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Coronary Artery Disease in South Asians

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It is well established that South Asians living in the western world have a higher burden of cardiovascular disease than other ethnicities. Additionally, South Asians develop cardiovascular disease at a younger age, have a more aggressive form of coronary artery disease, and a higher overall mortality. This predilection seems to be multifactorial and includes a combination of traditional and emerging risk factors with an absence of ethnic-specific prevention and control measures. Future direction points toward ongoing research with the aim of discovering technology for earlier detection. Additionally, coronary artery disease in South Asians could be addressed by increasing awareness, modifying health beliefs through health-promotion strategies, and instituting ethnic-specific control measures including appropriate and early pharmacological intervention.
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rEviEw articlE
Abstract: It is well established that South Asians living in the western world
have a higher burden of cardiovascular disease than other ethnicities. Addi-
tionally, South Asians develop cardiovascular disease at a younger age, have a
more aggressive form of coronary artery disease, and a higher overall mortal-
ity. This predilection seems to be multifactorial and includes a combination
of traditional and emerging risk factors with an absence of ethnic-specific
prevention and control measures. Future direction points toward ongoing
research with the aim of discovering technology for earlier detection. Addi-
tionally, coronary artery disease in South Asians could be addressed by
increasing awareness, modifying health beliefs through health-promotion
strategies, and instituting ethnic-specific control measures including appro-
priate and early pharmacological intervention.
Key Words: coronary artery disease, ethnicity, South Asian
(Cardiology in Review 2012;20: 304–311)
South Asians comprise 25% of the world’s population and account
for nearly 60% of the global cardiovascular disease (CVD) bur-
den.1–3 In this population, coronary artery disease (CAD) occurs at
a younger age, is more aggressive, and has a higher overall mortal-
ity.4–11 Accordingly, it is imperative for health practitioners to under-
stand the burden of CVD in patients of South Asian descent.
EPIDEMIOLOGY
The term South Asians refers to people who are originally from
the Indian subcontinent, that is, from India, Pakistan, Nepal, Bangla-
desh, and Sri Lanka. As a result of worldwide migration (Figure 1)11
standardized comparisons among different ethnic groups have pro-
vided valuable information regarding clinical outcomes in South
Asians with CAD. The traditional CAD risk factors occur at a
younger age with higher mortality rates from CAD.12–14 Over the past
30 years, the incidence of CAD among South Asians has doubled,
and has exponentially risen for South Asians who have immigrated to
the United States.13,14 Contemporary data from the United States sug-
gest the proportional mortality ratio for South Asians with CAD is at
least two times that of any other ethnicity (Figure 2).9 Although CAD
affects only 3% to 4% of the rural population in South Asia, it affects
10% of South Asian urban populations who live in South Asia, and
who have immigrated to western countries.14 As such, environmental
factors related to urbanization play a role in the premature develop-
ment of CAD among the South Asian community.
The CAD burden of South Asians is projected to worsen in the
next decade to more than half of the global CVD. The current control
measures that have proven effective in other ethnic groups may not
be optimal in the South Asian population.13
Are All South Asians the Same?
Variations in the distribution of CAD and associated risk fac-
tors have been observed among South Asian countries, with Ban-
gladesh having the highest prevalence of risk factors and the lowest
prevalence of risk modification (ie, regular exercise and daily con-
sumption of fruits and vegetables) with the lowest mean age of acute
myocardial infarction (MI). When South Asian migrant groups liv-
ing in the United Kingdom were studied, similar heterogeneities in
cardiovascular risk factors have been observed among Bangladeshi
migrants compared with Indian and Pakistani migrants. Further-
more, the metabolic profiles of Bangladeshi migrants demonstrate
higher levels of triglycerides, low-density lipoprotein (LDL), and
fasting glucose, and the lowest levels of high-density lipoprotein
(HDL) when compared with Pakistanis, Indians, and Europeans.15–17
These exaggerated differences in Bangladeshis are of particular con-
cern and require further investigation.
Future Generations
Unfortunately, South Asian children are showing increased
susceptibility to the metabolic syndrome and CAD. A comparative
study done in the United Kingdom between white and South Asian
children showed higher mean fasting and postglucose load insulin
concentrations, increased mean heart rate, and elevated mean serum
triglyceride and fibrinogen levels among South Asian children.18
A higher incidence of adiposity was seen in South Asian children
compared with white children, yet an increased prevalence of insulin
resistance persisted after adjusting for adiposity and pubertal status.18
In addition to the children from native and migrant South
Asian populations who have been reported to have such tendencies,
children of South Asian descent born and raised in Western societ-
ies have altered metabolic profiles when compared with their white
counterparts. Case Western Reserve University (Cleveland, OH) com-
pared metabolic and anthropometric measures of young adults of South
Asian ethnicity, who were born and raised in the United States. Men
had significantly higher total cholesterol (TC), LDL, TC: HDL ratios,
triglycerides, and fasting insulin levels and lower HDL than their white
counterparts. Women demonstrated higher plasma insulin levels than
their white counterparts. The entire South Asian group had higher trun-
cal skin-fold thickness and lower insulin-like growth factor-binding
protein-1 levels. Plasma leptin levels were also significantly higher
in the South Asian cohort, whereas no differences were observed in
lean body mass, homocysteine, or serum lipoprotein(a) [Lp(a)]. These
findings point to an altered metabolic profile that supports a genetic
predisposition to altered body fat pattern (thin muscle/visceral fat phe-
notype), and contributes to the deleterious consequences of the meta-
bolic syndrome.19
TRADITIONAL RISK FACTORS
Traditional risk factors for atherosclerotic vascular disease,
which had been described by the Framingham study were mainly
assessed in white subjects.20 Although they play a part in the South
Asian population, they cannot fully explain the excess risk.14 South
Copyright © 2012 by Lippincott Williams & Wilkins
ISSN: 1061-5377/12/304-311
DOI: 10.1097/CRD.0b013e3182532286
Cardiology in Review
20
6
Copyright © 2012 by Lippincott Williams & Wilkins
1061-5377/12/304-311
10.1097/CRD.0b013e3182532286
From the *The Albert Einstein College of Medicine, Bronx, New York; †Division
of Cardiology, Montefiore-Einstein Heart Center, Bronx, New York; ‡Faculty
of Nursing, University of Alberta, Edmonton, Canada; and §Mazankowski
Alberta Heart Institute, University of Alberta, Edmonton, Canada.
Disclosure: The authors have no conflicts of interest to report.
Correspondence: Seshasayee Narasimhan, MBBS, MRCP, FRACP, Department of
Medicine, Cardiovascular Division, Montefiore-Einstein Heart Center, Jack D.
Weiler Hospital of the Albert Einstein College of Medicine, 1825 Eastchester
Road, Bronx, NY 10461-2373. E-mail: docsesh@gmail.com.
