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Systematic review
Paradoxically lower prevalence of peripheral arterial disease in South Asians: a systematic review and meta-analysis
  1. Meghan Sebastianski1,
  2. Mark J Makowsky2,
  3. Marlene Dorgan3,
  4. Ross T Tsuyuki1,4
  1. 1Epidemiology Coordinating and Research (EPICORE) Centre, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
  2. 2Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
  3. 3Health Sciences Libraries, University of Alberta, Edmonton, Alberta, Canada
  4. 4Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
  1. Correspondence to Ross T Tsuyuki, Epidemiology Coordinating and Research (EPICORE) Centre, Dept of Medicine, University of Alberta, 220 College Plaza, Edmonton, Alberta, Canada T6G 2C8; ross.tsuyuki{at}ualberta.ca

Abstract

Background While people of South Asian (SA) descent have higher rates of cardiovascular disease compared with people of White European (WE) descent, a lower prevalence of lower extremity peripheral arterial disease (PAD) has been suggested in SA. Our intent was to systematically review the literature on PAD prevalence in people of SA descent and to conduct a meta-analysis to identify differences in PAD prevalence between SA and WE.

Methods Standard Cochrane systematic review methodology was used for conducting a literature review of published research. Population prevalence studies of PAD in SA with a WE comparison group were included. Full text studies were selected and reviewed by two authors with independent data extraction. Prevalence differences between SA and WE were analysed using ORs.

Findings 129 studies were initially identified and ultimately 15 (n=240 003 patients) studies were included. Only one study reported direct comparative general PAD prevalence between SA and WE (OR=0.26, 95%CI 0.17 to 0.38, p<0.001, n=77 855). Fourteen studies with comparative prevalence data between SA and WE in high-risk populations confirm significantly lower odds of PAD in SA with coronary artery disease (CAD) (OR=0.47, 95%CI 0.39 to 0.56, p<0.001, n=139 313) and diabetes (OR=0.44; 95% CI 0.30 to 0.63, p<0.001, n=22 835).

Interpretation Reported PAD prevalence is significantly lower in SA than WE for both the CAD and diabetes populations. Explanations for these findings, if true, are unclear. These results underscore the need for further study to clarify mechanisms of ethnic divergence in PAD prevalence.

  • PERIPHERAL VASCULAR DISEASE

https://doi.org/10.1136/heartjnl-2013-303605

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    Introduction

    Lower extremity peripheral arterial disease (PAD) is a recognised risk factor for amputation, myocardial infarction and stroke.1 ,2 In fact, PAD is more than a risk factor, it is a direct indicator of the extent of atherosclerotic disease. PAD itself shares a number of common contributing risk factors with coronary artery disease (CAD) and cerebrovascular disease, including hypertension, dyslipidemia, smoking and diabetes.1 ,2 Therefore, the presence of PAD can indicate widespread atherosclerotic disease in other vascular beds.3–5 Despite the benefits of detecting PAD early, the majority of PAD cases are asymptomatic and, as such, PAD is underdiagnosed.4 ,6

    South Asians (SAs), people of Indian, Pakistani, Sri Lankan and Bangladeshi descent, experience higher rates of cardiovascular disease and cardiovascular mortality when compared to persons of White European (WE) descent.7–11 Even SA immigrants to Western countries who have adopted the cultural, behavioural and dietary patterns of their new country continue to have higher CAD risk than the local population. 10 ,12 This risk is partially driven by the fact that SAs also have one of the highest prevalence of diabetes, a well-known cardiovascular risk factor.8 ,13 ,14 From other PAD studies focusing on ethnicity, particularly in African Americans, high rates of CAD and diabetes have translated into high PAD prevalence as expected by the physiological linkages between atherosclerotic disease and diabetes even after adjustment for both traditional and novel cardiovascular risk factors.15 ,16 Despite high incidence of diabetes and cardiovascular disease in SAs, some studies have suggested lower PAD prevalence in this ethnic group.9 ,14 ,17 ,18 This may lead to decreased vigilance of a condition already under-diagnosed and may also impact diagnosis and treatment of cardiovascular risk factors.

