METHODS: We used data from an ongoing individual participant meta-analysis involving 17 population-based cohorts worldwide. We selected 60,211 participants without cardiovascular disease at baseline with available data on ethnicity (White, Black, Asian or Hispanic). We generated a multivariable linear regression model containing risk factors and ethnicity predicting mean common carotid intima-media thickness (CIMT) and a multivariable Cox regression model predicting myocardial infarction or stroke. For each risk factor we assessed how the association with the preclinical and clinical measures of cardiovascular atherosclerotic disease was affected by ethnicity.
RESULTS: Ethnicity appeared to significantly modify the associations between risk factors and CIMT and cardiovascular events. The association between age and CIMT was weaker in Blacks and Hispanics. Systolic blood pressure associated more strongly with CIMT in Asians. HDL cholesterol and smoking associated less with CIMT in Blacks. Furthermore, the association of age and total cholesterol levels with the occurrence of cardiovascular events differed between Blacks and Whites.
CONCLUSION: The magnitude of associations between risk factors and the presence of atherosclerotic disease differs between race/ethnic groups. These subtle, yet significant differences provide insight in the etiology of cardiovascular disease among race/ethnic groups. These insights aid the race/ethnic-specific implementation of primary prevention.
OBJECTIVE: To determine (i) proportions of patients with CHD in Singapore who achieved goals for serum low-density lipoprotein-cholesterol (LDL-C); and (ii) factors influencing goal attainment.
METHODS: A historical cohort study was conducted using records from the Singapore Cardiac Databank, a national registry of CHD patients. Serum LDL-C goal attainment was assessed in 5174 survivors of acute myocardial infarction or coronary revascularization (i.e. coronary artery bypass graft surgery or percutaneous coronary interventions), of whom 3811 (73.7%) were at very high risk.
RESULTS: At baseline, the mean patient age was 60.3 years, mean serum value of total cholesterol was 228 mg/dL, and mean LDL-C was 163 mg/dL. Of all CHD patients, approximately 70% did not achieve a serum LDL-C target of <100 mg/dL. Most patients receiving HMG-CoA reductase inhibitor (statin) regimens were treated initially with low- to medium-equipotency regimens and were never titrated to stronger regimens. The vast majority (approximately 94%) of patients at very high risk did not achieve the stringent serum LDL-C target of <70 mg/dL. Patients receiving higher potency statins were significantly more likely to achieve LDL-C goals, whereas those with higher baseline LDL-C levels or Malaysian ethnicity were less likely to achieve LDL-C goals.
CONCLUSIONS: Most CHD patients in the large group of Singapore residents with CHD in the present study did not achieve recommended LDL-C targets. A more effective disease-management approach, including patient education concerning lifestyle modification (e.g. diet, physical activity), efforts to enhance medication adherence, and more effective, well tolerated therapies such as high-equipotency or high-dose statins and statin combination regimens, may be needed to improve achievement of consensus cholesterol targets. This is the first study of cholesterol goal attainment in a large group of Southeast Asians and serves as a baseline for future evaluations in Asian populations.
OBJECTIVE: To examine treatment patterns, goal attainment, and factors influencing treatment among patients in 6 Asian countries who were taking statins.
METHODS: A retrospective cohort study was conducted in China, Korea, Malaysia, Singapore, Taiwan, and Thailand, where 437 physicians (41% cardiologists) recruited adults with hypercholesterolemia newly initiated on statin monotherapy.
RESULTS: Of 2622 patients meeting inclusion and exclusion criteria, approximately 66% had coronary heart disease (CHD)/diabetes mellitus, 24% had no CHD but > or =2 risk factors, and 10% had no CHD and <2 risk factors. Most patients ( approximately 90%) received statins at medium or lower equipotency doses. Across all cardiovascular risk categories, 48% of patients attained ATP III targets for low-density lipoprotein cholesterol (LDL-C), including 38% of those with CHD/diabetes (goal: <100 mg/dL), 62% of those without CHD but with > or =2 risk factors (goal: <130 mg/dL), and 81% of those without CHD and <2 risk factors (goal: <160 mg/dL). Most patients who achieved goals did so within the first 3 months. Increasing age (odds ratio (OR)=1.015 per 1-year increment; 95% confidence interval (CI)=1.005-1.206; p=0.0038) and initial statin potency (OR=2.253; 95% CI=1.364-3.722; p=0.0015) were directly associated with goal attainment, whereas increased cardiovascular risk (OR=0.085; 95% CI=0.053-0.134; p<0.0001 for CHD/diabetes mellitus at baseline compared with <2 risk factors,) and baseline LDL-C (OR=0.990; 95% CI=0.987-0.993); p<0.0001 per 1-mg/dL increment) were inversely associated with LDL-C goal achievement. Limitations of this study include potential differences in treatment settings and cardiovascular risk factors between different countries and centers. In addition, the effects on cholesterol goal achievement of concomitant changes in lifestyle were not assessed.