Coronary Artery Disease in South Asians
Seshasayee Narasimhan, MBBS, MRCP,*†§ Katrina McKay, RN, and Kevin R. Bainey, MD§
CRD
CRD200331
Coronary Artery Disease in South Asians
Narasimhan et al
2012
November/December
© 2012 Lippincott Williams & Wilkins www.cardiologyinreview.com  |  305
Cardiology in Review • Volume 20, Number 6 November/December 2012  Coronary Artery Disease in South Asians
Asians seem to have a combination of traditional and novel risk
factors, which contribute to their heightened risk of CAD. In general,
traditional risk factors are noted to be rare with the exception of
diabetes mellitus.1,5,21 In fact, the contribution of insulin resistance
plays a major role in the higher prevalence of CAD and may be
associated with the contribution of excessive central abdominal
obesity/visceral fat.12,14,22,23 In fact, when compared with other
ethnicities of comparable body mass index, South Asians have higher
visceral fat mass,24,25 thicker truncal skin fold, and lower lean body
mass with the distribution focused in the abdominal visceral space
(thin muscle/visceral fat phenotype).19,26–32 Central adiposity has
been correlated with insulin resistance and hyperinsulinemia,28,29 and
has been noted to have a direct relationship with increased risk of
CAD.33 The International Diabetes Federation utilizes ethnic-specific
waist circumference, which helps better identify those South Asian
patients having the highest cardiovascular risk factors.34 For the
South Asian population, the waist circumference cutoff for men was
90 cm or more and for women was 80 cm or more(Table 1).35
One of the modifiable risk factors, smoking, is low in South
Asians, and virtually nonexistent in women.12 However, a high intake
of dietary fats and little or no exercise contributes to characteristic
lipid profiles, including higher triglyceride levels, higher Lp(a)
levels, increased ratio of apolipoprotein B to apolipoprotein A-1
(ApoB/ApoA-I), smaller HDL and LDL particle size, and lower
levels of HDL.12 ApoB 100 is the major apolipoprotein found
in LDL, intermediate-density lipoprotein, and very LDL, and it
is the primary ligand for the LDL receptor. ApoA-I is the major
protein constituent of HDL. The ApoB 100/ApoA-I ratio provides
an atherogenic to antiatherogenic lipoprotein ratio that has been
shown to be a better predictor of CVD than LDL level, HDL level
or LDL/HDL ratio.36–39 Furthermore, the ApoB 100/ApoA-I ratio
can identify individuals with a preponderance of small dense LDL
particles, but with seemingly normal LDL levels.40,41 The landmark
International Heart (INTERHEART) study was among the first
studies to demonstrate that elevated ApoB100/ApoA-I ratio was the
risk factor associated with the highest population-attributable risk for
MI (46.8%), with waist-to-hip ratio (37.7%), and smoking (37.5%)
also being important risk factors in the South Asian population.41–43
EMERGING RISK FACTORS
Although contributory, traditional risk factors do not fully
explain the heightened risk of CAD in South Asians. Thus, novel and
emerging risk factors have been explored. This is particularly impor-
tant as testing for these parameters (if available) will certainly help
risk stratification in South Asian patients.
Lipoprotein (a)
The National Cholesterol Education Program Adult Treat-
ment Panel III considers Lp(a) an important and emerging risk
factor for CAD. Lp(a) has been implicated in the development of
premature atherosclerotic disease in the South Asian cohort.44–48 It
FIGURE 1. South Asian migration patterns from the Indian subcontinent to different areas across the world. Reprinted with 
permission from Atherosclerosis 2009;204:1–10.
TABLE 1. New Metabolic Syndrome (MS) Criteria
Measures (Any 3 of 5 Constitutes
Diagnosis of MS) Categorical Cutoff Points
Elevated waist circumference*† Men: 102 cm (40 inches)
Women: 88 cm (35 inches)
Elevated triglycerides (TGL) 150 mg/dL (1.7 mM)
Or on drug therapy for elevated
TGL
Reduced HDL-cholesterol (HDL-C) Men: 40 mg/dL (1.03 mM)
Women: 50mg/dL (1.3 mM)
Or on drug therapy for reduced
HDL-C‡
Elevated blood pressure 130 mm Hg systole (or) 85
mm Hg diastole (or) on
antihypertensive therapy for
history of hypertension
Elevated fasting blood glucose 100 mg/dL (5.6 mM)
or on drug therapy for
hyperglycemia
Adapted from Diagnosis and management of the metabolic syndrome: an
American Heart Association/National Heart, Lung, and Blood Institute Scientific
Statement.35
*To measure the waist circumference, locate top of right iliac crest. Place
measuring tape in a horizontal plane around abdomen at the level of iliac crest. Ensure
tape is snug, does not compress abdomen skin and is parallel to the floor. Measurement
is made at the end of normal expiration.
†Non-Asian adults (black, Hispanic and white) with marginally increased waist
circumference, men: 94 cm to 101 cm (37–39 inches), women: 80 cm to 87 cm (31–34
inches) may have a strong genetic contribution to insulin resistance and should benefit
from lifestyle changes similar to those in the categorical cutoff group. Asian adults have
a lower waist circumference cut off, men: 90 cm (35 inches) and women: 80 cm (31
inches).
‡Fibrates and nicotinic acid are the most commonly used drugs for elevated TGL
and reduced HDL-C. Patients on either of these drugs are presumed to have elevated
TGL.
TGL indicates triglycerides; HDL, high-density lipoprotein.
306 | www.cardiologyinreview.com © 2012 Lippincott Williams & Wilkins
Narasimhan et al Cardiology in Review Volume 20, Number 6 November/December 2012
represents a class of LDL particles that contains the plasminogen-
like apolipoprotein A moiety attached to the ApoB100 protein.
Unlike other lipids that are influenced by diet, age, sex, and other
environmental factors, Lp(a) levels are primarily driven by genetics
and ethnicity.49–52 In whites, Lp(a) levels more than 30 mg/dL are
considered a risk factor for premature CAD. In South Asians, levels
less than 20 mg/dL are considered optimal.48,53 There is a two- to
threefold increased risk of acute myocardial infarction and reste-
nosis after coronary angioplasty or coronary artery bypass grafting
in those South Asian patients with Lp(a) levels between 20 and 30
mg/dL.54–56 When Lp(a) levels are more than 55 mg/dL with low
HDL and high TC/HDL ratio, MI risk increases 100-fold.46,57,58 Due
to its homology to plasminogen, Lp(a) is highly thrombogenic and
antifibrinolytic.59
Homocysteine
Mager et al60 acknowledges that treating hyperhomocyste-
inemia (>15 µM) in CAD as both primary and secondary strate-
gies have failed to show benefit. However, they also noted that
all the prior studies have focused on white cohorts, which ques-
tions ethnic variation. Hyperhomocysteinemia is also known to
occur due to alcohol abuse,61 and seems to be a novel risk fac-
tor in South Asian patients.13,62–66 It contributes to cardiovascular
risk and tends to be higher in South Asians compared with the
white population.64–67 Boushey et al63 reported that a 1-µM increase
in hyperhomocysteinemia level is associated with an increase in
CAD risk of 12% in men and 16% in women.63 Refsum et al66
reported a high prevalence of hyperhomocysteinemia (15 µM) in
Indians. They also observed that dietary difference made no dif-
ference, and that hyperhomocysteinemia strongly correlated with
cobalamine deficiency.66 Further ethnic-specific studies are needed
to fully understand the contribution of hyperhomocysteinemia to
CAD in South Asians.
Adipokines
Adipokines or adipose-tissue–derived circulating hormones
seem to link insulin resistance and premature atherosclerosis, par-
ticularly in South Asians given the propensity toward central abdom-
inal obesity. Certainly proinflammatory adipokines, such as leptin,
PAI-1, tumor necrosis factor-α, interleukin-6, and C-reactive protein,
contribute to endothelial dysfunction and the development of ath-
erosclerotic disease. Adipose tissue also produce anti-inflammatory
substances such as adiponectin (a cytokine with insulin sensitizing,
antiatherogenic, and anti-inflammatory properties), but seem to be
suppressed in individuals with central obesity. In fact, studies sup-
port the direct association between hypoadiponectinemia (both total
adiponectin levels and high molecular-weight adiponectin levels) and
the development of CAD in South Asians. Yet, this association has
not been observed in whites.68,69
Other Novel Cardiac Biomarkers
Abnormalities in markers of endothelial dysfunction, such
as vascular-cell adhesion molecule-1,70 impaired endothelium
dependant dilation,71 proinflammatory HDL,72–78 and Apo A-I poly-
morphisms,14,79–81have been described in the South Asian population.
