients with ischemic stroke. This study aimed to demonstrate the sensitivity and specificity of TC/HDL-C and LDL-C/HDL-C ratios as atherogenic markers for young adult ischemic strokes. This trial was conducted as a retrospective case—control study. A total of 123 patients (patient group) and 86 healthy individuals (control group) aged 18–50 years were randomly selected from four different hospitals. Lipid parameters and TC/HDL-C and LDL-C/HDL-C ratios were compared between these two groups. The mean age was 38.8 ± 7.3 years in patients and 37.7 ± 9 years in controls (p > 005). The HDL-C levels were 39.1 ± 10.8 mg/dL in patients and 48.4 ± 13.8 mg/dL in controls (p < 0.001). LDL-C/HDL-C ratios were 3.23 ± 1.74 and 2.38 ± 0.87, and TC/HDL-C ratios were 5.24 ± 2.31 and 4.10 ± 1.25 in the patient and control groups, respectively (p < 0.001). The LDL-C/HDL-C and TC/HDL-C cutoff values in ROC analyses were 2.61 and 4.40 respectively; the AUCs (95% CI) were determined to be 0.680 (0.608–0.753) and 0.683 (0.610–0.755) (p < 0.001), respectively. An increased risk of stroke was observed in those with a high LDL-C/HDL-C ratio (OR = 1.827; 95% CI = 1.341–2.488; p < 0.001). Our study obtained similar results when we compared the mean TC and LDL-C levels between the two groups. However, considering the TC/HDL-C and LDL-C/HDL-C ratios, it is noteworthy that there was a significant difference between the patient and control groups.
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Langlois, Michel R., M. John Chapman, Christa Cobbaert, Samia Mora, Alan T. Remaley, Emilio Ros, Gerald F. Watts, et al. "Quantifying Atherogenic Lipoproteins: Current and Future Challenges in the Era of Personalized Medicine and Very Low Concentrations of LDL Cholesterol. A Consensus Statement from EAS and EFLM." Clinical Chemistry 64, no. 7 (July 1, 2018): 1006–33. http://dx.doi.org/10.1373/clinchem.2018.287037.
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Abstract BACKGROUND The European Atherosclerosis Society–European Federation of Clinical Chemistry and Laboratory Medicine Consensus Panel aims to provide recommendations to optimize atherogenic lipoprotein quantification for cardiovascular risk management. CONTENT We critically examined LDL cholesterol, non-HDL cholesterol, apolipoprotein B (apoB), and LDL particle number assays based on key criteria for medical application of biomarkers. (a) Analytical performance: Discordant LDL cholesterol quantification occurs when LDL cholesterol is measured or calculated with different assays, especially in patients with hypertriglyceridemia >175 mg/dL (2 mmol/L) and low LDL cholesterol concentrations <70 mg/dL (1.8 mmol/L). Increased lipoprotein(a) should be excluded in patients not achieving LDL cholesterol goals with treatment. Non-HDL cholesterol includes the atherogenic risk component of remnant cholesterol and can be calculated in a standard nonfasting lipid panel without additional expense. ApoB more accurately reflects LDL particle number. (b) Clinical performance: LDL cholesterol, non-HDL cholesterol, and apoB are comparable predictors of cardiovascular events in prospective population studies and clinical trials; however, discordance analysis of the markers improves risk prediction by adding remnant cholesterol (included in non-HDL cholesterol) and LDL particle number (with apoB) risk components to LDL cholesterol testing. (c) Clinical and cost-effectiveness: There is no consistent evidence yet that non-HDL cholesterol-, apoB-, or LDL particle-targeted treatment reduces the number of cardiovascular events and healthcare-related costs than treatment targeted to LDL cholesterol. SUMMARY Follow-up of pre- and on-treatment (measured or calculated) LDL cholesterol concentration in a patient should ideally be performed with the same documented test method. Non-HDL cholesterol (or apoB) should be the secondary treatment target in patients with mild to moderate hypertriglyceridemia, in whom LDL cholesterol measurement or calculation is less accurate and often less predictive of cardiovascular risk. Laboratories should report non-HDL cholesterol in all standard lipid panels.
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Shawa, Hassan, Ferhat Deniz, Hadil Bazerbashi, Mike Hernandez, Rena Vassilopoulou-Sellin, Camilo Jimenez, and Mouhammed Amir Habra. "Mitotane-Induced Hyperlipidemia: A Retrospective Cohort Study." International Journal of Endocrinology 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/624962.