CONCLUSION: LDL-C goal attainment is low in Asians, particularly those with CHD/diabetes. More effective patient monitoring, treatments, including combining regimens and dose titration, and adherence to these treatments along with therapeutic lifestyle counseling may facilitate goal attainment.
METHODS: FH patients attending clinics in seven countries were invited to participate in a cross-sectional survey study. Consenting patients (N = 551) completed self-report measures of generalized beliefs about medication overuse and harms, beliefs in treatment effectiveness, specific beliefs about taking medication (attitudes, subjective norms, perceived behavioral control), and intentions to take medication. Participants also completed measures of demographic variables (age, gender, education level, income, cardiovascular disease status). Data were analysed using path analysis controlling for country and demographic variables.
RESULTS: Attitudes (β = .331, p<0.001), subjective norms (β = .121, p=0.009), and beliefs about medication overuse (β = -.160, p<0.001) were significant predictors of intentions to take medication. Treatment beliefs predicted intentions indirectly (β = .088, p<0.001) through attitudes and subjective norms. There was also an indirect effect of beliefs about medication overuse on intentions (β = -.045, p=0.056), but the effect was small compared with the direct effect.
CONCLUSIONS: The findings indicate the importance among FH patients of specific beliefs about taking medication and generalized beliefs about medication overuse and treatment in predicting medication intentions. When managing patients, clinicians should emphasize the efficacy of taking cholesterol-lowering drugs and the importance of treatment outcomes, and allay concerns about medication overuse.
OBJECTIVE: The objective of this study was to compare the health care of FH in countries of the Asia-Pacific region and Southern Hemisphere.
METHODS: A series of questionnaires were completed by key opinion leaders from selected specialist centers in 12 countries concerning aspects of the care of FH, including screening, diagnosis, risk assessment, treatment, teaching/training, and research; the United Kingdom (UK) was used as the international benchmark.
RESULTS: The estimated percentage of patients diagnosed with the condition was low (overall <3%) in all countries, compared with ∼15% in the UK. Underdetection of FH was associated with government expenditure on health care (ϰ = 0.667, P cholesterol targets on conventional therapies. Treatment gaps included suboptimal availability and use of lipoprotein apheresis and proprotein convertase subtilsin-kexin type 9 inhibitors. A deficit of FH registries, training programs, and publications were identified in less economically developed countries. The demonstration of cost-effectiveness for cascade screening, genetic testing, and specialized treatments were significantly associated with the availability of subsidies from the health care system (ϰ = 0.571-0.800, P
METHODS: A total of 20 healthy volunteers were challenged with 3 test meals, similar in fat content (~31% en) but varying in saturated SFA content and polyunsaturated/saturated fatty acid ratios (P/S). The 3 meals were lauric + myristic acid-rich (LM), P/S 0.19; palmitic acid-rich (POL), P/S 0.31; and stearic acid-rich (STE), P/S 0.22. Blood was sampled at fasted baseline and 2, 4, 5, 6, and 8 hours. Plasma lipids (triacylglycerol [TAG]) and lipoproteins (TC, LDL-C, high density lipoprotein-cholesterol [HDL-C]) were evaluated.
RESULTS: Varying SFA in the test meal significantly impacted postprandial TAG response (p < 0.05). Plasma TAG peaked at 5 hours for STE, 4 hours for POL, and 2 hours for LM test meals. Area-under-the-curve (AUC) for plasma TAG was increased significantly after STE treatment (STE > LM by 32.2%, p = 0.003; STE > POL by 27.9%, p = 0.023) but was not significantly different between POL and LM (POL > LM by 6.0%, p > 0.05). At 2 hours, plasma HDL-C increased significantly after the LM and POL test meals compared with STE (p < 0.05). In comparison to the STE test meal, HDL-C AUC was elevated 14.0% (p = 0.005) and 7.6% (p = 0.023) by the LM and POL test meals, respectively. The TC response was also increased significantly by LM compared with both POL and STE test meals (p < 0.05).
CONCLUSIONS: Chain length of saturates clearly mediated postmeal plasma TAG and HDL-C changes.
OBJECTIVE: The primary study objective was to evaluate the postprandial fate of tocotrienols and alpha-tocopherol in human plasma and lipoproteins.
DESIGN: Seven healthy volunteers (4 males, 3 females) were administered a single dose of vitamin E [1011 mg palm tocotrienol-rich fraction (TRF) or 1074 mg alpha-tocopherol] after a 7-d conditioning period with a tocotrienol-free diet. Blood was sampled at baseline (fasted) and 2, 4, 5, 6, 8, and 24 h after supplementation. Concentrations of tocopherol and tocotrienol isomers in plasma, triacylglycerol-rich particles (TRPs), LDLs, and HDLs were measured at each interval.