Further research is needed to delineate the magnitude of cardiovascu-
lar risk these novel risk factors will confer upon this high-risk patient
population.
NOVEL CONSIDERATIONS
Genetics
The Coronary Artery Disease Genetic Consortium (C4D)
recently reported the discovery of five new loci for CAD. They
focused on two populations, whites and South Asians, and found
the same five loci were implicated in the development of CAD in
both populations. Yet, there may be other genes causing premature
CAD in South Asians, which remain undiscovered. Currently, the
best available genetic information is one of the Lp(a) variants, which
occur in approximately one in every six persons, and confers a 50%
increase in risk, and the 9p21 gene, which confers an approximate
25% increase in risk. Still, this does not entirely explain the heightened
risk of CAD in the South Asian population.82,83 As such, two major
genome-wide association studies are currently being performed in the
United Kingdom (the London Life Sciences Prospective Population
Study) and Pakistan (the Prosecutor’s Management Information
System).
FIGURE 2. Mortality of different ethnic groups from ischemic heart disease. Reprinted with permission from Ann Epidemiol
2004;14:499–506.
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Cardiology in Review • Volume 20, Number 6 November/December 2012  Coronary Artery Disease in South Asians
Coronary Artery Size
Currently, there is a lack of consensus regarding the contribu-
tion of coronary artery size in South Asian patients. Nonetheless, the
South Asian cohort still has a higher prevalence of both severe diffuse
and three-vessel CAD. Vascular remodeling based on ethnic differ-
ences has been implicated because, in comparison with whites, the
South Asian cohort exhibits a greater narrowing of the proximal left
anterior descending artery in association with more advanced athero-
sclerosis.84 Another small retrospective study using strict inclusion/
exclusion criteria showed that proximal coronary artery size and
the number of significant coronary stenoses did not differ between
matched pairs of South Asian and white men.85 Dhawan and Bray86
compared coronary angiograms from a consecutive series of South
Asian men with those from randomly selected white men and found a
smaller mean total coronary artery diameter in the South Asian group
than in the white cohort. They also demonstrated a correlation between
body surface area and coronary artery size. However, when the inves-
tigators adjusted total coronary artery diameter for body surface area,
the interethnic difference in coronary artery size between South Asian
and white patients was negligible.86 A recent article by Hasan et al87
used quantitative coronary angiography to assess the coronary size
and distribution of disease between South Asians and whites, and
concluded that South Asians have smaller coronary artery luminal
diameters compared with whites, which reiterates a possible role of
coronary artery size in affecting increased CAD risk and mortality
among South Asians. Furthermore, they noted the observation that
South Asians exhibit heightened CAD at an earlier age when com-
pared with whites.87 Intravascular ultrasound may be a worthwhile
investigative modality, although this has not been currently explored.
Alcohol
Regular alcohol consumption (once per week) is noted to be
cardioprotective in some ethnicities. The beneficial effects are depen-
dent on the amount of alcohol consumed and the pattern of drinking.
In their meta-analysis, Di Castelnuovo et al88 reported the beneficial
effects of alcohol when limited in the light-to-moderate drinkers who
have less risk than abstainers. Heavy drinkers are at the highest risk.
They also showed that consumption of one drink daily by women and
one or two drinks daily by men was associated with a reduction in
total mortality of 18%. Conversely, intakes of more than two drinks
daily in women and three drinks daily in men were associated with
increased mortality in a dose-dependent fashion.88 Alcohol consump-
tion was not cardioprotective in the South Asian group, and was actu-
ally harmful in the Indian subgroup.16,17 Perhaps this could be related
to the lower prevalence or the pattern of drinking (binge vs daily
drinking) in South Asians.88
FUTURE DIRECTIONS
Is it Time to Revise the Framingham’s Risk Factor
Profile Score?
Traditionally, the Framingham’s risk factor profile score
(FRFPS) includes age, cholesterol levels, blood pressure, smoking,
and diabetes mellitus to help determine the 10-year risk of nonfatal
MI or coronary death. The FRFPS underestimates the CAD risk in
South Asians.10 Certainly the metabolic syndrome is contributory in
South Asians and should be included in risk stratification. Figure 3
provides a modified FRFPS in South Asians at risk for CAD and may
be a useful tool in risk stratification.11
Are We Missing Something?
Despite conventional and novel risk factors, it has been shown
that the beliefs and attitudes of South Asian patients have a direct
result on their health outcomes. Health beliefs are important in influ-
encing health behaviors.89 The ability to embrace or reject lifestyle
modifications could possibly be influenced by a lack of appreciation
for CAD and the consequences of the disease.90 Various studies based
in the United Kingdom and the United States have identified a gen-
eral deficit in knowledge concerning CAD, its prevention and health
FIGURE 3. A proposed cardiovascular risk stratication tool for patients of South Asian descent. Reprinted with permission from 
Atherosclerosis 2009;204:1–10.
1. Target LDL <2.0 mmol/L
2. Total cholesterol/HDL <4.0
3. Anti-platelet therapy
4. Healthy lifestyle
Moderate Risk
in SA population
High Risk
in SA population
Yes No Yes No
Low Risk
in SA population
Moderate Risk
in SA population
1. Target LDL <2.0
2. Total cholesterol/
HDL <4.0
3. Anti-platelet therapy
4. Healthy lifestyle
1. Target LDL <3.5
2. Total cholesterol/
HDL <5.0
3. Anti-platelet therapy
4. Healthy lifestyle
1. Target LDL <3.5
2. Total cholesterol/
HDL <5.0
3. Anti-platelet therapy
4. Healthy lifestyle
1. Target LDL <5.0
2. Total cholesterol/
HDL <6.0
3. Healthy lifestyle
High Risk
(10 year risk of CAD 20%
or history of DM or any
atherosclerotic diease)
according to FRS
Low Risk
(10 year risk of CAD10%)
according to FRS
Moderate Risk
(10 year risk of CAD 11% -19%)
according to FRS
AB C
High Risk in SA
population
?
Metabolic Syndrome
(Waist circumference 90 in
Males; 80 in females)
?
Metabolic Syndrome
(Waist circumference 90 in
Males; 80 in females )
Primary Prevention of Coronary Artery Disease (CAD)
in a South Asian (SA) Patient
Adjusted Framingham
Risk Score (FRS)
Add 10 years to age criteria
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Narasimhan et al Cardiology in Review Volume 20, Number 6 November/December 2012
promotion.91–93 Furthermore, Rankin and Bhopal92 identified that the
lack of knowledge was influenced by the country of birth, noting that
the Bangladeshi community fared the worst.
This lack of knowledge of CAD is linked to poor dietary
habits, low levels of physical activity, and social support. Beishon
and Nazroo89 noted that despite healthy-eating campaigns, there was
a definite lack of information among the South Asian community
regarding dietary intake and its correlation with CAD. Most South
Asians believe in a healthy diet, yet few adhere to dietary constraints.
Reddy and Yusuf94 highlighted the global availability of vegetable
oils and fats, which resulted in increased fat consumption among
low-income countries. The usual diet for South Asian countries con-
sisted of high carbohydrates and low fat. This has been replaced with
a decline in complex carbohydrates and a high intake of dietary fat.