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Limited data are available about mitotane-nduced hyperlipidemia. We retrospectively analyzed lipid data in 38 patients with adrenocortical carcinoma (ACC) who received mitotane therapy with emphasis on HDL cholesterol (HDL-c) and clinical predictors of lipid changes. At baseline, the mean levels of HDL-c, LDL-c, and triglycerides were 53.3 mg/dL, 114.4 mg/dL, and 149 mg/dL, respectively. HDL-c, LDL-c, and triglyceride concentrations significantly increased with mitotane therapy to a mean HDL peak (HDL-P) of 86.3 mg/dL (P<0.001), a mean LDL peak of 160.1 mg/dL (P<0.001), and a mean triglyceride peak (Tg-P) of 216.7 mg/dL (P=0.042). HDL-P positively correlated with mitotane concentration (r=0.52,P<0.001), while LDL-P levels and Tg-P did not. Gender, body mass index, cortisol overproduction, baseline levels of HDL-c, and triglyceride did not predict change in HDL-c. Similar changes were noticed in subgroup analysis after excluding patients who were using lipid-lowering agents. In conclusion, in ACC patients, mitotane caused significant increases in HDL-c that may counteract the deleterious atherosclerotic effects of LDL-c and Tg rise. Understanding the mechanism of HDL change may lead to the discovery of novel HDL-c-elevating drugs.
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Aoua, Hanene, Ymène Nkaies, Ali Ben Khalfallah, Mohsen Sakly, Ezzedine Aouani, and Nebil Attia. "Association between Small Dense Low-Density Lipoproteins and High-Density Phospolipid Content in Patients with Coronary Artery Disease with or without Diabetes." Laboratory Medicine 51, no. 3 (October 17, 2019): 271–78. http://dx.doi.org/10.1093/labmed/lmz067.
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Abstract Objective To evaluate the phospholipid profile in total plasma, non–high-density lipoprotein (HDL), and HDL fractions. We tried to correlate the phospholipid profile to low-density lipoprotein (LDL) size, as reflected by cholesterol content in each LDL subclass. Methods We measured small dense LDL-C levels after heparin-magnesium precipitation and measured high-density lipoprotein phospholipid (HDL-P) levels using a colorimetric enzymatic method. Results The correlation of the phospholipid profile to small dense LDL-C (sdLDL-C) in patients with coronary problems showed a negative association between small dense low-density lipoprotein (sdLDL) and HDL-P (r = −0.73; P = .02). Moreover, a strong positive correlation was detected between TG and the ratio HDL-P/HDL-C (r = 0.83; P <.001). Conclusions HDL phospholipid has an antiatherogenic effect in coronary artery disease with or without diabetes. Further, large LDL modulation seems to be associated with diabetes rather than coronaropathy.
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Wang, Yanan, Chenchen Wei, Quhong Song, Junfeng Liu, Yajun Cheng, Yisong Li, Bo Wu, and Ming Liu. "Reduction in the Ratio of Low-density Lipoprotein Cholesterol to Highdensity Lipoprotein Cholesterol is Associated with Increased Risks of Hemorrhagic Transformation in Patients with Acute Ischemic Stroke." Current Neurovascular Research 16, no. 3 (September 17, 2019): 266–72. http://dx.doi.org/10.2174/1567202616666190619151914.
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Background and Purpose: Hemorrhagic transformation (HT) is a potentially serious complication in patients with acute ischemic stroke (AIS). Whether the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (LDL-C/HDL-C) is associated with HT remains unclear. Methods: Ischemic stroke patients within 7 days of stroke onset from January 2016 to November 2017 were included in this study. Lipid profiles were measured within 24h after admission. HT was determined by a second computed tomography or magnetic resonance imaging within 7 days after admission. Univariate and multivariate logistic regression analysis was used to assess the association between LDL-C/HDL-C and HT. Results: We enrolled 1239 patients with AIS (788 males; mean age, 64 ± 15 years), of whom 129 (10.4%) developed HT. LDL-C/HDL-C was significantly lower on admission in patients with HT than those without HT (2.00 ± 0.89 vs. 2.25 ± 1.02, P=0.009). The unadjusted odds ratio (OR) of low LDL-C/HDL-C for HT was 2.07 (95% confidence interval [CI] 1.42-3.01, P＜0.001). After adjustment for possible confounders, lower LDL-C/HDL-C (≤1.52) was significantly associated with HT (OR 1.53, 95% CI: 1.02-2.31, P=0.046). Similar results were observed between lower LDL-C (≤ 4 mmol/L) and HT (OR 4.17, 95% CI: 1.25-13.90, P=0.02). However, no significant association was found between HT and high HDL-C, low triglycerides or low total cholesterol. Conclusion: Lower LDL-C/HDL-C and LDL-C were significantly associated with increased risk of HT after AIS. Further investigations are warranted to confirm these findings and then optimize lipid management in stroke patients with lower LDL/HDL-C or LDL-C.
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Kartikasari, Nur Indah, and Ahmad Syauqy. "PERBEDAAN KADAR KOLESTEROL LDL DAN HDL SEBELUM DAN SESUDAH PEMBERIAN JUS KACANG HIJAU (Phaseolus radiatus Linn) PADA PRIA DISLIPIDEMIA." Journal of Nutrition College 3, no. 4 (October 27, 2014): 698–705. http://dx.doi.org/10.14710/jnc.v3i4.6870.
