scholarly journals The joint effects of apolipoprotein B, apolipoprotein A1, LDL cholesterol, and HDL cholesterol on risk: 3510 cases of acute myocardial infarction and 9805 controls

2009 ◽  
Vol 30 (17) ◽  
pp. 2137-2146 ◽  
Author(s):  
S. Parish ◽  
R. Peto ◽  
A. Palmer ◽  
R. Clarke ◽  
S. Lewington ◽  
...  
2016 ◽  
Vol 62 (7) ◽  
pp. 930-946 ◽  
Author(s):  
Børge G Nordestgaard ◽  
Anne Langsted ◽  
Samia Mora ◽  
Genovefa Kolovou ◽  
Hannsjörg Baum ◽  
...  

Abstract AIMS To critically evaluate the clinical implications of the use of non-fasting rather than fasting lipid profiles and to provide guidance for the laboratory reporting of abnormal non-fasting or fasting lipid profiles. METHODS AND RESULTS Extensive observational data, in which random non-fasting lipid profiles have been compared with those determined under fasting conditions, indicate that the maximal mean changes at 1–6 h after habitual meals are not clinically significant [+0.3 mmol/L (26 mg/dL) for triglycerides; −0.2 mmol/L (8 mg/dL) for total cholesterol; −0.2 mmol/L (8 mg/dL) for LDL cholesterol; +0.2 mmol/L (8 mg/dL) for calculated remnant cholesterol; −0.2 mmol/L (8 mg/dL) for calculated non-HDL cholesterol]; concentrations of HDL cholesterol, apolipoprotein A1, apolipoprotein B, and lipoprotein(a) are not affected by fasting/non-fasting status. In addition, non-fasting and fasting concentrations vary similarly over time and are comparable in the prediction of cardiovascular disease. To improve patient compliance with lipid testing, we therefore recommend the routine use of non-fasting lipid profiles, whereas fasting sampling may be considered when non-fasting triglycerides are >5 mmol/L (440 mg/dL). For non-fasting samples, laboratory reports should flag abnormal concentrations as triglycerides ≥2 mmol/L (175 mg/dL), total cholesterol ≥5 mmol/L (190 mg/dL), LDL cholesterol ≥3 mmol/L (115 mg/dL), calculated remnant cholesterol ≥0.9 mmol/L (35 mg/dL), calculated non-HDL cholesterol ≥3.9 mmol/L (150 mg/dL), HDL cholesterol ≤1 mmol/L (40 mg/dL), apolipoprotein A1 ≤1.25 g/L (125 mg/dL), apolipoprotein B ≥1.0 g/L (100 mg/dL), and lipoprotein(a) ≥50 mg/dL (80th percentile); for fasting samples, abnormal concentrations correspond to triglycerides ≥1.7 mmol/L (150 mg/dL). Life-threatening concentrations require separate referral for the risk of pancreatitis when triglycerides are >10 mmol/L (880 mg/dL), for homozygous familial hypercholesterolemia when LDL cholesterol is >13 mmol/L (500 mg/dL), for heterozygous familial hypercholesterolemia when LDL cholesterol is >5 mmol/L (190 mg/dL), and for very high cardiovascular risk when lipoprotein(a) >150 mg/dL (99th percentile). CONCLUSIONS We recommend that non-fasting blood samples be routinely used for the assessment of plasma lipid profiles. Laboratory reports should flag abnormal values on the basis of desirable concentration cutpoints. Non-fasting and fasting measurements should be complementary but not mutually exclusive.


2014 ◽  
Vol 04 (01) ◽  
pp. 009-014
Author(s):  
A. Harish Rao

Abstract: Objective: to know the glycemic and lipidaemic status in patients with acute myocardial infarction, and with the secondary objective to know the effect of age, gender, diabetes, smoking, hypertension on fasting glucose and lipid levels. Methods and materials: The 74 patients admitted for acute myocardial infarction during the study period of one year were analysed for fasting glucose values and serum levels of total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides. Results: The mean serum concentrations of total cholesterol, triglycerides, HDL cholesterol and LDL cholesterol were 233.28±45.34, 139.22±41.71, 171.43±36.53 and 27.07±36.53 respectively. Mean levels of total cholesterol, HDL cholesterol, triglycerides and fasting glucose values were not affected by age, gender, BMI, hypertension and smoking. BMI >30kg/m2 was associated with increased levels of total cholesterol(p=0.013) and LDL cholesterol(p=0.014). Also increase LDL cholesterol was seen in male gender(p=0.04). The prevalence of hypercholesterolemia, hypertriglyceridemia and low HDL cholesterol was 82.4%,77% and 78% respectively. Diabetes had no effect on lipid profile. Conclusion: our study highlighted the prevalence of dyslipidemias associated with myocardial infarction but not significant impact of fasting glucose levels.