As well, South Asians are unaware of the varied types of oils and fats
(saturated and unsaturated) and their effects on CVD.89 This deficit
in dietary knowledge, along with urbanization, has translated to poor
dietary habits for Indians immigrating to the United Kingdom, lead-
ing to central obesity and a predisposition to accelerated atheroscle-
rotic disease.95
In general, South Asians have lower levels of physical activ-
ity.86,96 Many South Asians do believe it is important, yet it seems only
younger men actually engage in regular physical activity. Women and
children believe daily activity is sufficient, whereas elderly South
Asians believe physical activity over a certain age would be detri-
mental to their health.89,96 Overall, Beishon and Nazroo89 found little
awareness among South Asians regarding types of activities and their
respective health benefits, especially in the presence of CAD. A study
conducted by Williams et al97 found ethnicity to be the most signifi-
cant risk factor for physical activity rates. This echoes the point of
ethnicity affecting knowledge levels, and once again the Bangladeshi
community has the worst rate of physical activity. It was also iden-
tified that urbanization and psychological distress for those South
Asians who immigrated to the United Kingdom, partially explains
the difference in physical activity. As a result, Bainey et al90 found
South Asians with CAD exhibit poor health-related quality of life
when compared with whites with CAD (Table 2).
Another important factor that is overlooked is social support.
For those South Asians who immigrated to the United Kingdom, there
is evidence to suggest poor social support outside of the home and
religious communities,98 where Pakistanis and Bangladeshis fared
worse than Indians.97 Pollard et al98 found there was no clear evidence
of social networks having a protective effect for abdominal obesity,
blood pressure, and serum lipid profiles. Barnett et al93 identified that
poor use of resources may be linked to an increase in CAD in UK
South Asians. It was also highlighted that South Asians are less likely
to be prescribed statins and other cardioprotective treatments.
How Do We Alter Health Beliefs Among
South Asians?
As there is a general deficit in knowledge regarding health,
and more specifically CAD, health information, and education is
essential. Rankin and Bhopal92 believe that there is an urgent need
for culturally appropriate education programs, especially for the
Bangladeshi community. The information required to decrease the
prevalence of CAD needs to be culturally sensitive and accessible to
patients.89,91 Tailoring and delivering the information on individual
and community levels can improve outcomes. The information in its
varying forms must be language specific and appropriate for effec-
tive communication.89,91 Additionally, extra support should be given
to complement the information that is available. This could be in the
form of healthy-cooking methods as an adjunct to dietary education.91
Accessibility can be accomplished by providing information from a
wide variety of sources, including primary-care physicians, media,
schools, the home, community centers, and family and friends.89
South Asians and health professionals alike need to be edu-
cated primarily on the predisposition of CAD. Additionally, health
professionals should be aware of the increased prevalence and risk of
CAD, and the prominent role of risk factors and metabolic dysfunc-
tion. Education will promote optimal standards of care. As an adjunct
to education, appropriate screening, which includes measuring waist
circumference, waist-to-hip ratios (appropriate for South Asians),
and frequent fasting glucose and lipid levels, need to be provided.11
An example of a health-promotion program that led to a
decrease in cardiovascular risk factors was the Khush Dil (Happy
Heart) intervention.99 The program aimed to develop and test meth-
ods for locally based and culturally sensitive CAD prevention and
control services for South Asians. In addition to decreasing the car-
diovascular risk factors, it changed the motivational status of the par-
ticipants, increasing the adherence to diet and lifestyle modifications.
CONCLUSIONS
It is well established that South Asian migrants living in the
western world have a higher burden of CVD than do other ethnic
groups. In addition, South Asians develop CVD at a younger age,
and have a higher cardiovascular mortality. This epidemic is multi-
factorial, which includes a combination of traditional and emerging
risk factors, a lack of awareness, and an absence of ethnic-specific
prevention/control measures. Future direction points toward ongoing
research with the aim of discovering technology for earlier detection.
Additionally, CAD in South Asians could be attenuated by increas-
ing awareness, modifying health beliefs through health-promotion
strategies, and instituting ethnic-specific control measures including
appropriate pharmacological intervention.
CLINICIAN’S TAKE-HOME POINTS
1. South Asians have an increased risk for early onset of CVD.
Among this population, they have the youngest mean age for MI
with poor clinical outcomes.
2. Besides the traditional risk factors (particularly diabetes melli-
tus), physicians should be aware of the emerging risk factors to
aid risk stratification in their South Asian patients. These include
the metabolic syndrome, visceral adiposity, hyperinsulinemia, el-
evated ApoB100/ApoA-I ratio, LP(a), homocysteine, and low ad-
iponectin levels. Of importance is the elevated Lp(a) levels in the
presence of normal TC and low HDL levels. Lp(a) levels less than
20 mg/dL are considered optimal. A raised ApoB100/ ApoA-I
ratio was the risk factor associated with the highest population-
attributable risk for MI.
TABLE 2. Propensity Score-Matched Analysis of SAQ Scores 
at 1 Year
SA SD
(n = 632)
EN SD
(n = 2681) P
Physical limitation 75 (23) 80 (23) 0.011
Angina stability 77 (28) 77 (27) 0.627
Angina frequency 86 (23) 80 (20) <0.001
Treatment
satisfaction
86 (19) 89 (16) <0.001
QOL 71 (24) 76 (21) <0.001
Adapted from Altered health status and quality of life in South Asians with
coronary artery disease.90
SAQ indicates Seattle angina questionnaire; SD standard deviation; SA, South
Asian; EN, European; QOL, quality of life.
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Cardiology in Review • Volume 20, Number 6 November/December 2012  Coronary Artery Disease in South Asians
3. Ethnic-specific targets should be utilized with the waist circum-
ference cutoff for men being 90 cm or more and women, 80 cm or
more in the definition of the metabolic syndrome.
4. The FRFPS underestimates CAD risk in both South Asian males
and females. Along with the established risk factors, the meta-
bolic syndrome could help risk stratify South Asian patients.
5. Raising awareness of this phenomenon through education and
health promotion among both physicians and patients is vital. It is
important to not only initiate appropriate and early pharmacologi-
cal therapy, but also include strategies to modify health beliefs
and improve lifestyle interventions to ensure continued success.
REFERENCES
1. Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atheroscle-
rosis, and cardiovascular disease between ethnic groups in Canada: the
Study of Health Assessment and Risk in Ethnic groups (SHARE). Lancet.
2000;356:279–284.
2. McKeigue PM, Miller GJ, Marmot MG. Coronary heart disease in south
Asians overseas: a review. J Clin Epidemiol. 1989;42:597–609.
3. Enas EA, Yusuf S, Mehta JL. Prevalence of coronary artery disease in Asian
Indians. Am J Cardiol. 1992;70:945–949.
4. Sheth T, Nair C, Nargundkar M, et al. Cardiovascular and cancer mortality
among Canadians of European, south Asian and Chinese origin from 1979 to
1993: an analysis of 1.2 million deaths. CMAJ. 1999;161:132–138.
5. Enas EA, Garg A, Davidson MA, et al. Coronary heart disease and its risk
factors in first-generation immigrant Asian Indians to the United States of
America. Indian Heart J. 1996;48:343–353.
6. Gupta M, Doobay AV, Singh N, et al. Risk factors, hospital management and
outcomes after acute myocardial infarction in South Asian Canadians and
matched control subjects. CMAJ. 2002;166:717–722.