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Latar belakang : Dislipidemia merupakan salah satu faktor risiko dari penyakit kardiovaskuler. Kacang hijau mengandung isoflavon, protein, dan serat yang diketahui dapat menurunkan kadar kolesterol LDL dan meningkatkan kolesterol HDL. Tujuan : Mengetahui perbedaan kadar kolesterol LDL dan HDL sebelum dan sesudah pemberian jus kacang hijau.Metode : Penelitian ini merupakan pretest - post test with control group design. Subjek adalah 28 pria dengan kadar kolesterol LDL 130-189 mg/dl dan kadar kolesterol HDL <60 mg/dl. Kelompok perlakuan mendapatkan jus kacang hijau 400 ml dan kelompok kontrol mendapatkan air minum kemasan selama 21 hari. Kelompok perlakuan dan kelompok kontrol diberikan konseling gizi sebelum intervensi. Kadar kolesterol LDL dan HDL diukur dengan menggunakan metode formula Friedewald dan phosphotungstic precipitation. Data dianalisis menggunakan uji Dependent t-test, Independent t-tes, Mann Whitney, dan Fisher.Hasil : Pemberian jus kacang hijau 400 ml selama 21 hari pada kelompok perlakuan dapat menurunkan kadar LDL (-17,49±22,61) dan meningkatkan kadar kolesterol HDL (8,87±5,24) secara bermakna. Pada kelompok kontrol, terdapat penurunan yang tidak signifikan terhadap kadar kolesterol LDL (-0,83±24,30) dan terdapat peningkatan yang signifikan terhadap kadar kolesterol HDL (2,84±4,60). Terdapat perbedaan rerata perubahan kadar kolesterol HDL (p=0,003) antara kelompok kontrol dengan kelompok perlakuan, tetapi tidak terdapat perbedaan rerata perubahan kolesterol LDL (p=0,072) antara kelompok kontrol dengan kelompok perlakuanSimpulan : Pemberian jus kacang hijau 400ml/hari selama 21 hari tidak menurunkan kadar kolesterol LDL secara signifikan, tetapi meningkatkan kadar kolesterol HDL secara signifikan.
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Mascarenhas-Melo, Filipa, José Sereno, Edite Teixeira-Lemos, Sandra Ribeiro, Petronila Rocha-Pereira, Ethan Cotterill, Frederico Teixeira, and Flávio Reis. "Markers of Increased Cardiovascular Risk in Postmenopausal Women: Focus on Oxidized-LDL and HDL Subpopulations." Disease Markers 35 (2013): 85–96. http://dx.doi.org/10.1155/2013/724706.
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Objective. To evaluate the effect of gender and menopause in cardiovascular risk (CVR) in a healthy population based on both classical and nontraditional markers.Methods. 56 men and 68 women (48 pre- and 20 postmenopause) were enrolled in the study. The following markers were analyzed: blood pressure (BP), body mass index (BMI), waist circumference (WC), glucose, total cholesterol (total-c), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-c), oxidized-LDL (Ox-LDL), HDL-c and subpopulations, paraoxonase-1 activity, hsCRP, uric acid, tumor necrosis factor alpha (TNF-α), adiponectin, vascular endothelial growth factor (VEGF), and intercellular adhesion molecular 1 (ICAM1).Results.Relative to the women, men present significantly increased BMI, WC, BP, glucose, total-c, TGs, LDL-c, Ox-LDL, uric acid, and TNF-αand reduced adiponectin and total and large HDL-c. The protective profile of women is lost after menopause with a significantly increased BMI, WC, BP, glucose, LDL-c, Ox-LDL, hsCRP, and VEGF and decreased total and large HDL-c. Significant correlations were found in women population and in postmenopausal women between Ox-LDL and total, large, and small HDL-c and between TNF-αand total, large, and small HDL-c, LDL-c, and Ox-LDL.Conclusions. Men present higher CVR than women who lost protection after menopause, evidenced by nontraditional markers, including Ox-LDL and HDL subpopulations.
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Stokic, Edita, and Jela Marinkov. "Treatment of low HDL-cholesterol levels in the reduction of cardiovascular risk." Medical review 60, no. 3-4 (2007): 145–50. http://dx.doi.org/10.2298/mpns0704145s.
