Ethnic differences in cardiovascular response to stress role of trait anger, sex and migrant status

To the best of our knowledge, few studies have examined risk factors related to coronary heart disease among women in an Asian context, let alone looked at ethnic differences.. Factors E

economic growth not only bring prosperity, but can also foster ill health with fast food, a sedentary lifestyle and little relaxation (Chockalingam, 2000)

Over the past few decades the majority of research with regards to risk factors associated with CHD has focused on risk associated with populations of Western

developed countries Although many of the risk factors identified are also relevant for non-Western populations, there is growing evidence that CHD incidence and mortality are unevenly distributed within and across populations of both developed and developing countries (Reddy &Yusuf, 1998)

Prevalence of Coronary Heart Disease

Epidemiological studies of international variations in CHD by specific ethnic groups and geographic regions have been highlighted in a report on the global burden of cardiovascular disease (Yusuf, Reddy, Ounpuu & Anand, 2001) Declining CHD death

rates were found in most industrialized countries except in Eastern Europe and Russia where the trends remained upwards Among the Asian countries, CHD rates in Japan have declined more rapidly than in the Western countries By contrast, death rates from

cardiovascular disease and CHD in particular, have shown an increasing trend in China (Woo & Donnan, 1989) and in India (Reddy & Yusuf, 1998) CHD rates in India are expected to rise further with increase in life expectancy and per capita income (Reddy, 1993) Murray and Lopez (1996) found that of all deaths in 1990, 25% were attributable to cardiovascular disease in India Although, the relatively few mortality studies from India make it difficult to present an accurate picture of disease prevalence in the country, there is some evidence that CHD prevalence has markedly increased in urban India (Gupta & Gupta, 1996)

Worldwide researchers have consistently found higher rates of CHD incidence and mortality among individuals of South Asian origin Sheth, Nair, Nargundkar, Anand, and Yusuf (1999) investigated ethnic variations in major causes of death in Canada and

documented trends within ethnic groups of South Asians, Chinese and Europeans, for heart disease Rates of death from ischemic heart disease, expressed per 100,000 population, were highest among the Canadians of South Asian origin (men 320.2, women 144.5) followed by Canadians of European origin (men 319.6, women 109.9) Mortality rates were lowest among Canadians of Chinese origin (men 107.0, women 40.0) Research done

in the United Kingdom also points out that South Asians are at excess risk of CHD (Bhopal, 2000) In comparing South Asians and Europeans, electrocardiograph evidence has shown

a 37% excess of CHD in South Asians (McKeigue, Ferrie, Pierpoint, & Marmot, 1993; Bhopal et al., 1999) To compare 10-year risk of CHD, stroke and combined CHD,

Cappuccio, Ookeshott, Strazzullo and Kerry (2002) applied the Framingham risk estimates

to ethnic minorities in UK Among the ethnic groups of Whites, South Asians and Blacks, people of African origin had the lowest 10-year risk estimate of CHD adjusted for age and sex (7%) The Whites showed 8.8% risk estimate, while the South Asians showed the highest estimated risk of 9.2% The estimated risk of combined cardiovascular risk was also highest in South Asians (12.5%) compared to 11.9% among Whites and 10.5% in people of African origin

Likewise, in the Asian context of Singapore, death rates for heart disease (22.1 %) are second only to those for cancer (Ministry of Health, Singapore, 2006) with the three major ethnic groups – Chinese, Malays and Indians showing variations in cardiovascular disease incidence and mortality In 1990, Hughes, Lun and Yeo found that Indians had higher mortality from ischemic heart disease than the Chinese and Malays, with

age-standardized relative risk ratios of Indians vs Chinese (males 3.8, females 3.4) and Indian vs Malays (males 1.9, females 1.6) For hypertensive disease Malays had highest mortality, while few ethnic differences were found for cerebrovascular disease across the

three ethnic groups In yet another study of risk factors and incident of CHD in Chinese, Malay, and Indian males, Lee et al (2001) found Indians to be at greatest risk of CHD, compared to Chinese (3.0; 2.0-4.8) and Malays (3.4; 1.9-3.3)