7. Gupta MSN, Warsi M, Reiter M, Ali K. Canadian South Asians have more
severe angiographic coronary disease than European Canadians despite hav-
ing fewer risk factors. Can J Cardiol. 2001; 17 (suppl C): 226C.
8. Singh N, Gupta M. Clinical characteristics of South Asian patients hospital-
ized with heart failure. Ethn Dis. 2005;15:615–619.
9. Palaniappan L, Wang Y, Fortmann SP. Coronary heart disease mortality for six
ethnic groups in California, 1990–2000. Ann Epidemiol. 2004;14:499–506.
10. Gupta M, Brister S. Is South Asian ethnicity an independent cardiovascular
risk factor? Can J Cardiol. 2006;22:193–197.
11. Bainey KR, Jugdutt BI. Increased burden of coronary artery disease in South-
Asians living in North America. Need for an aggressive management algo-
rithm. Atherosclerosis. 2009;204:1–10.
12. Ghumman M. Coronary Artery Disease in South Asians. Clinical Correlations:
http://www.clinicalcorrelations.org/?p=1023 GMCADiSACC.
13. Jayasinghe SR, Jayasinghe SH. Variant metabolic risk factor profile lead-
ing to premature coronary disease: time to define the syndrome of acceler-
ated atherocoronary metabolic syndrome in Asian Indians. Singapore Med J.
2009;50:949–955.
14. Dodani S. Can conventional risk factors explain excess coronary artery dis-
ease risk in South Asians: Dyslipidemias and dysfunctional high density lipo-
protein (HDL). The Open Epidemiology Journal 2009;2:55–62.
15. Bhopal R, Unwin N, White M, et al. Heterogeneity of coronary heart disease
risk factors in Indian, Pakistani, Bangladeshi, and European origin popula-
tions: cross sectional study. BMJ. 1999;319:215–220.
16. Joshi P, Islam S, Pais P, et al. Risk factors for early myocardial infarc-
tion in South Asians compared with individuals in other countries. JAMA.
2007;297:286–294.
17. Eapen D, Kalra GL, Merchant N, et al. Metabolic syndrome and cardiovascu-
lar disease in South Asians. Vasc Health Risk Manag. 2009;5:731–743.
18. Whincup PH, Gilg JA, Owen CG, et al. British South Asians aged 13-16 years
have higher fasting glucose and insulin levels than Europeans. Diabet Med.
2005;22:1275–1277.
19. Kalhan R, Puthawala K, Agarwal S, et al. Altered lipid profile, leptin, insu-
lin, and anthropometry in offspring of South Asian immigrants in the United
States. Metab Clin Exp. 2001;50:1197–1202.
20. Dawber TR, Kannel WB, Revotskie N, et al. Some factors associated with the
development of coronary heart disease: six years’ follow-up experience in the
Framingham study. Am J Public Health Nations Health. 1959;49:1349–1356.
21. McKeigue PM, Ferrie JE, Pierpoint T, et al. Association of early-onset coro-
nary heart disease in South Asian men with glucose intolerance and hyperin-
sulinemia. Circulation. 1993;87:152–161.
22. Patel JV, Lim HS, Gunarathne A, et al. Ethnic differences in myocardial
infarction in patients with hypertension: effects of diabetes mellitus. QJM.
2008;101:231–236.
23. Forouhi N, McKeigue P. How far can risk factors account for excess coronary
mortality in South Asians? Can J Cardiol 1997; 13: 47B.
24. Misra A. Body composition and the metabolic syndrome in Asian Indians: a
saga of multiple adversities. Natl Med J India. 2003;16:3–7.
25. Misra A, Athiko D, Sharma R, et al. Non-obese hyperlipidemic Asian north-
ern Indian males have adverse anthropometric profile. Nutr Metab Cardiovasc
Dis. 2002;12:178–183.
26. Miller GJ, Beckles GL, Maude GH, et al. Ethnicity and other characteristics
predictive of coronary heart disease in a developing community: principal
results of the St James Survey, Trinidad. Int J Epidemiol. 1989;18:808–817.
27. Banerji MA, Faridi N, Atluri R, et al. Body composition, visceral fat, leptin,
and insulin resistance in Asian Indian men. J Clin Endocrinol Metab.
1999;84:137–144.
28. Miller GJ, Kotecha S, Wilkinson WH, et al. Dietary and other characteristics
relevant for coronary heart disease in men of Indian, West Indian and Euro-
pean descent in London. Atherosclerosis. 1988;70:63–72.
29. Sharp PS, Mohan V, Levy JC, et al. Insulin resistance in patients of Asian
Indian and European origin with non-insulin dependent diabetes. Horm Metab
Res. 1987;19:84–85.
30. Chandalia M, Abate N, Garg A, et al. Relationship between generalized and
upper body obesity to insulin resistance in Asian Indian men. J Clin Endocri-
nol Metab. 1999;84:2329–2335.
31. Chowdhury B, Lantz H, Sjostrom L. Computed tomography-determined body
composition in relation to cardiovascular risk factors in Indian and matched
Swedish males. Metab Clin Exp. 1996;45:634–644.
32. Kamath SK, Hussain EA, Amin D, et al. Cardiovascular disease risk factors in
2 distinct ethnic groups: Indian and Pakistani compared with American pre-
menopausal women. Am J Clin Nutr. 1999;69:621–631.
33. Raji A, Seely EW, Arky RA, et al. Body fat distribution and insulin resis-
tance in healthy Asian Indians and Caucasians. J Clin Endocrinol Metab.
2001;86:5366–5371.
34. Misra A, Vikram NK, Gupta R, et al. Waist circumference cutoff points and
action levels for Asian Indians for identification of abdominal obesity. Int J
Obes (Lond). 2006;30:106–111.
35. Grundy SM, Cleeman JI, Daniels SR, et al. American Heart Association
National Heart, Lung, and Blood Institute. Diagnosis and management of the
metabolic syndrome: an American Heart Association/National Heart, Lung,
and Blood Institute Scientific Statement. Circulation. 2005;112:2735–2752.
36. Durrington PNLS, Charlton-Menys V. Apolipoproteins as predictors of car-
diovascular risk in the Collaborative Atorvastin Diabetes Study (CARDS)
[abstract]. Atherosclerosis. 2006; 7(Suppl 37): Mo-W14: 14.
37. Olsson AGHI, Pedersen, T. Apolipoprotein B/A1 ratio is a better discriminator
of risk of coronary heart disease than is LDL/HDL-cholesterol ratio in the
IDEAL study. Atherosclerosis. 2006; 7 (Suppl): 161.
38. Pedersen TR, Faergeman O, Kastelein JJ, et al. Incremental Decrease in End
Points Through Aggressive Lipid Lowering (IDEAL) Study Group. High-dose
atorvastatin vs usual-dose simvastatin for secondary prevention after myo-
cardial infarction: the IDEAL study: a randomized controlled trial. JAMA.
2005;294:2437–2445.
39. Walldius G, Jungner I, Holme I, et al. High apolipoprotein B, low apolipo-
protein A-I, and improvement in the prediction of fatal myocardial infarction
(AMORIS study): a prospective study. Lancet. 2001;358:2026–2033.
40. Walldius GJ, Jungner I. The apoB/apo A-1 ratio- a new predictor of fatal
stroke, myocardial infarction and other ischaemic diseases stronger than LDL
and lipid ratios. Atherosclerosis. 2006; 7 (Suppl): 468.