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Introduction. Although reduction of LDL-C levels is a priority in the treatment of dyslipidemia, not all coronary events are prevented despite aggressive LDL-C lowering, and risk reduction can be improved by treating additional lipid abnormalities. The Framingham Study was the first to demonstrate the inverse relationship between HDL-C and risk of coronary heart disease (CHD). This relationship was present at all levels of LDL-C, whereas the highest risk was associated with low HDL-C and high LDL-C. The antiatherogenic actions of HDL-cholesterol. The antiatherogenic actions of HDL-C are complex. HDL-C plays a major role in reverse cholesterol transport, mobilizing cholesterol from the periphery to the liver. In addition, cardioprotective effects of HDL-C include endothelial protection, anti-inflammatory activity, as well as antioxidant and antithrombotic effects. Treatment of low HDL cholesterol. In addition to lowering LDL-C, statins increase HDL-C by 5 to 15% by increasing apolipoprotein A-I synthesis. Fibrate therapy results in an increase in HDL-C of 10 to 25 % by activating PPAR-, which stimulates hepatic apolipoprotein A-I gene expression. Niacin is the most effective agent used for increasing HDL-C, causing increase of 15 to 35%. The side effects of niacin therapy, which is largely mediated by prostaglandins, may be minimized by the use of prolonged-release formulation of nicotinic acid. Combination therapy with HDL-raising agents, such as nicotinic acid and statin, markedly increases HDL-C, lowers LDL-C and improves the lipoproteins subclass distribution. Conclusion. New therapeutic modalities in the treatment of low HDL-C and lowering LDL-C, either in combination or as a monotherapy, may provide additional benefits in reducing CHD risk. .
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Adam, Leonie, and Thomas Bobbert. "Non-HDL-Cholesterin." Diabetes aktuell 18, no. 06 (October 2020): 242–46. http://dx.doi.org/10.1055/a-1237-6894.
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ZUSAMMENFASSUNGDie diabetische Stoffwechsellage korreliert häufig mit einer Dyslipidämie, die sich typischerweise durch erhöhte Triglyzeride, niedriges HDL-Cholesterin und eine hohe Konzentration an small dense LDL-Cholesterin (LDL: low-density lipoprotein) auszeichnet. Zur kardiovaskulären Risikostratifizierung bei Diabetes mellitus Typ 2 eignet sich die Verwendung von Non-HDL-Cholesterin (HDL: high-density lipoprotein), um sämtliche potenziell atherogene Lipoproteine – VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein), LDL, Lipoprotein(a), Chylomikronen, Remnants – zu erfassen.
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Rütti, Sabine, Jan A. Ehses, Rahel A. Sibler, Richard Prazak, Lucia Rohrer, Spiros Georgopoulos, Daniel T. Meier, et al. "Low- and High-Density Lipoproteins Modulate Function, Apoptosis, and Proliferation of Primary Human and Murine Pancreatic β-Cells." Endocrinology 150, no. 10 (July 23, 2009): 4521–30. http://dx.doi.org/10.1210/en.2009-0252.
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Abstract A low high-density lipoprotein (HDL) plasma concentration and the abundance of small dense low-density lipoproteins (LDL) are risk factors for developing type 2 diabetes. We therefore investigated whether HDL and LDL play a role in the regulation of pancreatic islet cell apoptosis, proliferation, and secretory function. Isolated mouse and human islets were exposed to plasma lipoproteins of healthy human donors. In murine and human β-cells, LDL decreased both proliferation and maximal glucose-stimulated insulin secretion. The comparative analysis of β-cells from wild-type and LDL receptor-deficient mice revealed that the inhibitory effect of LDL on insulin secretion but not proliferation requires the LDL receptor. HDL was found to modulate the survival of both human and murine islets by decreasing basal as well as IL-1β and glucose-induced apoptosis. IL-1β-induced β-cell apoptosis was also inhibited in the presence of either the delipidated protein or the deproteinated lipid moieties of HDL, apolipoprotein A1 (the main protein component of HDL), or sphingosine-1-phosphate (a bioactive sphingolipid mostly carried by HDL). In murine β-cells, the protective effect of HDL against IL-1β-induced apoptosis was also observed in the absence of the HDL receptor scavenger receptor class B type 1. Our data show that both LDL and HDL affect function or survival of β-cells and raise the question whether dyslipidemia contributes to β-cell failure and hence the manifestation and progression of type 2 diabetes mellitus.
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Damirin, Alatangaole, Hideaki Tomura, Mayumi Komachi, Jin-Peng Liu, Chihiro Mogi, Masayuki Tobo, Ju-Qiang Wang, et al. "Role of lipoprotein-associated lysophospholipids in migratory activity of coronary artery smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (May 2007): H2513—H2522. http://dx.doi.org/10.1152/ajpheart.00865.2006.