2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
José Luis Pérez-Castrillón ◽  
Laura Abad Manteca ◽  
Gemma Vega ◽  
Javier del Pino Montes ◽  
Daniel de Luis ◽  
...  

Adequate vitamin D levels are necessary for good vascular health. 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. The objective of this study was to evaluate the response of cholesterol and triglycerides to atorvastatin according to vitamin D levels. Sixty-three patients with acute myocardial infarction treated with low and high doses of atorvastatin were included. Levels of total cholesterol, triglycerides, HDL cholesterol, and LDL cholesterol were measured at baseline and at 12 months of follow-up. Baseline levels of 25-hydroxyvitamin D (25-OHD) were classified as deficient (30 nmol/L), insufficient (30–50 nmol/L), and normal (50 nmol/L). In patients with 25-OHD  nmol/L, there were no significant changes in levels of total cholesterol ( mg/dL versus  mg/dL), triglycerides ( mg/dL versus  mg/dL), and LDL cholesterol ( mg/dL versus 92  mg/dL); whereas patients with insufficient (30–50 nmol/L) and normal vitamin D (50 nmol/L) had a good response to atorvastatin. We suggest that vitamin D concentrations 30 nmol/L may be required for atorvastatin to reduce lipid levels in patients with acute myocardial infarction.


1997 ◽  
Vol 82 (8) ◽  
pp. 2653-2659
Author(s):  
Kamal A. S. Al-Shoumer ◽  
Katharine H. Cox ◽  
Carol L. Hughes ◽  
William Richmond ◽  
Desmond G. Johnston

Hypopituitary patients, particularly women, have excess mortality, mostly due to vascular disease. We have studied circulating lipid and lipoprotein concentrations, fasting and over 24 h, in hypopituitary women and men and in matched controls. Firstly, 67 hypopituitary patients (36 women) and 87 normal controls (54 women) were studied after an overnight fast. Secondly, 12 patients (6 women) and 14 matched controls (7 women) were studied over 24 h of normal meals and activity. The patients were all GH deficient and were replaced with cortisol, T4, and sex hormones where appropriate, but not with GH. In the first study, circulating triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, and low density lipoprotein (LDL) cholesterol were measured after an overnight fast. In the second study, fasting levels of apolipoprotein B, apolipoprotein A1, and lipoprotein(a) were also measured, and then circulating triglyceride and total cholesterol concentrations were measured over 24 h. Fasting concentrations of triglyceride (mean ± sem, 1.73 ± 0.22 vs. 1.11 ± 0.09 mmol/L; P = 0.0025), total cholesterol (6.45 ± 0.25 vs. 5.59± 0.21 mmol/L; P = 0.002), LDL cholesterol (4.58 ± 0.24 vs. 3.80 ± 0.19 mmol/L; P = 0.007), and apolipoprotein B (135 ± 10 vs. 111 ± 9 mg/dL; P = 0.048) were elevated in hypopituitary compared to control women. The lipid alterations were observed in older and younger women and occurred independently of sex hormone or glucocorticoid replacement. Fasting values were not significantly different in hypopituitary and control men. Patients and controls (women and men) had similar fasting HDL cholesterol, apolipoprotein A1, and lipoprotein(a) concentrations. Although the differences that existed in fasting lipid values were most marked in women, the men were also abnormal in this respect, in that a higher proportion of hypopituitary than control men had total and LDL cholesterol above recommended values (≥6.2 and ≥4.1 mmol/L, respectively). In the postprandial period (0730–2030 h), the areas under the curve (AUC) for circulating triglyceride and total cholesterol were significantly higher in hypopituitary than control women (P = 0.0089 and P = 0.0016, respectively). The AUC for triglyceride and total cholesterol over 24 h were also significantly increased (P= 0.009 and P = 0.0004, respectively). No significant differences were observed for postprandial and 24-h AUC for triglyceride and total cholesterol concentrations in men. We conclude that hypopituitarism with conventional replacement therapy is associated with unfavorable fasting and postprandial lipid and lipoprotein concentrations, particularly in women. The changes may contribute to the observed increased vascular morbidity and mortality.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chuang Li ◽  
Jingxun Chen ◽  
Siyue Wei ◽  
Mei Zhang ◽  
Yushun Chu ◽  
...  