41. Yusuf S, Hawken S, Ounpuu S, et al. INTERHEART Study Investigators.
Effect of potentially modifiable risk factors associated with myocardial infarc-
tion in 52 countries (the INTERHEART study): case-control study. Lancet.
2004;364:937–952.
42. Rosengren A, Hawken S, Ounpuu S, et al. INTERHEART investigators.
Association of psychosocial risk factors with risk of acute myocardial
infarction in 11119 cases and 13648 controls from 52 countries (the
INTERHEART study): case-control study. Lancet. 2004;364:953–962.
43. Ezzati M. How can cross-country research on health risks strengthen interven-
tions? Lessons from INTERHEART. Lancet. 2004;364:912–914.
44. Enas EA, Dhawan J, Petkar S. Coronary artery disease in Asian Indians: les-
sons learnt and the role of lipoprotein(a). Indian Heart J. 1997;49:25–34.
45. Enas EA, Mehta J. Malignant coronary artery disease in young Asian Indians:
thoughts on pathogenesis, prevention, and therapy. Coronary Artery Disease
in Asian Indians (CADI) Study. Clin Cardiol. 1995;18:131–135.
310 | www.cardiologyinreview.com © 2012 Lippincott Williams & Wilkins
Narasimhan et al Cardiology in Review Volume 20, Number 6 November/December 2012
46. Enas EA, Mehta JL. Lipoprotein (a): an important risk factor in coronary
artery disease. J Am Coll Cardiol. 1998;32:1132–1134.
47. Gambhir JK, Kaur H, Gambhir DS, et al. Lipoprotein(a) as an independent
risk factor for coronary artery disease in patients below 40 years of age. Indian
Heart J. 2000;52:411–415.
48. Gupta R, Kastia S, Rastogi S, et al. Lipoprotein(a) in coronary heart disease: a
case-control study. Indian Heart J. 2000;52:407–410.
49. Anand SS, Enas EA, Pogue J, et al. Elevated lipoprotein(a) levels in South
Asians in North America. Metab Clin Exp. 1998;47:182–184.
50. Haffner SM, Gruber KK, Morales PA, et al. Lipoprotein(a) concentrations in
Mexican Americans and non-Hispanic whites: the San Antonio Heart Study.
Am J Epidemiol. 1992;136:1060–1068.
51. Howard BV, Le NA, Belcher JD, et al. Concentrations of Lp(a) in black and
white young adults: relations to risk factors for cardiovascular disease. Ann
Epidemiol. 1994;4:341–350.
52. Wang W, Hu D, Lee ET, et al. Lipoprotein(a) in American Indians is low and
not independently associated with cardiovascular disease. The Strong Heart
Study. Ann Epidemiol. 2002;12:107–114.
53. Hoogeveen RC, Gambhir JK, Gambhir DS, et al. Evaluation of Lp[a] and
other independent risk factors for CHD in Asian Indians and their USA coun-
terparts. J Lipid Res. 2001;42:631–638.
54. Desmarais RL, Sarembock IJ, Ayers CR, et al. Elevated serum lipoprotein(a)
is a risk factor for clinical recurrence after coronary balloon angioplasty. Cir-
culation. 1995;91:1403–1409.
55. Hoff HF, Beck GJ, Skibinski CI, et al. Serum Lp(a) level as a predictor of vein
graft stenosis after coronary artery bypass surgery in patients. Circulation.
1988;77:1238–1244.
56. von Eckardstein A, Schulte H, Cullen P, et al. Lipoprotein(a) further increases
the risk of coronary events in men with high global cardiovascular risk. J Am
Coll Cardiol. 2001;37:434–439.
57. Hopkins PN, Wu LL, Hunt SC, et al. Lipoprotein(a) interactions with lipid
and nonlipid risk factors in early familial coronary artery disease. Arterioscler
Thromb Vasc Biol. 1997;17:2783–2792.
58. Solymoss BC, Marcil M, Wesolowska E, et al. Relation of coronary artery dis-
ease in women <60 years of age to the combined elevation of serum lipopro-
tein (a) and total cholesterol to high-density cholesterol ratio. Am J Cardiol.
1993;72:1215–1219.
59. Scanu AM. Lipoprotein(a): a genetically determined cardiovascular pathogen
in search of a function. J Lab Clin Med. 1990;116:142–146.
60. Mager A, Orvin K, Koren-Morag N, et al. Impact of homocysteine-lowering
vitamin therapy on long-term outcome of patients with coronary artery dis-
ease. Am J Cardiol. 2009;104:745–749.
61. Robinson G, Narasimhan S, Weatherall M, et al. Raised plasma homocysteine
levels in alcoholism: increasing the risk of heart disease and dementia? N Z
Med J. 2005;118:U1490.
62. Stubbs PJ, Al-Obaidi MK, Conroy RM, et al. Effect of plasma homocysteine
concentration on early and late events in patients with acute coronary syn-
dromes. Circulation. 2000;102:605–610.
63. Boushey CJ, Beresford SA, Omenn GS, et al. A quantitative assessment of
plasma homocysteine as a risk factor for vascular disease. Probable benefits of
increasing folic acid intakes. JAMA. 1995;274:1049–1057.
64. Chambers JC, Obeid OA, Refsum H, et al. Plasma homocysteine concentra-
tions and risk of coronary heart disease in UK Indian Asian and European
men. Lancet. 2000;355:523–527.
65. Hughes K, Ong CN. Homocysteine, folate, vitamin B12, and cardiovascular
risk in Indians, Malays, and Chinese in Singapore. J Epidemiol Community
Health. 2000;54:31–34.
66. Refsum H, Yajnik CS, Gadkari M, et al. Hyperhomocysteinemia and elevated
methylmalonic acid indicate a high prevalence of cobalamin deficiency in
Asian Indians. Am J Clin Nutr. 2001;74:233–241.
67. Chandalia M, Abate N, Cabo-Chan AV Jr, et al. Hyperhomocysteinemia
in Asian Indians living in the United States. J Clin Endocrinol Metab.
2003;88:1089–1095.
68. Retnakaran R, Hanley AJ, Zinman B. Does hypoadiponectinemia explain the
increased risk of diabetes and cardiovascular disease in South Asians? Diabe-
tes Care. 2006;29:1950–1954.
69. Zornitzki T, Reshef N, Ayzenberg O, et al. High-molecular weight adiponec-
tin is associated with coronary artery angiographic findings in Asian Indians.
Metab Clin Exp. 2009;58:632–637.
70. Deepa R, Velmurugan K, Arvind K, et al. Serum levels of interleukin 6,
C-reactive protein, vascular cell adhesion molecule 1, and monocyte chemo-
tactic protein 1 in relation to insulin resistance and glucose intolerance–the
Chennai Urban Rural Epidemiology Study (CURES). Metab Clin Exp.
2006;55:1232–1238.
71. Chambers JC, McGregor A, Jean-Marie J, et al. Abnormalities of vascular
endothelial function may contribute to increased coronary heart disease risk in
UK Indian Asians. Heart. 1999;81:501–504.
72. Navab M, Anantharamaiah GM, Reddy ST, et al. Mechanisms of disease:
proatherogenic HDL–an evolving field. Nat Clin Pract Endocrinol Metab.
2006;2:504–511.
73. Ansell BJ, Fonarow GC, Fogelman AM. High-density lipoprotein: is it always
atheroprotective? Curr Atheroscler Rep. 2006;8:405–411.
74. Ansell BJ, Watson KE, Fogelman AM, et al. High-density lipoprotein function
recent advances. J Am Coll Cardiol. 2005;46:1792–1798.