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The migration of vascular smooth muscle cells (SMCs) is a hallmark of the pathogenesis of atherosclerosis and restenosis after angioplasty. Plasma low-density lipoprotein (LDL), but not high-density lipoprotein (HDL), induced the migration of human coronary artery SMCs (CASMCs). Among bioactive lipids postulated to be present in LDL, lysophosphatidic acid (LPA) appreciably mimicked the LDL action. In fact, the LDL-induced migration was markedly inhibited by pertussis toxin, an LPA receptor antagonist Ki-16425, and a small interfering RNA (siRNA) targeted for LPA1 receptors. Moreover, LDL contains a higher amount of LPA than HDL does. HDL markedly inhibited LPA- and platelet-derived growth factor (PDGF)-induced migration, and sphingosine 1-phosphate (S1P), the content of which is about fourfold higher in HDL than in LDL, mimicked the HDL action. The inhibitory actions of HDL and S1P were suppressed by S1P2 receptor-specific siRNA. On the other hand, the degradation of the LPA component of LDL by monoglyceride lipase or the antagonism of LPA receptors by Ki-16425 allowed LDL to inhibit the PDGF-induced migration. The inhibitory effect of LDL was again suppressed by S1P2 receptor-specific siRNA. In conclusion, LPA/LPA1 receptors and S1P/S1P2 receptors mediate the stimulatory and inhibitory migration response to LDL and HDL, respectively. The balance of not only the content of LPA and S1P in lipoproteins but also the signaling activity between LPA1 and S1P2 receptors in the cells may be critical in determining whether the lipoprotein is a positive or negative regulator of CASMC migration.
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Laksana, Iqbal, Purwo Sri Rejeki, Lilik Herawati, Mohammad Anam Al Arif, and Indrayuni Lukitra Wardhani. "High-Fat Diet Increases Serum HDL, but Not for LDL and HDL/LDL Ratio in MICE." Folia Medica Indonesiana 57, no. 2 (June 1, 2021): 117. http://dx.doi.org/10.20473/fmi.v57i2.16123.
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The use of a ketogenic diet with an increased proportion of fat is rampant lately, both as a therapy or even lifestyle. The use of a ketogenic diet is feared to cause dyslipidemia. It will also lead to atherosclerosis and thrombosis. This study aimed to determine the effect of a high-fat diet on HDL, LDL, and HDL/LDL ratio in mice. Thirty male Mus Musculus, 2-3 mo, 15-25 g divided into five groups diet. K1 (12% fat, 20% protein, 62% carb), K2 (30% fat, 60%protein), K3 (45% fat, 45% protein), K4 (60% fat, 30% protein) and K5 (75% fat, 15% protein) for 4 weeks. Feed and water by adlibitum. Blood for serum was taken from the ventricle, while in the measurement of HDL serum level, the LDL used ELISA. Normality of data analyzed by Shapiro Wilk, and homogeneity by Levene test. HDL serum was analyzed using equality test followed by Games Howell, LDL serum and ratio of HDL/LDL was tested by ANOVA followed by LSD with significance 0,05. HDL serum in K1 (62,50±9.94) mg/dL, K2 (78,40±18,76) mg/dL, K3 (79,00±3,81) mg/dL, K4 (80,00±2,16) mg/dL, and K5 (83,50±5,62) mg/dL with p<0,05 in K1, K2 to K3, K4 and K5. LDL serum in K1 (21,67± 4,80) mg/dL, K2 (23,00±12,70) mg/dL, K3 (18,40±4,34) mg/dL, K4 (24,00 ±1,83) mg/dL and K5 (22,00 ± 4,08) mg/dL with p>0,05. Ratio HDL/LDL K1 (3,01±0,91), K2 (4,10±1,86), K3 (4,53±1,5), K4 (3,35±0,34), and K5 (3,96 ± 1,25) with p>0,05.
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Ikhsan, Mohd, and Tatik Mulyati. "PENGARUH PEMBERIAN NATA DE COCO TERHADAP KADAR KOLESTEROL LDL DAN HDL PADA WANITA DISLIPIDEMIA." Journal of Nutrition College 2, no. 2 (May 30, 2013): 242–49. http://dx.doi.org/10.14710/jnc.v2i2.2749.
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Latar Belakang : Kadar kolesterol LDL yang tinggi dan HDL yang rendah berkaitan dengan penyebab utama terjadinya penyakit jantung dan pembuluh darah. Serat diketahui dapat menurunkan kadar kolesterol LDL serta meningkatkan kolesterol HDL. Nata de coco mengandung selulosa, hemiselulosa dan lignin yang memiliki efek hipokolesterolemia dalam darah.Metode : Jenis penelitian adalah true experimental dengan rancangan control group pre-test-post-test. Sebanyak 52 wanita dengan kadar kolesterol LDL ≥100 mg/dl dan HDL ≤50 mg/dl menjadi subyek dalam penelitian ini. Subyek dibagi menjadi 3 kelompok, yaitu kelompok kontrol, perlakuan 1 mendapat 160 g nata de coco/hari (serat 4.8 g) dan perlakuan 2 mendapat 320 g nata de coco/hari (serat 9.6 g). Intervensi dilakukan selama 14 hari. Metode phosphotungstic precipilation digunakan untuk menganalisis kadar HDL sementara kadar LDL dianalisis mengunakan rumus Friedewald. Darah diambil setelah subyek berpuasa selama 10 jam. Analisis statistik yang digunakan antara lain paired-samples t test, ANOVA dan Kruskal-Wallis. Hasil : Konsumsi nata de coco sebanyak 160 g/hari dan 320 g/hari berturut-turut menurunkan kadar kolesterol LDL sebanyak 4.47% (p=0.091) dan 6.25% (p=0.044) serta meningkatkan kadar kolesterol HDL sebanyak 12.1% (p=0.001) dan 3.6% (p=0.361). Tidak terdapat perbedaan pengaruh pemberian nata de coco terhadap perubahan kadar kolesterol LDL antar kedua kelompok (p=0.863), namun terdapat pengaruh yang bermakna terhadap kolesterol HDL antar kedua kelompok (p=0.043). Sedangkan pada kelompok kontrol terjadi peningkatan kadar kolesterol LDL sebebesar 2.54% (p=0.005) dan penurunan kadar kolesterol HDL sebesar 0,56% (p=0.570).Kesimpulan : Konsumsi nata de coco sebanyak 320 g/hari berpengaruh terhadap penurunan kadar kolesterol LDL secara bermakna sedangkan pemberian nata de coco sebanyak 160 g/hari berpengaruh terhadap peningkatan kolesterol HDL secara bermakna.Kata kunci : nata de coco; kolesterol LDL; kolesterol HDL; wanita; dislipidemia.