    Given the increasing ethnic diversity in Western countries, it is important to recognise the differences in the epidemiology of PAD between ethnic groups and respond with appropriate treatments and guidelines. Our objective is to compare the population prevalence of PAD in persons of SA descent to persons of WE descent through a systematic review and meta-analysis of the literature.

    Methods

    Search strategy

    Standard Cochrane systematic review methodology as outlined by the Cochrane Collaboration19 was used to conduct a librarian-assisted literature review of published papers on PAD prevalence. The following databases were searched: MEDLINE (1950-Apr 2013), EMBASE (1980-Apr 2013), BIOSIS Previews (1926-Apr 2013), PubMed (1966-Apr 2013), Web of Science (1900-Apr 2013), and Scopus (1982-Apr 2013). A manual search and a review of reference lists from primary studies were also undertaken. Search terms were determined by review of previous related literature and included, but were not limited to, ‘peripheral vascular disease,’ ‘peripheral arterial disease,’ ‘atherosclerosis,’ ‘peripheral occlusive artery disease,’ ‘claudication,’ ‘peripheral ischaemia,’ ‘PAD,’ ‘PVD,’ ‘diabetes mellitus,’ ‘ diabetes complications,’ ‘diabetic foot,’ ‘Asian continental ancestry group,’ ‘Asian,’ ‘Indian,’ ‘Indo-Asian,’ ‘South Asian,’ ‘ethnic difference,’ ‘ethnicity,’ ‘race difference’ ‘ankle brachial,’ ‘doppler,’ ‘foot pulse’ and ‘prevalence.’ To ensure a comprehensive search, term truncation, subject heading explosion and validated search filters were used when appropriate. A complete search strategy is available from the authors.

    Selection criteria

    We included population prevalence studies of PAD in SAs with a WE comparison group. SAs were defined as persons of Indian, Pakistani, Bangladeshi, Sri Lankan, Ceylonese, Nepalese, Bhutanese or Maldivian descent. The comparison group of WEs refers to light-skinned persons who are of European ancestry. As the term Caucasian is often misused when referring to WEs, articles using this term were included in the review. Eligible studies included patients with other comorbidities such as CAD or diabetes mellitus where PAD prevalence was a secondary measure. Each publication was assessed for quality; however, risk of bias did not disqualify the study for inclusion. We did not place any limitations on the PAD diagnosis methods or year of publication and there were no restrictions on the language of publication.

    Study selection process

    Initial screening of abstracts and/or titles was undertaken by the primary author (MS). Studies identified for full review were then examined by two authors (MS, RT) to assess eligibility according to the inclusion criteria specified. Outcomes of interest were extracted independently by two reviewers (MS, MM) and compared for discrepancies. During the appraisal for inclusion and subsequent data extraction, any issues or differences of opinion were resolved by discussion until a consensus was reached. In one case, we contacted the author for further clarification on their study.

    Data extraction and analysis

    Extracted variables included ethnicity, sample size, age, gender, body mass index (BMI), smoking, comorbid conditions, method of PAD diagnosis and reported PAD prevalence. The denominator for PAD prevalence was assumed to be the sample size of the study unless otherwise stated. Any studies that did not indicate PAD diagnosis method were assumed to not have used ankle-brachial index (ABI).

    All studies identified for inclusion underwent data analysis. PAD prevalence was divided a priori into three groups: the general population with no comorbidities and two chronic disease populations: CAD and diabetes. Data were combined and reported as weighted averages with SD or 95% CIs using SPSS software (V.17. IBM: Chicago, Illinois, USA) and STATA (V.12.1. StataCorp LP: College Station, Texas, USA). Random-effects meta-analysis illustrated by forest plots within Review Manager (RevMan) (V.5.1. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2011) was used to calculate ORs and heterogeneity. Measures of heterogeneity between the studies were reported as I2. Studies were further divided by method of PAD diagnosis: the gold standard ABI versus other diagnosis methods.