75. Navab M, Ananthramaiah GM, Reddy ST, et al. The double jeopardy of HDL.
Ann Med. 2005;37:173–178.
76. Fogelman AM. When good cholesterol goes bad. Nat Med. 2004;10:902–903.
77. Zheng L, Nukuna B, Brennan ML, et al. Apolipoprotein A-I is a selective
target for myeloperoxidase-catalyzed oxidation and functional impairment in
subjects with cardiovascular disease. J Clin Invest. 2004;114:529–541.
78. Navab M, Anantharamaiah GM, Reddy ST, et al. Human apolipoprotein A-I
and A-I mimetic peptides: potential for atherosclerosis reversal. Curr Opin
Lipidol. 2004;15:645–649.
79. Perez-Mendez O, Bruckert E, Franceschini G, et al. Metabolism of apoli-
poproteins AI and AII in subjects carrying similar apoAI mutations, apoAI
Milano and apoAI Paris. Atherosclerosis. 2000;148:317–325.
80. Hovingh GK, Brownlie A, Bisoendial RJ, et al. A novel apoA-I mutation
(L178P) leads to endothelial dysfunction, increased arterial wall thick-
ness, and premature coronary artery disease. J Am Coll Cardiol. 2004;44:
1429–1435.
81. Islam MS, Raitakari OT, Juonala M, et al. Apolipoprotein A-I/C-III/A-IV SstI
and apolipoprotein B XbaI polymorphisms and their association with carotid
artery intima-media thickness in the Finnish population. The Cardiovascular
Risk in Young Finns Study. Atherosclerosis. 2005;180:79–86.
82. A genome-wide association study in Europeans and South Asians identifies
five new loci for coronary artery disease. Nat Genet. 2011;43:339–344.
83. Large-Scale Gene-Centric Analysis Identifies Novel Variants for Coronary
Artery Disease. PLoS Genet. 7(9):e1002260. AQ: Please provide year for ref-
erence 83.
84. Tillin T, Dhutia H, Chambers J, et al. South Asian men have different patterns
of coronary artery disease when compared with European men. Int J Cardiol.
2008;129:406–413.
85. Zindrou D, Taylor KM, Bagger JP. Coronary artery size and disease in UK
South Asian and Caucasian men. Eur J Cardiothorac Surg. 2006;29:492–495.
86. Dhawan J, Bray CL. Are Asian coronary arteries smaller than Caucasian? A
study on angiographic coronary artery size estimation during life. Int J Car-
diol. 1995;49:267–269.
87. Hasan RK, Ginwala NT, Shah RY, et al. Quantitative angiography in South
Asians reveals differences in vessel size and coronary artery disease severity
compared to Caucasians. Am J Cardiovasc Dis. 2011;1:31–37.
88. Di Castelnuovo A, Costanzo S, Bagnardi V, et al. Alcohol dosing and total
mortality in men and women: an updated meta-analysis of 34 prospective stud-
ies. Arch Intern Med. 2006;166:2437–2445.
89. Beishon S, Nazroo JY. Contrasting the health beliefs and behaviours of South
Asian communities. 1997. www.nice.org.uk/nicemedia/documents/coron_
heartdis.pdf BSaNJCthbaboSAc. Accessed July 6, 2011.
90. Bainey KR, Norris CM, Gupta M, et al. Altered health status and quality of
life in South Asians with coronary artery disease. Am Heart J. 2011;162:
501–506.
91. Mehrotra N. South Asian Total Health Initiative (SATHI) 2010. www.rwjms.
umdnj.edu/sathi MNSATHIS.
92. Rankin J, Bhopal R. Understanding of heart disease and diabetes in a South
Asian community: cross-sectional study testing the ‘snowball’ sample method.
Public Health. 2001;115:253–260.
93. Barnett AH, Dixon AN, Bellary S, et al. Type 2 diabetes and cardiovascular
risk in the UK south Asian community. Diabetologia. 2006;49:2234–2246.
94. Reddy KS, Yusuf S. Emerging epidemic of cardiovascular disease in
developing countries. Circulation. 1998;97:596–601.
95. Patel JV, Vyas A, Cruickshank JK, et al. Impact of migration on coronary
heart disease risk factors: comparison of Gujaratis in Britain and their
contemporaries in villages of origin in India. Atherosclerosis. 2006;185:
297–306.
© 2012 Lippincott Williams & Wilkins www.cardiologyinreview.com  |  311
Cardiology in Review • Volume 20, Number 6 November/December 2012  Coronary Artery Disease in South Asians
96. Farooqi A, Nagra D, Edgar T, et al. Attitudes to lifestyle risk factors for coro-
nary heart disease amongst South Asians in Leicester: a focus group study.
Fam Pract. 2000;17:293–297.
97. Williams ED, Stamatakis E, Chandola T, et al. Assessment of physical activity
levels in South Asians in the UK: findings from the Health Survey for Eng-
land. J Epidemiol Community Health. 2011;65:517–521.
98. Pollard TM, Carlin LE, Bhopal R, et al. Social networks and coronary heart
disease risk factors in South Asians and Europeans in the UK. Ethn Health.
2003;8:263–275.
99. Mathews G, Alexander J, Rahemtulla T, et al. Impact of a cardiovascular risk
control project for South Asians (Khush Dil) on motivation, behaviour, obe-
sity, blood pressure and lipids. J Public Health (Oxf). 2007;29:388–397.
... Not only there is heightened susceptibility in the SA population to ACS and its related adverse outcomes, but emerging evidence also suggests a demographic shift in ACS occurrence, with SAs experiencing ACS at notably younger ages (5-10 years younger) compared to other ethnic groups. This is worrisome and underscores the need for early intervention and contextual and age-appropriate healthcare approaches [6][7][8][9][10]. ...
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Background There is dearth of literature addressing early outcomes of acute coronary syndrome (ACS) among young patients, particularly South Asians descent who are predisposed to premature coronary artery disease (CAD). Therefore, we compared presentation, management, and early outcomes of young vs. old ACS patients and explored predictors of in-hospital mortality. Methods We extracted data of 23,560 ACS patients who presented at Tabba Heart Institute, Karachi, Pakistan, from July 2012-June 2020, from the Chest pain-MI-Registry™. We categorized data into young ≤ 45 and old ACS patients > 45 years. Chi-sq/Fischer exact tests were used to assess the difference between presentation, disease management, and in-hospital mortality between both groups. Logistic regression was used to determine odds ratio along with 95% confidence interval of factors associated with early mortality. Results The younger patients were 12.2% and women 23.5%. The prevalence of dyslipidemia (34.5% vs. 22.4%), diabetes (52.1% vs. 27.4%), and hypertension (68.3% vs. 42.9%) was higher in older patients. Family history of premature CAD (18.1% vs. 32.7%), smoking (40.0% vs. 22.9%), and smokeless tobacco use (6.5% vs. 8.4%) were lower in older patients compared to younger ones. Younger patients were more likely to present with STEMI (33.2% vs. 45%). The median symptom-to-door time was 125 min longer (p-value < 0.01) in the young patients compared to the older age group. In-hospital mortality (4.3% vs. 1.7%), cardiac arrest (1.9% vs. 0.7%), cardiogenic shock (1.9% vs. 0.9%), and heart failure (1% vs. 0.6%) were more common in older patients. After adjusting for other factors, younger age (AOR 0.6, 95% CI 1.5–3.7) had significantly lesser odds of in-hospital mortality. Other factors associated with early mortality included women, family history of premature CAD, STEMI, Killip class III and IV, coronary angiography, revascularization, CABG, and use of aspirin and beta blockers within the first 24 h. Conclusion We found every tenth ACS patient was younger than 45 years of age despite a lesser number of comorbidities such as hypertension and diabetes. Overall, the in-hospital prognosis of young patients was more favorable than that of older patients. The study emphasizes the need for tailored primary prevention programs for ACS, considering the varying risks among different age groups.
