Elsevier

Atherosclerosis

Volume 209, Issue 2, April 2010, Pages 579-584
Atherosclerosis

Triglycerides and small dense low density lipoprotein in the discrimination of coronary heart disease risk in South Asian populations

https://doi.org/10.1016/j.atherosclerosis.2009.10.010Get rights and content

Abstract

Introduction

Coronary heart disease (CHD) is exceptionally prevalent amongst globally dispersed migrant groups originating from the Indian subcontinent, but the contribution of dyslipidaemia to their increased risk remains poorly defined.

Methods

Fasting lipids and lipoproteins, apolipoproteins (Apo), low density lipoprotein (LDL) diameter and oxidised LDL were measured amongst rural Indians in India (n = 294) and their migrant contemporaries in the UK (n = 242). The performance of qualitative and quantitative measures of lipid metabolism were compared in the discrimination of WHO defined metabolic risk and raised Framingham CHD risk scores (>15%) using Receiver Operating Characteristic (ROC) curves.

Results

LDL diameter was correlated with triglycerides (R2 = 0.12, P < 0.001) and with high density lipoprotein (HDL) cholesterol levels (R2 = 0.15, P < 0.001) in both groups. Migrants had less small dense LDL (95% CI: 12.5–14.2%) vs. rural Indians (15.7–17.2, P < 0.05). On ROC analysis, triglycerides were the only consistent discriminators of metabolic and CHD risk scores (all P  0.001). Apo B was also a strong indicator of raised CHD risk scores. Irrespective of site, individuals with raised triglycerides also had higher total cholesterol and Apo B, denser LDL, lower HDL and more oxidised LDL (all P  0.01).

Discussion

Fasting triglycerides reflect both qualitative and quantitative aspects of lipid metabolism, and are a comprehensive discriminator of CHD risk in this South Asian population.

Introduction

Populations originating from the Indian subcontinent have a higher prevalence [1], [2], and earlier progression of coronary heart disease (CHD) compared with individuals in other countries [3]. In the UK, rates of CHD mortality amongst South Asians migrants are 40% greater than those for the general British population [4], and this excess risk may be even higher amongst newer generations of British South Asians [5]. A lack of targeted healthcare initiatives prolongs health inequality for this ethnic minority in the UK [6]. The detection and management of CHD risk associated with hyperlipidaemia are at the forefront of primary and secondary healthcare approaches in cardiovascular medicine [7], but the contribution of dyslipidaemia in South Asians to their increased CHD susceptibility remains poorly defined. Historically, much of the research has focused on ethnic differences, comparing lipid levels amongst South Asian migrants only relative to the indigenous population of Britain [8] using diagnostic thresholds defined by studies biased by a large Caucasian contingency.

Ethnic differences include lower levels of HDL cholesterol, and higher triglycerides amongst South Asians relative to European populations [8], [9]. Intuitively, this dyslipidaemia may be a manifestation of the pre-diabetic state amongst South Asians, as rates of glucose intolerance are also excessively high for this group [10], [11]. Raised triglyceride levels promote the preponderance of LDL particles that are small and dense [12], another interrelated feature of the abnormal lipid distribution amongst individuals with diabetes, and an adverse consequence for CHD risk [13], [14]. The oxidative susceptibility of LDL represents another qualitative measure of the atherogenic potential of the lipid profile [15]. Precise quantitative measures of lipoproteins include apolipoproteins (Apo) AI and B [16], which may explicate CHD risk better than routine lipid measures [17], [3].

To further describe the nature of dyslipidaemic tendencies in a South Asian population [18], we measured qualitative aspects of lipid metabolism in a population of Indian Gujarati migrants living in Britain and their contemporaries still living in Indian villages of origin. We investigated which measures of lipid metabolism were needed to support our existing clinical approaches to estimate of CHD risk in this population. Due to the innate nature of raised triglycerides in the clustering of CHD risk factors [19], our hypothesis was that circulating concentrations of fasting triglycerides were better discriminators of metabolic and CHD risk than clinically routine measures of total cholesterol and HDL cholesterol within this South Asian population.

Section snippets

Methods

Methodology of this migration study is described in detail elsewhere [18]. In brief, we compared a Gujarati community who had migrated to Sandwell (West Midlands, UK) from the rural village area around Navsari, Gujarat (India) with age, gender, and caste matched contemporaries still living in those villages in India. Randomly selected subjects drawn from electoral rolls (at both sites) were invited to clinic appointments, which included venepuncture during an oral glucose tolerance test. Blood

Results

Individual data were available from 140 male, 162 female Gujaratis living in rural villages in India and 120 male, 123 female migrant Gujaratis living in Britain. The impact of migration on CHD risk factors is reported elsewhere where rates of glucose intolerance were comparable between sites, but mean body-mass indices, blood pressure and serum cholesterol and triglycerides were greater amongst migrants (all of whose 95% CI were ≥6.6–13.1% higher) [18]. Nearly a quarter of men and women had a

Discussion

As hypothesised, serum triglycerides were better in their discrimination of metabolic and CHD risk compared to other lipid and lipoprotein measures within this South Asian population. Within both rural and western sites, raised triglycerides amongst individuals were co-ordinated with a more atherogenic lipid profile that included higher cholesterol, lower HDL cholesterol, greater Apo B, smaller and denser LDL, and more oxidised LDL. The implication of these findings is that the measurement of

Conflict of interest

None declared.

Acknowledgement

This research was supported by the British Heart Foundation.

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