    Results

    Literature search

    A total of 21 615 citations were reviewed; 15 studies, with a total of 240 003 patients, were included for the complete statistical analysis (figure 1). The studies were published between 1991 and 2013 with 13 studies published after 2000.

    Figure 1
    Figure 1

    Identification of included studies.

    Of the included studies, one study was conducted in the general population (n=77 855), seven (n = 162 148) focused on CAD patients and seven (n=22 835) focused on diabetes patients (table 1). Of the CAD studies, three were from the UK (UK) (n=10 028) and four were from Canada (n=129 285). All of the diabetes studies originated in the UK (n=22 835).

    View this table:
    Table 1

    Included studies

    Quality of studies

    Many of the studies included in the analysis were limited by unclear PAD diagnosis methods. Only 3 of the 15 studies (one CAD, two DM, n=636) used the gold standard ABI to diagnose PAD cases. An additional six (41%, n=17 898) studies made PAD diagnoses using clinical symptoms, six (41%, n=221 469) used information from databases with or without International Classification of Disease (ICD) Codes (table 1). For the studies that used ABI, the cut-off value for a positive diagnosis of PAD ranged from 0.85 to 1.00.

    There is a possibility of selection bias, as 80% (12 studies, n=146 539) of included studies drew samples from research centres, hospitals and diabetes clinics where patients generally have more advanced disease profiles with multiple comorbidities when compared to the population at large. In reporting their sampling methods, 80% (12 studies, n=238 438) used either all available patients, consecutive or random sampling.

    Population characteristics

    There was evidence of heterogeneity across the comparison studies that underwent meta-analysis (CAD I2=25%, DM I2=66%) with demographic variation between the population groups of patients with CAD and diabetes (figures 2 and 3). The CAD population was significantly older and had a higher percentage of males than the diabetes population in both ethnic groups, while BMI and smoking rates were lower in the CAD population than the diabetes population (all p<0.001).

    Figure 2
    Figure 2

    Forest plot of coronary artery disease comparison studies.

    Figure 3
    Figure 3

    Forest plot of diabetes comparison studies.

    Within each disease subgroup of CAD and diabetes, when compared to WEs the SA populations were significantly younger (CAD: 60.4±1.2 years vs 64.6±0.4 years, p<0.001; diabetes: 54.8±5.5 years vs 61.4±5.3 years, p<0.001); had more males (CAD: 76.9% vs 72.8%; diabetes: 55.7% vs 54.3%), had a lower BMI (CAD: 25.7±0.5 vs 28.0±0.3, p<0.001; diabetes 28.6±1.7 vs 30.5±2.8, p<0.001) and lower smoking rates (CAD: 20.4% vs 20.7%, p=0.004; diabetes 21.4% vs 52.4%, p<0.001) (table 2).

    View this table:
    Table 2

    Population characteristics for South Asian and White European PAD comparison studies

    PAD prevalence

    PAD prevalence in the general population

    There was one comparative study between SAs and WEs in a general population. They reported a significantly different PAD prevalence of 1.4% in the SA population and 1.9% in the WE population (OR=0.26, 95% CI 0.17 to 0.38, p<0.001).20

    PAD prevalence in studies of people with CAD

    In the pooled analysis of the CAD comparison studies, PAD prevalence in the SA ethnic group was significantly lower than the WE group (OR=0.47, 95%CI 0.39 to 0.56, p<0.001) with low heterogeneity (I2=25%) (figure 2, table 3). Only one CAD study reported use of ABI and the reported PAD prevalence for both SAs and WEs was significantly higher than the non-ABI studies (p<0.001) (table 4). The difference in PAD prevalence between the two ethnic groups in the ABI study was only marginally statistically significant (OR=0.53, 95%CI 0.26 to 1.06; p=0.07) (figure 2).