Abstract Background The optimum lipid indexes, predicting the coronary lesion in postmenopausal women are not clear. Objective To evaluate the optimum lipid predicter for coronary lesion in routine and advanced lipid tests. Method 300 postmenopausal women were enrolled and assigned into coronary heart disease (CHD) Group (242), and non-CHD Group (58). Routine and advanced lipid indexes were measured with standard laboratory test and nuclear magnetic resonance (NMR) spectroscopy. The correlation and predictivities for CHD of routine and advanced lipid indexes were performed with Logistic regression, Spearman correlation analysis and receiver operating characteristic (ROC). Results Age (hazard ratio (HR) 2.58, 95% confidence interval (CI) 1.08–5.86, P = 0.03), apolipoprotein B (ApoB) (HR 1.35, 95% CI 1.15–1.59, P < 0.001), corrected particles of low-density lipoprotein (LDL-p-corr) (HR 1.05, 95% CI 1.03–1.06, P < 0.001) and corrected particles of non-high-density lipoprotein (non-HDL-p-corr) (HR 1.02, 95% CI 1.01–1.03, P < 0.001) were the risk factors of CHD. LDL cholesterol (LDL-C), LDL-p, LDL-p-corr, HDL cholesterol (HDL-C), non-HDL cholesterol (non-HDL-C), non-HDL-p and non-HDL-p-corr were in linear correlation with Gensini score. Advanced lipid indexes LDL-p (area under curve (AUC) = 0.750, P = 0.02), LDL-p-corr (AUC = 0.759, P = 0.02), non-HDL-p (AUC = 0.693, P = 0.03) and non-HDL-p-corr (AUC = 0.699, P = 0.03) were more predictive for CHD than the routine ones (LDL-C and non-HDL-C). Conclusion In postmenopausal women, age, ApoB, LDL-p-corr and non-HDL-p-corr were risk factors of CHD. Compared with traditional lipid items, LDL-p, LDL-p-corr, non-HDL-p and non-HDL-p-corr may be better lipid indexes for CHD in postmenopausal women.


2013 ◽  
Vol 2013 ◽  
pp. 1-7
Author(s):  
Andrew W. Gardner ◽  
Petar Alaupovic ◽  
Donald E. Parker ◽  
Polly S. Montgomery ◽  
Omar L. Esponda ◽  
...  

Apolipoprotein B is a stronger predictor of myocardial infarction than LDL cholesterol, and it is inversely related to physical activity and modifiable with exercise training. As such, apolipoprotein measures may be of particular relevance for subjects with PAD and claudication. We compared plasma apolipoprotein profiles in 29 subjects with peripheral artery disease (PAD) and intermittent claudication and in 39 control subjects. Furthermore, we compared the plasma apolipoprotein profiles of subjects with PAD either treated (n=17) or untreated (n=12) with statin medications. For the apolipoprotein subparticle analyses, subjects with PAD had higher age-adjusted Lp-B:C (P<0.05) and lower values of Lp-A-I:A-II (P<0.05) than controls. The PAD group taking statins had lower age-adjusted values for apoB (P<0.05), Lp-A-II:B:C:D:E (P<0.05), Lp-B:E + Lp-B:C:E (P<0.05), Lp-B:C (P<0.05), and Lp-A-I (P<0.05) than the untreated PAD group. Subjects with PAD have impaired apolipoprotein profiles than controls, characterized by Lp-B:C and Lp-A-I:A-II. Furthermore, subjects with PAD on statin medications have a more favorable risk profile, particularly noted in multiple apolipoprotein subparticles. The efficacy of statin therapy to improve cardiovascular risk appears more evident in the apolipoprotein sub-particle profile than in the more traditional lipid profile of subjects with PAD and claudication. This trial is registered with ClinicalTrials.govNCT00618670.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Jaeun Yang ◽  
Christopher Naugler ◽  
Lawrence de Koning