... In addition, it has been found that the presence of abnormal lipid profile has a higher characteristic of CAD risk in South Asians when matched to other ethnic groups. 19 Moreover, the association between alcohol consumption and cardiovascular mortality and morbidity has been debated for a long time. Several international comparisons show a negative association between alcohol usage and mortality due to coronary heart disease. ...
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Background Trinidad and Tobago ranks number 45 in the world for total deaths due to coronary heart disease. Predictive tests for coronary angiographic results set the basis for earlier monitoring of the disease before additional complications become obvious. Aims and Methods This study aimed to evaluate the anthropometric and biochemical parameters of 124 patients with suspected coronary artery disease (CAD) in Trinidad and how these parameters correlate to the findings at angiography. Results The biochemical parameters showed statistically significant correlations with CAD severity by Spearman's rank-order correlation. Two clinical parameters showed significant associations with CAD severity—ethnicity (χ2 (4) = 12.925, p = 0.012) and presence of type 2 diabetes at baseline (χ2 (4) = 21.483, p < 0.001). Conclusion Biochemical parameters such as fasting blood sugar, N-terminal pro B-type natriuretic peptide, creatinine, and hemoglobin A1c were well correlated and well associated with the severity of CAD after diagnosis by the process of coronary angiography. Hence, these factors can be taken into consideration to predict the severity of CAD.
... Оценочная распространенность ИБС в Соединенных Штатах Америки (США), включая инфаркт миокарда (ИМ), составляет около 6% населения [2,31]. Национальный реестр Американского колледжа кардиологии сообщил о 2,5 миллионах случаев ИМ в период с 1990 по 2006 год и дополнительно продемонстрировал увеличение доли случаев, вызванных ОКС без подъема сегмента ST (ОКСбпST), с 14,2% до 59,1% в течение последних 10 лет [33,35]. ...
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The review is based on the analysis of current literature data on acute coronary syndrome (ACS): definition, epidemiology, classification, and methods of modern therapy methods. The article presents in detail the premedication and reperfusion strategies of introduction with an emphasis on a differential approach in the choice of therapy depending on the state of the ST-segment elevation. According to the literature the choice of treatment differs in patients with ACS with ST. The results of multicenter studies on the use of anticoagulant therapy in ACS and the need for double anticoagulant therapy against the background of the use of statins, ACE inhibitors, and beta blockers are presented.
... South Asians including Sri Lankans have a distinct genetic make-up, a higher prevalence of hypertension, diabetes mellitus, central obesity, insulin resistance, and metabolic syndrome than whites in the UK and America [2,[4][5][6][7][8][9]. South Asians also have a higher salt intake and are undergoing huge lifestyle and socioeconomic transformations, all leading to a high cardiovascular (CV) risk [10][11][12][13]. Furthermore, it is reported that their absolute CV risk is higher than the predictions of standard European scores [14]. ...
... Sex and ancestry were the potential causes of CAD differences [18,[43][44][45]. However, previous studies were limited to small sample sizes, which made it difficult to overcome the defects of heterogeneity. ...
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Significant differences may exist among different descents, but the current studies are mainly based on European populations. In the present study, we analyzed the population-specific differences of coronary artery disease (CAD) between European and East Asian descents. In stage 1, we identified CAD susceptibility genes by gene-based tests in European and East Asian populations. We identified two novel susceptibility genes for CAD, namely, CUX2 and OAS3. In stage 2, we carried out meta-analyses for the population-specific variants. rs599839 (PSRC1) represented a protective variant for CAD in East Asian populations (ORASN = 0.72. 95% CI: 0.63-0.81) but a risk factor in European populations (OREUR = 1.13, 95% CI: 0.93-1.36). In stage 3, we enriched the risk genes and explored the population-specific differences in Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), regulatory element, tissues, and cell types. In stage 4, in order to predict genes that showed pleiotropic/potentially causal association with CAD, we integrated summary-level data from independent genome-wide association studies (GWAS) and expression quantitative trait loci (eQTLs) by using summary data-based Mendelian randomization (SMR). The results showed that NBEAL1 and FGD6 were population-specific pleiotropic/causal genes. Although some potential mutations and risk genes of CAD are shared, it is still of great significance to elucidate the genetic differences among different populations. Our analysis provides a better understanding of the pathogenic mechanisms and potential therapeutic targets for CAD.
... South Asians including Sri Lankans have a distinct genetic make-up, a higher prevalence of hypertension, diabetes mellitus, central obesity, insulin resistance, and metabolic syndrome than whites in the UK and America [2,[4][5][6][7][8][9]. South Asians also have a higher salt intake and are undergoing huge lifestyle and socioeconomic transformations, all leading to a high cardiovascular (CV) risk [10][11][12][13]. Furthermore, it is reported that their absolute CV risk is higher than the predictions of standard European scores [14]. ...
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Introduction and objectives There are no cardiovascular (CV) risk prediction models for Sri Lankans. Different risk prediction models not validated for Sri Lankans are being used to predict CV risk of Sri Lankans. We validated the WHO/ISH (SEAR-B) risk prediction charts prospectively in a population-based cohort of Sri Lankans. Method We selected 40–64 year-old participants from the Ragama Medical Officer of Health (MOH) area in 2007 by stratified random sampling and followed them up for 10 years. Ten-year risk predictions of a fatal/non-fatal cardiovascular event (CVE) in 2007 were calculated using WHO/ISH (SEAR-B) charts with and without cholesterol. The CVEs that occurred from 2007–2017 were ascertained. Risk predictions in 2007 were validated against observed CVEs in 2017. Results Of 2517 participants, the mean age was 53.7 year (SD: 6.7) and 1132 (45%) were males. Using WHO/ISH chart with cholesterol, the percentages of subjects with a 10-year CV risk <10%, 10–19%, 20%-29%, 30–39%, ≥40% were 80.7%, 9.9%, 3.8%, 2.5% and 3.1%, respectively. 142 non-fatal and 73 fatal CVEs were observed during follow-up. Among the cohort, 9.4% were predicted of having a CV risk ≥20% and 8.6% CVEs were observed in the risk category. CVEs were within the predictions of WHO/ISH charts with and without cholesterol in both high (≥20%) and low(<20%) risk males, but only in low(<20%) risk females. The predictions of WHO/ISH charts, with-and without-cholesterol were in agreement in 81% of subjects (ĸ = 0.429; p<0.001). Conclusions WHO/ISH (SEAR B) risk prediction charts with-and without-cholesterol may be used in Sri Lanka. Risk charts are more predictive in males than in females and for lower-risk categories. The predictions when stratifying into 2 categories, low risk (<20%) and high risk (≥20%), are more appropriate in clinical practice.
... Ventricular tachycardia and ventricular fibrillation are point of concern in patients with STEMI and some studies suggest double or even triple the burden of these fatal arrhythmias when STEMI is associated with LVSD. [9][10][11] In our study the incidence of ventricular arrhythmias was two times higher in patients who developed left ventricular systolic dysfunction (36.36%) as compared to normal left ventricular systolic function (72.72%), (p 0.001), respectively. Previously conducted studies can validate the findings of our study. ...
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