|Year : 2018 | Volume
| Issue : 1 | Page : 8-14
Association of serum triglycerides with microalbuminuria in nondiabetic hypertensive patients
Lei Huang1, Jing Luo1, Yifei Dong2, Peng Lu1, Xi-Xin Ji1, Jian Liu1, Ping Li1, Xiaoshu Cheng1
1 Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China
2 Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University; Jiangxi Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China
|Date of Web Publication||16-May-2018|
Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, No 1, Minde Road, Nanchang, Jiangxi, 330006
Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, No. 1, Minde Road, Nanchang, Jiangxi 330006
Source of Support: None, Conflict of Interest: None
Background: Triglycerides (TG) levels were associated with microalbuminuria in diabetes. However, this association was barely investigated in non-diabetic hypertensive patients. We aimed to investigate such an association in non-diabetic hypertensive patients and the factors would affect it. Methods: We enrolled 445 eligible non-diabetic hypertensive patients and analyzed the association between TG and microalbuminuria. Results: Urinary microalbumin levels were significantly increased in patients with high TG levels (≥ 1.7 mmol/L). Multivariate logistic regression analysis identified that ln (TG) [odds ratio (OR): 2.273, 95% confidence interval (CI): 1.140 to 4.532, P = 0.020] were independently associated with microalbuminuria in all patients. Multinomial logistic regression analysis further revealed that highest tertile of TG level (≥ 1.76 mmol/L) significantly correlated with microalbuminuria (OR: 2.164, 95% CI: 1.336 to 3.507, P = 0.002) and the association remained significant after adjustments of sex, body mass index, ln(age), ln(systolic blood pressure), ln[diastolic blood pressure (DBP) (OR: 1.990, 95% CI: 1.197 to 3.308, P = 0.008). Association between TG and microalbuminuria was no longer significant when patients were limited to those with low-density lipoprotein cholesterol (LDL-C) treatment target achieved. However, in a forced model of multivariate regression analysis by eliminating ln (DBP), ln (TG) resumed the association with microalbuminuria (OR: 2.722, 95% CI: 1.122 to 6.605, P = 0.027). Conclusions: TG levels were associated with microalbuminuria in non-diabetic hypertensive patients, and the independence of association was supposed to be affected by baseline LDL-C and blood pressure levels.
Keywords: Hypertension, microalbuminuria, nondiabetic hypertensive patients, triglycerides
|How to cite this article:|
Huang L, Luo J, Dong Y, Lu P, Ji XX, Liu J, Li P, Cheng X. Association of serum triglycerides with microalbuminuria in nondiabetic hypertensive patients. Cardiol Plus 2018;3:8-14
|How to cite this URL:|
Huang L, Luo J, Dong Y, Lu P, Ji XX, Liu J, Li P, Cheng X. Association of serum triglycerides with microalbuminuria in nondiabetic hypertensive patients. Cardiol Plus [serial online] 2018 [cited 2018 Dec 12];3:8-14. Available from: http://www.cardiologyplus.org/text.asp?2018/3/1/8/232551
Lei Huang, Jing Luo. These authors contributed equally to this work.
| Introduction|| |
Hypertension is frequently accompanied by serum lipid and lipoprotein disorders including elevated levels of triglycerides (TGs) and low-density lipoprotein-cholesterol (LDL-C) and reduced level of high-density lipoprotein-cholesterol (HDL-C). Accompanied by high blood pressure (BP), dyslipidemia is one of the top 10 risk factors for death in China. The baseline lipid profiles in the general population vary in different countries and regions. Compared with Euro-American populations, Chinese populations show lower levels of total cholesterol (TC) and LDL-C and higher TG levels., In Asian populations, TG and non-HDL-C (TC minus HDL-C) levels have been found to be significantly higher in hypertensive patients when compared with normotensive controls, and with greater statistical significance than LDL-C levels.
Urinary albumin leakage is a manifestation of generalized vascular damage. Microalbuminuria (urinary albumin excretion of 20–200 mg/L or 30–300 mg/24 h) has been determined as an important prognostic indicator and has been reported to be associated with increased cardiovascular risk and progressive renal damage., In patients with hypertension, microalbuminuria has been identified as a predictor of cardiovascular complications including ischemic heart diseases., The overall prevalence of microalbuminuria is 4.1% in Chinese adults. The prevalence doubles in individuals with hypertension, triples in those with diabetes, and quadruples in those with both.