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Ben Tekaya, A., E. Hannech, A. Fendri, S. Boukriba, O. Saidane, S. Bouden, R. Leila, et al. "AB0848 ATHEROGENIC INDEX IS THE BEST DETERMINANT OF SUBCLINICAL ATHEROSCLEROSIS IN SPONDYLOARTHRITIS PATIENTS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1549.2–1549. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3840.
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BackgroundBlood lipid levels particularly total cholesterol (CT), low-density lipoprotein cholesterol (C-LDL), high-density lipoprotein cholesterol (C-HDL), and triglycerides (TG), are commonly used to predict cardiovascular risk. However, it has been demonstrated that atherogenic index (CT/HDL, C-LDL/C-HDL) are prognostic indicators of atherosclerosis [1].ObjectivesThe purpose of our study was to determine the role of lipid indicators in predicting subclinical atherosclerosis among SpA patients.MethodsIt was a cross sectional study over a period of 12 months including patients with established SpA (ASAS Criteria). They were cardiovascular disease free. Lipid analyses were performed for all patients including the determination of: C-LDL, C-HDL, CT, and TG. The ratios CT/C-HDL, C-LDL/C-HDL were calculated. Atherosclerosis was assessed by Doppler ultrasound with measurement of the carotid Intima-Media Thickness (cIMT).ResultsThere were 47 SpA patients: 14 female (28.8%) and 33 male (70.2%). The median age was 36 years (18-50). The median disease duration was 11 years (1-32). The median lipid factors levels were respectively 3.66 mmol/l (2.27-6.34) for CT, 0.84 mmol/l (0.43-2.88) for TG, 2.17 mmol/l (0.93-3.9) for C-LDL, and 1.08 mmol/l (0.63-1.49) for C-HDL. The median CT/C-HDL, C-LDL/C-HDL ratios were respectively 3.48 (2.21-6.79) and 1.99 (0.86-3.77). There were 17% of patients with a high ratio CT/C-HDL (>4.5) and 9.3% of patients with high ratio C-LDL/C-HDL (>3.22).The median cIMT was 0.55 millimeters (0.32-0.83). cIMT was positively correlated with low linearity with CT (p=0.007; r=0.404) and with the CT/C-HDL ratio (p=0,028; r=0.34).ConclusionIn our study, CT/HDL ratio and CT were the best determinant of subclinical atherosclerosis in SpA patients.References[1]Acevedo M, Krämer V, Tagle R, Corbalán R, Arnaíz P, Berríos X, Navarrete C. Total/HDL cholesterol ratio and non HDL cholesterol as predictors for increased intima media thickness. Rev Med Chil. 2012;140(8):969-76.Disclosure of InterestsNone declared
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Patricia, Venny, Nining Kurniati, Citra Trisna, and Nana Munawar. "Description of The Risk Level of Heart Disease to The Ratio of LDL/HDL Patients at Rsud Dr. Adjidarmo." Journal of Noncommunicable Diseases Prevention and Control 1, no. 1 (April 30, 2023): 8–12. http://dx.doi.org/10.61843/jondpac.v1i1.497.
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The increased risk of stroke is associated with high low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, and a high ratio of LDL and HDL cholesterol, and will be amplified if other stroke risk factors are present. The purpose of this study was to determine the ratio of LDL and HDL cholesterol in patients at RSUD Dr. Adjidarmo. The research design is descriptive research. With a total population of 150 people, a sample of 20% of the population, namely 30 people, was taken. The data collection technique in this study was primary data, namely through the medical records of heart patients who had received outpatient care at the Cardiac and Vascular Polyclinic at RSUD Dr. Adjidarmo Rangkasbitung. The data analysis technique was performed by entering data into tables and calculating the ratio between LDL and HDL for the group of patients at risk of heart disease based on the ratio obtained. The results of the study of the 30 respondents who were examined gave an overview of the results of the examination, with low risk LDL/HDL ratio values (low risk) of 21 people (70%); the average risk LDL/HDL ratio was 5 people (16.67%); the moderate risk LDL/HDL ratio was 1 person (3.3%); and the high risk LDL/HDL ratio was 3 people (10%). Patients who have a risk of developing coronary heart disease are 16 men (53.3%) and 14 women (46.7%). The average age of patients with coronary heart disease is over 50 in men and over 39 in women.