Emerging Factors of Ethnicity, Sex and Migrant populations

Ethnicity is emerging as an important demographic factor in heart disease

prevalence and mortality In fact, the American Heart Association Taskforce on Strategic Research Direction (S.C Smith et al., 2001) identified ethnicity as one of the priority topics

in understanding why subgroups in a population experience CHD differently compared to other populations in terms of prevalence of risk factors, risk-factor management, access to care, lifestyle and metabolic risk factors, psycho-social risk factors, as well as genetic variations (Roberts, Bonow, Loscalzo & Mosca, 2000)

Ethnicity is a construct that encompasses both genetic and cultural differences (Anand, 1999) As individuals of different ethnic backgrounds tend to live in specific regions, disparity in disease by ethnicity is a function of geographic differences, which in turn reflect distinct lifestyles and socio-economic status Such differences in rates of CHD become apparent in studies across countries For instance, the Seven Countries Study (Menotti et al., 1993) found low CHD rates in Japan and Mediterranean countries as compared to higher CHD rates in Finland and the United States (US) These differences were largely attributed to differences in diet, serum cholesterol and blood pressure

However, this study did not look beyond traditional biological risk factors at other aspects such as psychosocial variables to explain differences in rates of CHD Such studies

highlight the need to examine ethnic differences associated with CHD in populations at risk with a focus on underlying psychosocial variables

Sex differences also exist in CHD Women are more likely than men, to have

angina pectoris with normal coronary arteries, more likely to have poor outcomes after bypass surgery, more likely to die after myocardial infarction and are influenced

differently by risk factors such as hypertension, diabetes, and inflammation (Maguire, 2003) CHD and stroke remain the leading killers of women in America and most

developed countries Although it is estimated that one in two women will eventually die

of heart disease or stroke, until recently misperceptions still existed that CHD is not a real problem for women (American Heart Association, 1997) In light of the paucity of

cardiovascular research among women, especially in the Asian context, there is a need to examine differences in CHD between men and women

Recent epidemiological findings have also clarified that, although CHD affects women on an average of a decade later in life than men, this disease is the leading cause

of death in women just as in men Despite their marked advantage in age-specific risk of CHD death, the greater likelihood of survival of women to advanced ages produces nearly equal numbers of actual deaths due to CHD in men and women United States data from

the National Center for Health Statistics (1997) shows that 39% more males than females die from heart disease between the ages of 45 and 64 However, after the age of 65 years, the death rate due to heart disease in women actually exceeds that in men by 22% This suggests that any protective effects of being female are largely gone by the age of 65 Substantial ethnic differences in CHD deaths in women have also been documented (Mosca et al., 1997) To the best of our knowledge, few studies have examined risk

factors related to coronary heart disease among women in an Asian context, let alone looked at ethnic differences

Migrant / minority populations have consistently been found to be at a higher

risk for CHD Literature on health behaviors and disease indicates an increase in

behavioral risk factors (e.g high fat diet, sedentary lifestyle) as well as biological risk factors (e.g obesity, hypertension) when individuals migrate to more prosperous

countries There is also increasing evidence that socio-cultural and psychological factors play a crucial role in an immigrant’s health across the world (Hovey & Magana, 2000)

As mentioned earlier, South Asian migrant populations (primarily Indians) have been found to show high rates of CHD incidence in Europe (Phillimore, Beattie, & Townsend, 1994), USA (Goslar et al., 1997; Brown & James, 2000) and Canada (Sheth et al, 1999) However, most of these studies drew no comparisons of these migrant Indian populations with their counterparts in India