RESULTS: After intervention with TRF, plasma tocotrienols peaked at 4 h (4.79 +/- 1.2 microg/mL), whereas alpha-tocopherol peaked at 6 h (13.46 +/- 1.68 microg/mL). Although tocotrienols were similarly detected in TRPs, LDLs, and HDLs, tocotrienol concentrations were significantly lower than alpha-tocopherol concentrations. In comparison, plasma alpha-tocopherol peaked at 8 h (24.3 +/- 5.22 microg/mL) during the alpha-tocopherol treatment and emerged as the major vitamin E isomer detected in plasma and lipoproteins during both the TRF and the alpha-tocopherol treatments.
CONCLUSIONS: Tocotrienols are detected in postprandial plasma, albeit in significantly lower concentrations than is alpha-tocopherol. This finding confirms previous observations that, in the fasted state, tocotrienols are not detected in plasma. Tocotrienol transport in lipoproteins appears to follow complex biochemically mediated pathways within the lipoprotein cascade.
METHODS: This human postprandial study evaluated 3 edible fat blends with differing polyunsaturated to saturated fatty acids (P/S) ratios (POL = 0.27, AHA = 1.00, PCAN = 1.32). A cross-over design included mildly hypercholestrolemic subjects (9 men and 6 women) preconditioned on test diets fats at 31% energy for 7 days prior to the postprandial challenge on the 8th day with 50 g test fat. Plasma lipids and lipoproteins were monitored at 0, 1.5, 3.5, 5.5 and 7 hr.
RESULTS: Plasma triacylglycerol (TAG) concentrations in response to POL, AHA or PCAN meals were not significant for time x test meal interactions (P > 0.05) despite an observed trend (POL > AHA > PCAN). TAG area-under-the-curve (AUC) increased by 22.58% after POL and 7.63% after PCAN compared to AHA treatments (P > 0.05). Plasma total cholesterol (TC) response was not significant between meals (P > 0.05). Varying P/S ratios of test meals significantly altered prandial high density lipoprotein-cholesterol (HDL-C) concentrations (P AHA > PCAN). Paired comparisons was significant between POL vs PCAN (P = 0.009) but not with AHA or between AHA vs PCAN (P > 0.05). A significantly higher HDL-C AUC for POL vs AHA (P = 0.015) and PCAN (P = 0.001) was observed. HDL-C AUC increased for POL by 25.38% and 16.0% compared to PCAN and AHA respectively. Plasma low density lipoprotein-cholesterol (LDL-C) concentrations was significant (P = 0.005) between meals and significantly lowest after POL meal compared to PCAN (P = 0.004) and AHA (P > 0.05) but not between AHA vs PCAN (P > 0.05). AUC for LDL-C was not significant between diets (P > 0.05). Palmitic (C16:0), oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids in TAGs and cholesteryl esters were significantly modulated by meal source (P
METHODS: Subjects underwent a randomized double-blind crossover trial, consuming diets supplemented with 20 g/day of either soybean oil-based mayonnaise (SB-mayo) or palm olein-based mayonnaise (PO-mayo) for 4 weeks each with a 2-week wash-out period. The magnitude of changes for metabolic outcomes between dietary treatments was compared with PO-mayo serving as the control. The data was analyzed by ANCOVA using the GLM model. Analysis was adjusted for weight changes.
RESULTS: Treatments resulted in significant reductions in TC (diff = -0.25 mmol/L; P = 0.001), LDL-C (diff = -0.17 mmol/L; P = 0.016) and HDL-C (diff = -0.12 mmol/L; P LDL-C:HDL-C ratio (P > 0.05). Lipoprotein particle change was significant with large LDL particles increasing after PO-mayo (diff = +63.2 nmol/L; P = 0.007) compared to SB-mayo but small LDL particles remained unaffected. Plasma glucose, apolipoproteins and oxidative stress markers remained unchanged.
CONCLUSIONS: Daily use with 20 g of linoleic acid-rich SB-mayo elicited reductions in TC and LDL-C concentrations without significantly changing LDL-C:HDL-C ratio or small LDL particle distributions compared to the PO-mayo diet.
TRIAL REGISTRATION: This clinical trial was retrospectively registered with the National Medical Research Register, National Institute of Health, Ministry of Health Malaysia, (NMRR-15-40-24035; registered on 29/01/2015; https://www.nmrr.gov.my/fwbPage.jsp?fwbPageId=ResearchISRForm&fwbAction=Update&fwbStep=10&pk.researchID=24035&fwbVMenu=3&fwbResearchAction=Update ). Ethical approval was obtained from the National University of Malaysia's Medical Ethics Committee (UKM 1.5.3.5/244/SPP/NN-054-2011, approved on 25/05/2011).