Background: It is unclear whether vitamin D deficiency is associated with a higher risk of cardiovascular disease, and through what biochemical pathways this could occur. We investigated the relationship between serum 25-OH vitamin D and typical cardiovascular risk markers as well as incident myocardial infarction (MI) in a large group of high-risk individuals from the community of Calgary, Alberta, Canada. Methods: Calgary Laboratory Services databases were queried for age, sex, body mass index (BMI), personal healthcare number (PHN) and first available serum 25-OH vitamin D measure from patients who received an electrocardiogram or urine creatinine clearance test from 2010-2013. Data was linked by PHN to first available laboratory results for total cholesterol, HDL cholesterol, triglycerides, LDL cholesterol, fasting glucose and HbA1c as well as Alberta Health Services hospital discharge data for first myocardial infarction (ICD-10: I21.1-9) occurring after 25-OH vitamin D measurement. Multiple linear and logistic regression were used to examine all associations. Results: There were 36 000-50 000 complete patient records for analysis of each of the risk markers, with a median follow-up of 8-11 months. A 30 mmol/L increase in serum 25-OH vitamin D was associated with significantly (p<0.001) lower total cholesterol (-0.07 mmol/L), LDL cholesterol (-0.06 mmol/L), triglycerides (-0.14 mmol/L), fasting glucose (-0.12 mmol/L), and HbA1c (-0.13% mmol/L), but higher HDL cholesterol (+0.06 mmol/L) after adjusting for age, sex, BMI, monthly hours of sun-exposure and time between measures. Among these individuals, there were 458 cases of MI occurring after 25-OH vitamin D measurement, with a median follow-up of 1 year. In a case-cohort analysis that included 2500 controls, a 30 mmol/L increase in 25-OH vitamin D was associated with a 21% (p<0.001) lower odds of MI after multivariate adjustment. This association was strongly attenuated after adjusting LDL, HDL, fasting glucose and HbA1c. Conclusion: In a high-risk group of community patients from Calgary, Alberta, Canada, higher serum 25-OH vitamin D was associated with a lower risk of MI, which was explained by changes in commonly measured cardiovascular risk markers. Further study is needed to determine whether changes in cardiovascular risk markers are causally related to changes in 25-OH vitamin D.


Author(s):  
Liv Tybjærg Nordestgaard ◽  
Anne Tybjærg-Hansen ◽  
Ruth Frikke-Schmidt ◽  
Børge Grønne Nordestgaard

Abstract Context To enable prevention and treatment of age-related macular degeneration(AMD), understanding risk factors for AMD is important. Objective We tested the hypotheses that elevated plasma apolipoprotein A1 and high-density lipoprotein(HDL) cholesterol, and low levels of low-density lipoprotein(LDL) cholesterol, are associated with increased risk of AMD. Design and Setting From the Danish general population, we studied 106,703 and 16,032 individuals in the Copenhagen General Population Study(CGPS) and the Copenhagen City Heart Study(CCHS) with median follow-up of respectively 9 and 32 years. Main Outcome Measures 1,787 AMD in CGPS and 206 in CCHS. Results Higher concentrations of plasma apolipoprotein A1 and HDL cholesterol, and lower concentrations of LDL cholesterol, were associated with higher risk of AMD in CGPS. After multifactorial adjustment, individuals in the highest versus lowest quartile of plasma apolipoprotein A1 and HDL cholesterol had hazard ratios for AMD of 1.40(95%CI:1.20-1.63) and 1.22(1.03-1.45). Corresponding hazard ratios for individuals in the lowest versus highest quartile of LDL cholesterol were 1.18(1.02-1.37). Per 100 mg/dL higher plasma apolipoprotein A1, 1 mmol/L(39 mg/dL) higher HDL, and 1 mmol/L(39mmol/L) lower LDL cholesterol, the hazard ratios for AMD were 1.53(1.31-1.80), 1.19(1.07-1.32), and 1.05(1.00-1.11), respectively, with similar results across strata of different risk factors. Higher concentrations of HDL cholesterol were also associated with higher risk of AMD in the CCHS. Conclusion Elevated plasma apolipoprotein A1 and HDL cholesterol, and lower LDL cholesterol, are associated with increased risk of age-related macular degeneration.


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