Hyperlipidemia has also been found to be a risk factor for microalbuminuria in patients with diabetes. Specifically, TG levels have been indicated as a strong independent determinant of microalbuminuria and macroalbuminuria in diabetes  and have been reported to be an important contributing factor in the progression of diabetic nephropathy. However, the relationship between TG and microalbuminuria is still unknown in nondiabetic hypertensive patients. In comparison with other lipid parameters, TG levels in hypertensive patients are not as prominent as in diabetic patients. Nevertheless, a more atherogenic lipoprotein profile has been described in hypertensive patients with microalbuminuria compared with those with normal urinary albumin excretion. We, therefore, aimed to investigate the association between TG and microalbuminuria in nondiabetic Chinese hypertensive patients in the present study.
| Subjects and Methods|| |
We evaluated 470 consecutive hypertensive patients from the Department of Cardiovascular Medicine at the Second Affiliated Hospital of Nanchang University from January 2015 to January 2016. Primary hypertension was defined as use of antihypertensive drugs or systolic blood pressure (SBP) ≥140 mmHg and/or diastolic blood pressure (DBP) ≥90 mmHg. Exclusion criteria were patients with diabetes, secondary hypertension including hypertension secondary to renal/kidney disease, renal artery stenosis, coarctation of the aorta, endocrine disorders, obstructive sleep apnea and usage of drugs, and the presence of severe systemic diseases including acute coronary syndrome, severe liver or kidney disorders, acute stroke, severe infections, and cancer. Of those eligible for participation, we excluded 25 patients because of urinary albumin excretion >200 mg/L.
All patients underwent an estimation of their atherosclerotic cardiovascular disease risk according to the Guidelines for the Prevention and Treatment of Dyslipidemia in Chinese Adults. Treatment targets of LDL-C were calculated according to risk stratification for each individual. For very high-risk patients, the LDL-C target was <1.8 mmol/L; for high-risk patients, the LDL-C target was <2.6 mmol/L; and for low-to-moderate risk patients, the LDL-C target was <3.4 mmol/L.
The study was approved by the Medical Research Ethics Committee of the Second Affiliated Hospital of Nanchang University, and signed informed consent was obtained from each patient before participation.
Medical history of coronary heart disease was obtained through questionnaires. The use of antihypertensive and cholesterol-lowering medications as well as smoking and alcohol consumption status was self-reported. Height and weight were measured in the standing position without shoes. Body mass index (BMI) was calculated as weight (kg) divided by height in meters squared.
A peripheral blood sample, used to determine biochemical variables, was taken after an 8-h fast. TC, TG, HDL-C, LDL-C, apolipoprotein A, apolipoprotein B, lipoprotein A, urinary microalbumin, creatinine, and uric acid were measured with standard assays for all patients. TC levels were determined by enzymatic colorimetric assay (Beckman Coulter, Suzhou, China), TG levels were evaluated by the Glycerol phosphate oxidase (GPO) - peroxidase (POD) method (Beckman Coulter, Suzhou, China), HDL-C and LDL-C were measured by direct homogeneous assay methods using detergents (Beckman Coulter, Suzhou, China), apolipoprotein A and apolipoprotein B levels were determined by immunoturbidimetry assay (Medicalsystem Biotechnology, Ningbo, China), lipoprotein A levels were determined by particle-enhanced turbidimetric assay (Kehua Bio-Engineering, Shanghai, China), and non-HDL levels were calculated by TC minus HDL-C. Urinary microalbumin levels were evaluated by immunoturbidimetry assay (Randox Laboratories, Crumlin, County Antrim, BT29 4QY, United Kingdom) and serum creatinine and uric acid concentrations were assayed by a direct enzyme method (Beckman Coulter, Suzhou, China). All biochemical variables were measured using an autoanalyzer (Olympus Corporation, OLYMPUS AU-2700, Japan) at the central laboratory of the Second Affiliated Hospital of Nanchang University as described previously. Estimated glomerular filtration rate (eGFR) was calculated according to the modified GFR-estimating equation for Chinese patients with chronic kidney disease as follows: eGFR Modification of Diet in Renal Disease (MDRD) = 186 × (serum creatinine in mg/dl) − 1.154 × (age in years) − 0.203 × 0.742 (if female) × 1.233.
Normally distributed data were expressed as mean ± standard deviation (SD). Nonnormally distributed results were expressed as the median value (interquartile range). Categorical values were presented as numbers (percentage). The study patients were stratified into two groups on the basis of microalbuminuria. Microalbuminuria was defined as albumin excretion in the urine within the range of 20–200 mg/L.