    View this table:
    Table 3

    PAD prevalence in comparative studies between South Asians and White Europeans

    View this table:
    Table 4

    PAD prevalence in comparative studies between South Asians and White Europeans using different PAD diagnosis methods

    PAD prevalence in studies of people with diabetes

    For the comparison studies between SAs and WE diabetes patients, SAs had significantly lower PAD prevalence rates than WEs (OR=0.44, 95% CI 0.30 to 0.63, p<0.001) with moderate heterogeneity (I2=66%) (figure 3, table 3). Two of the five comparison studies used ABI for PAD diagnosis (OR=0.44; 95% CI 0.24 to 0.81; p=0.009; I2=0%) (figure 4) and the difference in PAD prevalence between the non-ABI and ABI studies was significant (p=0.001 and p=0.044 for SAs and WEs respectively) (table 4).

    Figure 4
    Figure 4

    Forest plot of diabetes comparison studies using ankle-brachial index.

    Ethnic differences in PAD prevalence and ABI

    In each disease subgroup, there was a significant difference in PAD prevalence between the ABI and non-ABI studies (table 4). However, the comparison studies that used ABI showed smaller differences in PAD prevalence between ethnic groups and had an OR closer to one when compared to studies using clinical diagnosis (figures 3 and 4).

    Discussion

    There is well-documented evidence that SAs have a markedly higher prevalence of diabetes and CAD compared to other ethnic groups.7 ,8 ,13 ,14 ,31 Based on known atherosclerotic risks, we would expect a higher PAD prevalence in SAs when compared to WEs, yet our systematic review data suggest a paradoxically lower prevalence of PAD in SAs. These findings support current research that certain ethnic groups are more prone to location-specific manifestations of atherosclerosis.32 The mechanism of the paradox (if true) is unknown and requires further investigation. This meta-analysis also confirms findings in previous individual studies that the prevalence of PAD is higher in studies using ABI. The underlying interpretation is that many patients are asymptomatic and, therefore, the true burden of PAD is unknown unless ABI is measured.

    Previous studies comparing ethnic differences in PAD prevalence have found ethnic disparities. A study of a multiethnic sample from the National Health and Nutrition Examination Survey (NHANES) reported an ABI-determined PAD prevalence of 7.8% among African Americans compared to 5.1% in Mexican Americans and 3.4% in Whites despite conventional risk factor control being similar between the different ethnic groups.33 African Americans have consistently reported higher PAD prevalence compared to Hispanics and Whites in multi-ethnic US studies.34 Not surprisingly, African Americans also have higher reported prevalence of cardiovascular disease, stroke and hypertension compared to all other ethnic groups in the USA.35

    SA studies suggest that the ethnic differences found in PAD prevalence are related to the heterogeneity of risk factors found in SAs where traditional risk factors alone do not explain the higher cardiovascular burden in this ethnic group.3 While smoking is a strong risk factor for PAD, smoking rates are generally less in SAs (particularly in females) than WEs; however, adjustment for smoking rates or pack years does not explain the ethnic discrepancy in PAD prevalence.3 ,18 Measuring carotid intima media thickness among SAs and WEs, the SHARE investigators discovered that despite a higher rate of cardiovascular events, SAs have significantly less carotid atherosclerotic thickness (p=0.00098).7 They suggested that the high prevalence of glucose and lipid abnormalities in this ethnic group could cause decreased plaque stability, leading to more cardiovascular events. SAs do indeed have a number of metabolic abnormalities, including high serum levels of apolipoprotein B, triglycerides, lipoprotein a, 7 ,36 ,37 as well as low levels of high density lipoproteins and apolipoprotein A.37 This unique lipid profile combined with higher levels of thrombotic factors of homocysteine, fibrinogen and the plasminogen activator inhibitor (PAI-1)37 along with insulin resistance38 may indicate that vascular disease risk in this ethnic group has less to do with the amount or location of the atherosclerotic plaque and more with its thrombotic tendency. In addition, C reactive protein (CRP), an inflammatory mediator, has been shown to be independently associated with cardiovascular disease even after adjustment of known confounders.39 CRP levels differ significantly between ethnic groups, with SAs having higher levels than persons of WE descent (adjusted mean CRP 2.59 mg/l (±0.12) SAs; 2.06 mg/l (±0.12) Europeans).39 From these findings, it is possible that despite having less atherosclerosis as evidenced by lower PAD prevalence and less intima media thickness, SAs still have higher rates of cardiovascular events and cardiovascular mortality due to inflammation and thrombosis of unstable plaque.

