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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2240-2242
doi: 10.1161/01.ATV.0000188507.89134.ef
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2240.)
© 2005 American Heart Association, Inc.

Editorials

Ethnic Differences in Arterial Responses, Inflammation, and Metabolic Profiles

Possible Insights into Ethnic Differences in Cardiovascular Disease and Stroke

Gregory Y.H. Lip; Christopher J. Boos

From the Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK

Correspondence to Professor Gregory Y.H. Lip, Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK. E-mail g.y.h.lip{at}bham.ac.uk

Despite enormous strides in our understanding of the potential risk factors implicated in cardiovascular disease (CVD), there has been a marked underrepresentation of data among ethnic minority groups in the published studies to date. It is critically important that this imbalance is addressed because it is clear that there are considerable variations in the rate of cardiovascular events and mortality among the differing ethnic groups, at least in the United Kingdom.

See page 2362

Compared with Caucasians, Afro-Caribbeans and people of African descent have an elevated risk (&1.5 to 2.5 times greater) of hypertension and diabetes mellitus, as well as related complications such as stroke, insulin resistance, and end-stage renal failure.1–6 Yet paradoxically, they have a far lower incidence of coronary artery disease than both south Asians (originating in the Indian subcontinent) and white Caucasians. The reasons for this apparent disparity are not clear but may relate to the clustering of known cardiovascular risk factors among the different ethnic groups. For example, when compared with Caucasians, Afro-Caribbeans are noted (in some studies) to have an increased incidence of obesity as well as lower levels of low-density lipoprotein cholesterol (yet higher high-density lipoprotein cholesterol) and of smoking rates and abnormal levels of adhesion molecules (which are implicated in coronary atheromatous plaque formation), such as vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and soluble P-selectin.2,3,5,7–11 In the Table we present an overview of some of the key studies that have compared the known cardiovascular risk factors and CVD among the two groups.


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  		TABLE 1. A Summary of Key Articles Comparing Cardiovascular Risk Factors Among Afro-Caribbeans Compared With Caucasians

Atherosclerosis beginning in the arterial wall and in the related endothelial damage/dysfunction represents the hallmark of CVD. In recent years, increasing emphasis has been placed on the noninvasive identification of patients at future risk of CVD so that preventative measures can be introduced before the establishment of overt disease. Among the noninvasive risk profiles that have taken center stage are the assessment of carotid intimal-medial thickness (CIMT), coronary artery calcium scoring, arterial stiffness, flow-mediated dilatation (a surrogate marker of endothelial function), and the quantification of known vascular risk markers, such as homocysteine, fibrinogen, cholesterol, and inflammatory parameters (eg, C-reactive protein [CRP]).12–14 Adverse derangement in any one of these indices has been linked to increased risk of future cardiovascular events.

The identification of increased arterial stiffness is important because it precedes a rise in systolic blood pressure and arterial pulse pressure, which in themselves are strongly linked to adverse cardiovascular events.15 Indeed, structural changes in the larger, more proximal conduit elastic arteries result in increased wall thickness (intimal-medial thickness), increased arterial pulse wave velocity, a reduction in arterial capacitance, and consequent increased arterial stiffness. It is also increasingly clear that the distal arterial tree and microvascular network is a vital determinant of long-term vascular resistance and itself is subject to increased stiffening as a consequence of atherosclerosis.16

In this issue of Atherosclerosis, Thrombosis, and Vascular Biology, Kalra et al attempt to further address the issues of cardiovascular risk and ethnicity, with a detailed and comprehensive assessment of ethnicity and CVD profiling.17 In this cross-sectional study, the authors compared a cohort of 78 apparently healthy Afro-Caribbeans (aged 35 to ≤75 years) with 82 age- and sex-matched Caucasian controls to ascertain whether important differences in known metabolic, vascular, and inflammatory markers as well as differences in physiological responses between large and small arteries might help to explain the excess of small vessel pathology among Afro-Caribbeans. Metabolic status was assessed by fasting measurements of blood glucose, total cholesterol, high-density lipoprotein cholesterol, triglycerides, homocysteine, insulin sensitivity, and insulin levels. Inflammatory status was assessed by quantification of CRP, tumor necrosis factor (TNF)-{alpha}, and interleukin (IL)-6. Vascular assessment included the measurement of CIMT, using B-mode ultrasound, as well as assessment of small vessel reactivity and large artery stiffness, using digital volume pulse photoplethysmography. Genotyping for important ß2-adrenoceptor polymorphisms, such as Arg16Gly and Gln27Glu, controversially linked to an increased risk of hypertension and coronary disease (with increased allele frequencies among Africans) was also performed. Overall, this was a most impressive and comprehensive attempt at cardiovascular risk profiling.

Kalra et al17 found that Afro-Caribbean patients had increased diastolic blood pressure, Arg16Gly and Gln27Glu polymorphisms, body mass index, and fasting insulin levels, but these results were unsurprising and somewhat consistent with previously published data. However, demonstration of higher levels of TNF-{alpha} and IL-6 despite equivalent CRP levels among the Afro-Caribbeans was interesting because this is in contrast with a previous article by Heald et al,18 which showed reduced CRP levels in Afro-Caribbeans (compared with both Europeans and Pakistanis) and noted that CRP was independently associated with an increased risk of having the metabolic syndrome (by homeostasis model assessment of insulin sensitivity). Kalra et al17 found a nonsignificant trend to lower homocysteine levels among the Afro-Carribbean patients in support of previous data.19 After adjustments for potential confounders, CIMT was greater among Afro-Carribeans when compared with Caucasians,17 again consistent with two previously published articles on the subject20,21; this might help explain the comparative increase in stroke risk among Afro-Carribeans. However, despite the increased CIMT among Afro-Carribeans, there was no significant difference in arterial stiffness (by quantification of stiffness index) between the two groups, which is contrary to previously published work.22,23

The reason for the disparity between the study by Kalra et al17 and previously published work is uncertain—perhaps differences in the patient populations studied, techniques used, and the increased statistical adjustments for additional confounders (beyond simply age and blood pressure) in this study versus the other published reports are possible causes. The great biological diversity of life also means that statistical adjustments can never fully adjust for all pathophysiological processes.