Differences between groups were evaluated using independent-samples t-test or Mann–Whitney U-test as appropriate for continuous variables and Chi-square test for categorical variables. Continuous variables with a skewed distribution were ln-transformed to attain normal distributions before regression analyses. Uni- and multi-variate logistic regression analyses were used to assess clinical covariates associated with the presence of microalbuminuria among all patients, as well as a subgroup of patients who achieved LDL-C treatment targets. Multinomial logistic regression analysis was used to assess the graded association between TG level tertiles (<1.12, 1.12–1.76, and ≥1.76 mmol/L) and microalbuminuria. A two-sided P < 0.05 was considered statistically significant. All statistical analyses were performed with SPSS software for Windows, version 16.0 (SPSS Inc., Chicago, Illinois, USA).
| Results|| |
Clinical characteristics of the study groups
[Table 1] details the clinical characteristics of all study groups. A total of 445 nondiabetic hypertensive patients were finally included in the study including 166 patients with normoalbuminuria (urinary albumin excretion <20 mg/L) and 279 patients with microalbuminuria (urinary albumin excretion 20–200 mg/L). More male patients had microalbuminuria. Patients with microalbuminuria were younger, had higher BMI, higher SBP, DBP, and serum TG levels, and had lower levels of HDL-C.
Association of triglyceride levels and microalbuminuria in all nondiabetic hypertensive patients
[Figure 1] shows the urinary microalbumin levels in patients with normal TC level (<5.2 mmol/L) and high TC level (≥5.2 mmol/L) [Figure 1]a; LDL-C treatment target-achieved and LDL-C treatment target-unachieved groups [Figure 1]b; normal-HDL-C level (≥1 mmol/L) and low-HDL-C level (<1 mmol/L) groups [Figure 1]c; and normal-TG level (<1.7 mmol/L) and high-TG level (≥1.7 mmol/L) groups [Figure 1]d. Urinary microalbumin level was significantly higher in patients with high TG levels (P = 0.019) and low HDL-C levels (P = 0.007). There was no significant difference in urinary microalbumin level between the two levels of TC or LDL-C.
|Figure 1: Urinary microalbumin levels in nondiabetic hypertensive patients with (a) normal TC level (<5.2 mmol/L) and high TC level (≥5.2 mmol/L); (b) LDL-C treatment target achieved and LDL-C treatment target unachieved; (c) normal HDL-C level (≥1 mmol/L) and low HDL-C level (<1 mmol/L); (d) normal TG level (<1.7 mmol/L) and high TG level (≥1.7 mmol/L). Data are expressed as median plus 2.5%–97.5% percentage range. Dots represent the data outside of the 2.5%–97.5% percentage range. HDL-C: High-density lipoprotein-cholesterol, LDL-C: Low-density lipoprotein-cholesterol; TG: Triglyceride, TC: Total cholesterol|
Click here to view
[Table 2] details the uni- and multi-variate logistic regression analyses used to evaluate the association of clinical covariates with the presence of microalbuminuria in all patients. Sex (male), ln(age), BMI, ln(SBP), ln(DBP), and ln(TG) were significantly associated with microalbuminuria in univariate logistic regression analyses. Multivariate regression analysis further identified that ln(DBP) (odds ratio [OR]: 8.621, 95% confidence interval [CI]: 2.184–34.037, P = 0.002) and ln(TG) (OR: 2.273, 95% CI: 1.140–4.532, P = 0.020) were significantly and independently associated with microalbuminuria in all patients. This model was reliable (P = 0.901 by the Hosmer–Lemeshow test).
|Table 2: Logistic regression analysis of clinical factors for presence of microalbuminuria in all patients|
Click here to view
Multinomial logistic regression analysis [Table 3] identified that, with the lowest tertile of TG level (<1.12 mmol/L) as the reference, the highest tertile of TG level (≥1.76 mmol/L) was significantly correlated with microalbuminuria (OR: 2.164, 95% CI: 1.336–3.507, P = 0.002) and this association remained significant after adjustment of sex, BMI, ln(age), ln(SBP), and ln(DBP) (OR: 1.990, 95% CI: 1.197–3.308, P = 0.008).