    Limitations

    A systematic review is retrospective by nature and is restricted to a secondary analysis of aggregate data. There was low heterogeneity between the CAD studies and moderate heterogeneity between the diabetes studies, which most likely originates from the different methods of PAD diagnosis and demographic variation. In addition, prevalence calculations were not adjusted for risk factors in all the original studies. Those studies for which prevalence was adjusted or matched for age and/or sex are noted in table 1. While heterogeneity between studies is a clear limitation, our conclusions are based on the best available evidence.

    In addition, the majority of papers included in this review originate in the UK and Canada. As a result, the study populations may be influenced by differing cultural perceptions and social factors that may contribute to a bias in reporting of symptoms such as claudication.9 These factors are difficult to account for in a combined analysis. It is also important to note that we cannot separate data from recent immigrant and local populations; however, as stated previously, research indicates that immigrants who adopt their new country's lifestyle maintain the same atherosclerotic risk as persons in their homeland.10 ,12

    Finally, these conclusions are drawn from studies sampled from clinical populations that may not reflect true population prevalence. The PAD prevalence may be higher than reported even in ABI studies as arteriosclerosis and arterial calcification, which are more common in diabetic patients, lead to non-compressible arteries, which can result in an underestimated PAD prevalence.9 ,17 We did exclude studies that involved amputation that could underestimate the PAD prevalence; however, there are many contributing factors to amputation outside of atherosclerotic disease.

    Implications

    SAs with CAD or diabetes appear to have less PAD than WEs; however, this information should not reduce the importance of PAD screening in SAs with multiple risk factors. In a number of populations, there is definitive evidence that PAD worsens prognosis and that diabetes is a strong risk factor for the development of PAD.2 Early detection of PAD is an opportunity for prevention and/or improved prognosis of cardiovascular outcomes that should not be overlooked.

    Conclusion

    Based upon the best available evidence from 15 studies in 240 003 patients, SAs have a paradoxically lower prevalence of PAD, both overall and in higher risk populations of those with CAD or diabetes. Further investigation is required to determine the underlying pathophysiological mechanism leading to differences in manifestations of atherosclerotic disease between ethnic groups; specifically if these differences are driven by novel risk factors or genetic susceptibility.

    Acknowledgments

    The authors would like to thank Mr. Quazi Ibrahim for his help with some of the statistical analysis.

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    Footnotes

    • Contributors MS and MD conducted the literature search, MS reviewed all citations, MS and RT determined criteria and papers for inclusion, MS and MM did independent data extraction, MS wrote the manuscript with input from MM and RT and undertook the statistical analysis with help from Mr. Quazi Ibrahim. MS and RT are the guarantors for this manuscript. All authors had full access to all of the data (including statistical reports and tables) in the study and can take responsibility for the integrity of the data and the accuracy of the data analysis.

    • Funding This study received no specific grant funding. MS is funded by a team grant from the Faculty of Medicine and Dentistry, University of Alberta to Drs. MS McMurtry and RT Tsuyuki.

    • Competing interests None.

    • Provenance and peer review Not commissioned; externally peer reviewed.