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Edes, Ashley N., Janine L. Brown, and Katie L. Edwards. "Testing lipid markers as predictors of all-cause morbidity, cardiac disease, and mortality risk in captive western lowland gorillas (<i>Gorilla gorilla gorilla</i>)." Primate Biology 7, no. 2 (December 17, 2020): 41–59. http://dx.doi.org/10.5194/pb-7-41-2020.
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Abstract. Great apes and humans develop many of the same health conditions, including cardiac disease as a leading cause of death. In humans, lipid markers are strong predictors of morbidity and mortality risk. To determine if they similarly predict risk in gorillas, we measured five serum lipid markers and calculated three lipoprotein ratios from zoo-housed western lowland gorillas (aged 6–52 years, n=61, subset with routine immobilizations only: n=47): total cholesterol (TC), triglycerides (TGs), high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (apoA1), TC∕HDL, LDL∕HDL, and TG∕HDL. We examined each in relation to age and sex, then analyzed whether they predicted all-cause morbidity, cardiac disease, and mortality using generalized linear models (GLMs). Older age was significantly associated with higher TG, TC∕HDL, LDL∕HDL, and TG∕HDL, and lower HDL and apoA1. With all ages combined, compared to females, males had significantly lower TG, TC∕HDL, LDL∕HDL, and TG∕HDL, and higher HDL. Using GLMs, age, sex, and lower LDL∕HDL were significant predictors of all-cause morbidity; this is consistent with research demonstrating lower LDL in humans with arthritis, which was the second most prevalent condition in this sample. In contrast to humans, lipid markers were not better predictors of cardiac disease and mortality risk in gorillas, with cardiac disease best predicted by age and sex alone, and mortality risk only by age. Similar results were observed when multimodel inference was used as an alternative analysis strategy, suggesting it can be used in place of or in addition to traditional methods for predicting risk.
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Asmariani, Widitha Gustining, and Enny Probosari. "PENGARUH PEMBERIAN BUAH PEPAYA (Carica papaya L.) TERHADAP KADAR KOLESTEROL LDL DAN KOLESTEROL HDL PADA TIKUS SPRAGUE DAWLEY DENGAN HIPERKOLESTEROLEMIA." Journal of Nutrition College 1, no. 1 (October 4, 2012): 258–64. http://dx.doi.org/10.14710/jnc.v1i1.369.
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Background: Increased LDL cholesterol concentrations and low plasma HDL cholesterol concentrations are well-established risk factors for cardiovascular disease. Diet modification is one of recommended theraphy to decrease LDL cholesterol level by increasing fiber intake from fruit. Papaya contains niacin, fiber, and antioxidant which can decrease LDL cholesterol level. It also contains quercetin to increase HDL cholesterol level. The aim of this study was to prove the effect of papaya of different dosages on LDL and HDL cholesterol of hypercholesterolemic rats. Methods: This research was true-experimental using pre-post test with control group design. Subjects were male Sprague Dowley rats, 7-8 weeks old, 100-200 grams weight, inducted hypercholesterolemia, given papaya diet using 5,4 gr, 7,2 gr, and 9,0 gr dosage for 4 weeks. LDL cholesterol and HDL cholesterol were measured by direct method using LDL-C Select (DiaSys) reagent and CHOP-PAP methods respectively. Normality of the data was tested by Shapiro Wilks test. Data were analyzed by paired t test continued with One Way Anova.and post-hoc LSD. Result: The study revealed that papaya of dosage 5,4 gr/day decreased LDL cholesterol (p<0,05) significantly from 45,29±9,05 mg/dl to 30,29±5,31 mg/dl but nonsignificantly decrease HDL cholesterol level (p=0,930) from 25,71 ± 5,09 to 25,57 ± 3,59 mg/dl at the same dosage. Other dosage of 7,2 mg/day and 9,0 gr/day neither significantly decrease LDL cholesterol level nor increase HDL cholesterol level. Conclusion: Papaya couldn’t decreased LDL cholesterol and increased HDL cholesterol in hypercholesterolemic rats.
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Meyer, B. "HDL/LDL - wie hoch, wie niedrig?" DMW - Deutsche Medizinische Wochenschrift 137, no. 22 (May 22, 2012): 1174–76. http://dx.doi.org/10.1055/s-0032-1304996.