|Table 3: Microalbuminuria according to triglyceride level tertiles in all nondiabetic hypertensive patients|
Click here to view
Interaction of triglyceride and blood pressure on microalbuminuria in nondiabetic hypertensive patients
Logistic regression analysis revealed a significant interaction between ln(TG) and ln(SBP) (OR: 1.212, 95% CI: 1.060–1.385, P = 0.005) and ln(TG) and ln(DBP) (OR: 1.262, 95% CI: 1.085–1.467, P = 0.003) with respect to microalbuminuria in all patients. In the subset of patients who had achieved their LDL-C treatment target, the interactions between ln(TG) and ln(SBP) (OR: 1.258, 95% CI: 1.065–1.486, P = 0.007) and ln(TG) and ln(DBP) (OR: 1.318, 95% CI: 1.091–1.592, P = 0.004) with respect to microalbuminuria remained statistically significant.
Association of triglyceride levels and microalbuminuria in nondiabetic hypertensive patients who were limited to low-density lipoprotein-cholesterol treatment target achieved
[Table 4] details the uni- and multi-variate logistic regression analyses investigating the association between clinical covariates and for the presence of microalbuminuria in nondiabetic hypertensive patients who had achieved their LDL-C treatment target. ln(age), current alcohol consumption, beta-blockers, ln(DBP), and ln(TG) were significantly associated with microalbuminuria in univariate logistic regression analysis. ln(TG) was no longer associated with microalbuminuria in multivariate regression analysis. However, in a forced model of multivariate regression analysis eliminating ln(DBP), ln(TG) was again found to be associated with microalbuminuria (OR: 2.722, 95% CI: 1.122–6.605, P = 0.027).
|Table 4: Multivariate logistic regression analysis of clinical factors for presence of microalbuminuria among hypertensive patients who achieved the treatment target of low-density lipoprotein-cholesterol (n=278)|
Click here to view
| Discussion|| |
A major finding of the present study was that TG was associated with microalbuminuria in nondiabetic hypertensive patients, and the independence of association was thought to be affected by baseline LDL-C and BP levels. Our findings were supported by the following results: (1) urinary microalbumin levels were significantly increased in the high TG group (≥1.7 mmol/L) [Figure 1]d; (2) TG levels were independently associated with microalbuminuria in all nondiabetic hypertensive patients [Table 2]; (3) risk of microalbuminuria significantly increased in the highest tertile of TG level patients (≥1.76 mmol/L) [Table 3]; (4) independent association between ln(TG) and microalbuminuria was lost when analyses were limited to the subset of patients who had met their LDL-C treatment target, and the association was again identified when the covariate ln(DBP) was excluded [Table 4].
Hyperlipidemia is associated with microalbuminuria not only in patients with diabetes, but also in those with essential hypertension. Microalbuminuria is a marker of cardiovascular complications and a reliable predictor of ischemic heart diseases in hypertensive patients., In hypertensive patients, a more atherogenic lipoprotein profile is seen in patients with microalbuminuria when compared with normoalbuminuric patients. In fact, combined lowering of LDL-C and BP can substantially reduce cardiovascular events in hypertensive patients at intermediate  to high risk  of cardiovascular disease (CVD). In addition to LDL-C, dyslipidemia-related CVD risk is also associated with elevated TG levels  and decreased HDL-C levels. The latter two lipid disorders may be the most common risk factors for residual cardiovascular risk in patients after lowering of LDL-C with statin therapy, especially in patients with diabetes.,
A meta-analysis of epidemiological data has shown that TG is an independent cardiovascular risk factor  and evidence has accumulated over the past 10 years showing the importance of TG as an independent risk factor for CAD., In Asian populations with relatively low TC levels, nonfasting TG levels predict the incidence of coronary heart disease. Also in Asian populations, TG appears to be more important than LDL-C and HDL-C as the major lipid parameters related to atherogenesis in the presence of hypertension. TG levels increase with BP. This relationship persists in patients with normal BP, across patients with high-normal BP, and those with hypertension, which indicates a biological interrelation between BP and TG. In our study, we identified a significant interaction between TG and both SBP and DBP on microalbuminuria in nondiabetic hypertensive patients, demonstrating a role for therapy targeting TG and BP in early renal impairment in hypertensive patients.