One novel observation by Kalra et al17 merits further discussion. Although there was a significant relationship between Caucasians, CIMT, and arterial stiffness, this relationship did not hold true for Afro-Caribbeans.17 Unlike Caucasians, Afro-Caribbeans also had selectively reduced small artery, but not large artery, function, as quantified by a change in reflectance index from baseline in response to stimuli, even after adjustment for potential confounders; however, there was a consistent and independent association between increasing CIMT and reducing small artery function among the Caucasian but not Afro-Caribbean patients.

Although large artery stiffness has been well studied,15 the situation with small artery stiffness is quite the opposite. Given the importance of small arteries in contributing to vascular resistance and blood pressure, as well as the consequent ventricular remodeling, it is plausible to suggest that some of the differences in CVD between Caucasians and Afro-Carribeans may relate to the propensity for small artery dysfunction among Afro-Caribbeans. It is also increasingly understood that arterial stiffness varies throughout the arterial tree, with likely variations in functional and structural changes in response to a host of hemodynamic and inflammatory insults.12

Nonetheless, the relationship between ethnicity and CVD is a highly complex one and is further compounded by a number of confounders, such as the effects of migration, generation gaps, and the clustering of ethnic minorities among the lower socioeconomic classes, which in itself is strongly linked to an increased CVD.9 Furthermore, the risk factors for CVD are only partly known, with an increasing number of CVD risk markers being recognized in recent years. The additive role of genes and genetic pleomorphisms to such CVD risk assessment is also uncertain but remains an active area of research.

In conclusion, Kalra et al17 have identified an association between small artery disease and a constellation of cardiovascular risk factors, such as increased TNF-{alpha} and IL-6 (proinflammatory markers), fasting insulin, body mass index, and diastolic blood pressure. Statistical association does not necessarily equate to causation, especially in a cross-sectional analysis, and this interesting article certainly raises more questions and research hypotheses that should ignite further research efforts toward a better understanding of the relationships between ethnicity and CVD so that we might be in a better position to prevent disease, rather than treat established disease, in the future.


*    References
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 *References
 

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  2. Khattar RS, Swales JD, Senior R, Lahiri A. Racial variation in cardiovascular morbidity and mortality in essential hypertension. Heart. 2000; 83: 267–271.[Abstract/Free Full Text]
  3. Lane D, Beevers DG, Lip GY. Ethnic differences in blood pressure and the prevalence of hypertension in England. J Hum Hypertens. 2002; 16: 267–273.[CrossRef][Medline] [Order article via Infotrieve]
  4. Gomez GB, Kerry SM, Oakeshott P, Rowlands G, Cappuccio FP. Changing from CHD to CVD risk-based guidelines for the management of mild uncomplicated hypertension in different ethnic groups: implications for primary care. J Hum Hypertens. 2005; 19: 321–324.[Medline] [Order article via Infotrieve]
  5. Strain WD, Chaturvedi N, Leggetter S, Nihoyannopoulos P, Rajkumar C, Bulpitt CJ, Shore AC. Ethnic differences in skin microvascular function and their relation to cardiac target-organ damage. J Hypertens. 2005; 23: 133–140.[Medline] [Order article via Infotrieve]
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  12. Boos CJ, Lip GY. Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension? J Hum Hypertens. 2005; 19: 511–513.[Medline] [Order article via Infotrieve]
  13. Fruchart JC, Nierman MC, Stroes ES, Kastelein JJ, Duriez P. New risk factors for atherosclerosis and patient risk assessment. Circulation. 2004; 109 (Suppl 1): III-15–III-19.
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  17. Kalra L, Rambaran C, Chowienczyk P, Goss D, Hambleton I, Ritter J, Rainford AS, Forrester T. Ethnic differences in arterial response and inflammatory markers in Afro-Caribbean and Caucasian subjects. Arterioscler Thromb Vasc Biol. 2005; 25: 2362–2367.[Abstract/Free Full Text]
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  23. Rajkumar C, Mensah R, Meeran K, Armstrong S, Bulpitt CJ. Peripheral arterial compliance is lower in Afro-Caribbeans compared to white Caucasians with type 2 diabetes after adjustment for blood pressure. J Hum Hypertens. 1999; 13: 841–843.[CrossRef][Medline] [Order article via Infotrieve]

Related Article:

Ethnic Differences in Arterial Responses and Inflammatory Markers in Afro-Caribbean and Caucasian Subjects
Lalit Kalra, Curtis Rambaran, Philip Chowienczyk, David Goss, Ian Hambleton, James Ritter, Ajay Shah, Rainford Wilks, and Terrence Forrester
Arterioscler. Thromb. Vasc. Biol. 2005 25: 2362-2367. [Abstract] [Full Text] [PDF]




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