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WENDLING, PATRICE. "HDL Soared, LDL Dropped With Anacetrapib." Family Practice News 40, no. 20 (December 2010): 9. http://dx.doi.org/10.1016/s0300-7073(10)71244-5.
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Desch, Karl. "LDL vs HDL: a sticky situation." Blood 142, no. 13 (September 28, 2023): 1110–11. http://dx.doi.org/10.1182/blood.2023021854.
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Arsenault, Benoit J., Isabelle Lemieux, Jean-Pierre Després, Nicholas J. Wareham, Erik SG Stroes, John JP Kastelein, Kay-Tee Khaw, and S. Matthijs Boekholdt. "Comparison between Gradient Gel Electrophoresis and Nuclear Magnetic Resonance Spectroscopy in Estimating Coronary Heart Disease Risk Associated with LDL and HDL Particle Size." Clinical Chemistry 56, no. 5 (May 1, 2010): 789–98. http://dx.doi.org/10.1373/clinchem.2009.140939.
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Abstract Background: Gradient gel electrophoresis (GGE) and nuclear magnetic resonance (NMR) spectroscopy are both widely accepted methods for measuring LDL and HDL particle size. However, whether or not GGE- or NMR-measured LDL or HDL particle size predicts coronary heart disease (CHD) risk to a similar extent is currently unknown. Methods: We used GGE and NMR to measure LDL and HDL particle size in a nested case-control study of 1025 incident cases of CHD and 1915 controls from the EPIC (European Prospective Investigation into Cancer and Nutrition)-Norfolk study. The study sample included apparently healthy men and women age 45–79 years followed for an average of 6 years. Results: Pearson correlation coefficients showed that the overall agreement between NMR and GGE was better for the measurement of HDL size (r = 0.78) than for LDL size (r = 0.47). The odds ratio for future CHD among participants in the bottom tertile of LDL size (smallest LDL particles) was 1.35 (95% CI, 1.12–1.63) for GGE and 1.74 (1.41–2.15) for NMR. For HDL size, these respective odds ratios were 1.41 (1.16–1.72) and 1.85 (1.47–2.32). After adjustment for potential confounders, the relationship between small LDL or HDL particles and CHD was no longer significant, irrespective of the method. Conclusions: In this prospective population study, we found that the relationships between NMR-measured LDL and HDL sizes and CHD risk were slightly higher than those obtained with GGE.
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Edyanto, Ermia, and Niken Puruhita. "PERBEDAAN KADAR KOLESTEROL LDL DAN HDL ANTARA WANITA VEGETARIAN TIPE VEGAN DAN NON-VEGAN." Journal of Nutrition College 1, no. 1 (October 4, 2012): 134–43. http://dx.doi.org/10.14710/jnc.v1i1.433.
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ABSTRACTBackground: Studies which investigated different risk for cardiovascular disease in vegetarian reported that each vegetarian diet type had different lipid serum level. Elevated LDL cholesterol level and reduced HDL cholesterol level are independent risk factors for coronary heart disease. This study was aimed to compare levels on LDL and HDL cholesterol between vegetarian vegan and non-vegan.Methods: Two groups of vegetarian women, 23 people in each group of vegan and non-vegan, participated in this cross-sectional study. The data taken of each subject were nutrient intakes (total fat, PUFA, MUFA, SFA, cholesterol, and total fiber), physical activity, body weight, height, LDL and HDL cholesterol serum levels. Data were analyzed by Shapiro-Wilk test, independent-t test, Mann-Whitney test and ANACOVA test.Results: There were no significant differences on LDL and HDL cholesterol serum levels between vegetarian vegan and non-vegan, both before and after variables i.e age, physical activity, body mass index (BMI), amount of total fat, PUFA, MUFA, SFA, cholesterol, and total fiber adjusted (p > 0,05). LDL cholesterol levels for vegetarian vegan and non-vegan were respectively: 97,8 ± 54,87 mg/dl and 112,6 ± 36,03 mg/dl, while for HDL cholesterol, those levels were 54,9 ± 11,15 mg/dl and 55,2 ± 10,82 mg/dl. In multivariant analysis, the most influential variables on LDL cholesterol serum level were age (p = 0,001) and physical activity (p = 0,010), while for HDL serum cholesterol were BMI (p = 0,010) and total fat (p = 0,012). This study also found the significant difference of BMI between vegetarian vegan and non-vegan (p = 0,011), whose for each of groups’ BMI, were respectively: 20,9 ± 3,08 kg/m2 and 23,5 ± 3,53 kg/m2. Conclusion: LDL and HDL cholesterol serum levels are not different between vegetarian vegan and non-vegan. BMI of both groups is different. Age and physical activity affect on LDL serum cholesterol level, while BMI and total fat affect on HDL serum cholesterol level. LDL cholesterol serum level and BMI in vegetarian vegan are lower than non-vegan. Key words: Vegetarian diet, vegan, non-vegan, LDL cholesterol, HDL cholesterol