An interesting finding in the present study is that urinary albumin excretion was significantly increased in nondiabetic hypertensive patients with low HDL-C and high TG, but not in patients with high TC or LDL-C [Figure 1]. Although a relatively low level of TC or LDL-C might be one of the possible reasons, the median levels of TG and HDL-C were normal in patients enrolled in the present study [Table 1]. We found a univariate association of TG with microalbuminuria in all nondiabetic hypertensive patients in the present study, and this association was still significant after adjustment for confounding factors [Table 2]. However, the association was no longer significant when the enrolled patients were limited to patients who had met their LDL-C treatment target [Table 4], which led to an inference that the association of TG and microalbuminuria in nondiabetic hypertensive patients was possibly based on an elevated TG level plus uncontrolled LDL-C, and this combination was associated with a higher level of risk stratification. Furthermore, the attenuation of the association of TG and microalbuminuria in those patients who had met their LDL-C treatment target occurred following the adjustment for DBP as shown in a forced multivariate model without the presence of DBP [Table 4]. This indicated that the association of TG and microalbuminuria could be mediated by baseline BP levels in nondiabetic hypertensive patients. Taken together, the independence of TG level as a risk factor for microalbuminuria in nondiabetic hypertensive patients remains debatable. Rather, TG levels appear to provide unique information for early renal impairment in nondiabetic hypertensive patients, especially when combined with uncontrolled LDL-C levels.
Limitations of our study include: (1) A cross-sectional design, which warrants a future prospective study to demonstrate the causal relationship between TG and microalbuminuria in nondiabetic hypertensive patients; (2) The variability of TG levels was high and increased with the level of TG. An average of multiple test result for TG may have reduced this variability. Medications are also likely to affect TG levels and were not taken into account in this study; (3) Patients did not receive ambulatory BP monitoring and thus BP in the present study might not reflect the patients' true BP levels; (4) This was a single-center study that investigated only a relatively small number of patients. Thus, the mechanism underlying the association between TG and microalbuminuria in nondiabetic hypertensive patients is not yet clear.
| Conclusion|| |
TG levels were associated with microalbuminuria in nondiabetic hypertensive patients, and the independence of association is hypothesized to be affected by baseline LDL-C and BP levels.
Financial support and sponsorship
This work was supported by the National Natural Science Foundation of China (grant number 81460071) and Key R&D Program of Jiangxi Province Department of Science and Technology (grant number 20171BBG70088).
Conflicts of interest
There are no conflicts of interest.
| References|| |
Nguyen NT, Magno CP, Lane KT, Hinojosa MW, Lane JS. Association of hypertension, diabetes, dyslipidemia, and metabolic syndrome with obesity: Findings from the national health and nutrition examination survey, 1999 to 2004. J Am Coll Surg 2008;207:928-34.
GBD 2015 Risk Factors Collaborators. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: A systematic analysis for the global burden of disease study 2015. Lancet 2016;388:1659-724.
Woo J, Lam CW. Serum lipid profile in an elderly Chinese population. Arteriosclerosis 1990;10:1097-101.
Carroll MD, Kit BK, Lacher DA, Shero ST, Mussolino ME. Trends in lipids and lipoproteins in US adults, 1988-2010. JAMA 2012;308:1545-54.
Yang W, Xiao J, Yang Z, Ji L, Jia W, Weng J, et al.
Serum lipids and lipoproteins in Chinese men and women. Circulation 2012;125:2212-21.
Yamamoto A, Temba H, Horibe H, Mabuchi H, Saito Y, Matsuzawa Y, et al.
Life style and cardiovascular risk factors in the Japanese population – From an epidemiological survey on serum lipid levels in Japan 1990 part 2: Association of lipid parameters with hypertension. J Atheroscler Thromb 2003;10:176-85.
Deckert T, Feldt-Rasmussen B, Borch-Johnsen K, Jensen T, Kofoed-Enevoldsen A. Albuminuria reflects widespread vascular damage. The steno hypothesis. Diabetologia 1989;32:219-26.
Lane JT. Microalbuminuria as a marker of cardiovascular and renal risk in type 2 diabetes mellitus: A temporal perspective. Am J Physiol Renal Physiol 2004;286:F442-50.
Pruijm MT, Madeleine G, Riesen WF, Burnier M, Bovet P. Prevalence of microalbuminuria in the general population of Seychelles and strong association with diabetes and hypertension independent of renal markers. J Hypertens 2008;26:871-7.
Jensen JS, Feldt-Rasmussen B, Strandgaard S, Schroll M, Borch-Johnsen K. Arterial hypertension, microalbuminuria, and risk of ischemic heart disease. Hypertension 2000;35:898-903.
Karalliedde J, Viberti G. Microalbuminuria and cardiovascular risk. Am J Hypertens 2004;17:986-93.
Yan L, Ma J, Guo X, Tang J, Zhang J, Lu Z, et al.
Urinary albumin excretion and prevalence of microalbuminuria in a general Chinese population: A cross-sectional study. BMC Nephrol 2014;15:165.
Hovind P, Tarnow L, Rossing P, Jensen BR, Graae M, Torp I, et al.
Predictors for the development of microalbuminuria and macroalbuminuria in patients with type 1 diabetes: Inception cohort study. BMJ 2004;328:1105.
Retnakaran R, Cull CA, Thorne KI, Adler AI, Holman RR; UKPDS Study Group, et al.
Risk factors for renal dysfunction in type 2 diabetes: U.K. Prospective diabetes study 74. Diabetes 2006;55:1832-9.
Kim DM, Ahn CW, Park JS, Cha BS, Lim SK, Kim KR, et al.
An implication of hypertriglyceridemia in the progression of diabetic nephropathy in metabolically obese, normal weight patients with type 2 diabetes mellitus in Korea. Diabetes Res Clin Pract 2004;66 Suppl 1:S169-72.
Campese VM, Bianchi S, Bigazzi R. Association between hyperlipidemia and microalbuminuria in essential hypertension. Kidney Int Suppl 1999;71:S10-3.
Joint Committee on the revision of the guidelines. Guidelines for the prevention and treatment of dyslipidemia in Chinese adults (revised edition, 2016). Chin Circul J 2016;31:937-50.
Cao C, Hu JX, Dong YF, Zhan R, Li P, Su H, et al.
Association of endothelial and mild renal dysfunction with the severity of left ventricular hypertrophy in hypertensive patients. Am J Hypertens 2016;29:501-8.
Hasslacher C, Ritz E, Wahl P, Michael C. Similar risks of nephropathy in patients with type I or type II diabetes mellitus. Nephrol Dial Transplant 1989;4:859-63.
Yusuf S, Lonn E, Pais P, Bosch J, López-Jaramillo P, Zhu J, et al.
Blood-pressure and cholesterol lowering in persons without cardiovascular disease. N
Engl J Med 2016;374:2032-43.
Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, Caulfield M, et al.
Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian cardiac outcomes trial – Lipid lowering arm (ASCOT-LLA): A multicentre randomised controlled trial. Lancet 2003;361:1149-58.
Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, Bingham S, et al.
Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 western prospective studies. Circulation 2007;115:450-8.
Mabuchi H, Kita T, Matsuzaki M, Matsuzawa Y, Nakaya N, Oikawa S, et al.
Large scale cohort study of the relationship between serum cholesterol concentration and coronary events with low-dose simvastatin therapy in Japanese patients with hypercholesterolemia and coronary heart disease: Secondary prevention cohort study of the Japan lipid intervention trial (J-LIT). Circ J 2002;66:1096-100.
Scott R, O'Brien R, Fulcher G, Pardy C, D'Emden M, Tse D, et al.
Effects of fenofibrate treatment on cardiovascular disease risk in 9,795 individuals with type 2 diabetes and various components of the metabolic syndrome: The fenofibrate intervention and event lowering in diabetes (FIELD) study. Diabetes Care 2009;32:493-8.
ACCORD Study Group; Ginsberg HN, Elam MB, Lovato LC, Crouse JR 3rd
, Leiter LA, et al.
Effects of combination lipid therapy in type 2 diabetes mellitus. N
Engl J Med 2010;362:1563-74.
Ahmad I, Miller M. Triglycerides and coronary heart disease: A global perspective. J Cardiovasc Risk 2000;7:303-7.
Gaziano JM, Hennekens CH, O'Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction. Circulation 1997;96:2520-5.
Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Relation of high TG-low HDL cholesterol and LDL cholesterol to the incidence of ischemic heart disease. An 8-year follow-up in the Copenhagen male study. Arterioscler Thromb Vasc Biol 1997;17:1114-20.
Iso H, Naito Y, Sato S, Kitamura A, Okamura T, Sankai T, et al.
Serum triglycerides and risk of coronary heart disease among Japanese men and women. Am J Epidemiol 2001;153:490-9.
Bønaa KH, Thelle DS. Association between blood pressure and serum lipids in a population. The Tromsø study. Circulation 1991;83:1305-14.
Saidu H, Karaye KM, Okeahialam BN. Plasma lipid profile in Nigerians with high – Normal blood pressure. BMC Res Notes 2014;7:930.
[Table 1], [Table 2], [Table 3], [Table 4]