Extensive research thus points to the diversity in prevalence and mortality due to coronary heart disease across countries and ethnic descent within a country, as well as sex More specifically, research findings indicate increased incidence of coronary heart

disease among people of South Asian origin Indians in particular seem to be at increased risk of CHD However, most studies have looked at South Asians as a group including people from India, Pakistan, and Bangladesh It must also be noted that research that has examined specific ethnic groups such as Indians, has been conducted among migrant populations – whether in the West (Canada, United Kingdom) or in South-East Asia

(Singapore) This raises the question of whether it is ethnicity per se that explains

increased incidence and risk of CHD, a migrant/minority status, other psychosocial

factors, or perhaps a combination of ethnic, minority, and psychosocial factors that

provide the underlying explanation We now continue with examining some of the

explanations that have been put forth to describe and understand ethnic differences in coronary heart disease

Factors Explaining Differences in Incidence of CHD

The possibilities of genetic determinism, inherent biological make-up, as well as traditional factors emerging from lifestyle aspects of individuals from different ethnic backgrounds, provide some explanations for increased cardiovascular risk for certain ethnic groups Researchers have long attributed cause of disease to an individual’s

biological make up with traditional risk factors being presented as potentially critical factors explaining differences in incidence and mortality due to CHD However, such factors including hypertension, obesity, cholesterol, parental history or cigarette smoking account for less than 50% of CHD cases (Siegman, 1994) Research with regards to these explanatory factors also suggests that rates of coronary heart disease may be explained in part by differences across ethnicity, although underlying mechanisms remain unclear

With increasing understanding that psychological and social processes play an important role in linking behavior and health (T.W Smith & Anderson, 1986), researchers have identified psychosocial factors such as stress, anger, depression and social support,

to be related to CHD Of these factors, anger / hostility has been found to be a critical factor involved in CHD incidence and mortality (Abel, Larkin, & Edens, 1995) and is also linked to other identified psychosocial factors These psychosocial risk factors do not occur in isolation, but tend to cluster in the same individuals and/or groups For instance, both men and women of lower socio-economic status are more likely to be depressed, hostile, socially isolated and engaged in high-risk behaviors such as smoking and

drinking (Wamala, Mittleman, Schenck-Gustafsson, & Orth-Gomer, 1999) that contribute

to CHD risk (Anand et al., 2001)

One of the proposed mechanisms that may link psychosocial factors to CHD is cardiovascular reactivity (CVR) – that is, psychosocial factors that lead to increased CVR

are considered to be critical risk factors for CHD Exaggerated cardiovascular responses to stressors have been associated with increased risk of hypertension (Everson, Kaplan, Goldberg, & Salonen, 1996), atherosclerosis (Barnett, Spence, Manuck, & Jennings, 1997), and ischemia (Krantz et al., 1991) It is the interaction between psychosocial factors such as anger / hostility and reactivity that the present study seeks to explore in an Asian

population, with emphasis on the Indian ethnic group (migrant and native), which evidence suggests, is at most risk of developing CHD among the Asian populations

Review of Literature

A brief review of some traditional risk factors that have been identified as crucial for South Asians as a high-risk population is presented We shall then scrutinize the psychosocial factors that have been recognized as potential risk factors for CHD In particular, we shall examine anger / hostility in relation to CHD as well as its links to other psychosocial factors, followed by a review of studies examining migratory status as a possible factor involved in ethnic differences in CHD Finally, an overview of research in the area of cardiovascular reactivity, which has unmasked some pathways in which

psychosocial factors produce different patterns of cardiovascular reactivity across

ethnicity, sex and tasks, is presented

Traditional Risk Factors Related To Coronary Heart Disease

Classical risk factors for CHD such as smoking, blood pressure (BP), obesity and cholesterol vary substantially across different ethnic groups and subgroups (Chaturvedi, 2003) Differences between European and non-European populations such as South Asians and people of African descent have been examined previously (Liu et al., 1996) Among established risk factors, R.Williams, Bhopal and Hunt (1994) found that South Asians in the UK had less exposure only for smoking while there was a relative excess of other known risk factors such as less exercise and more diabetes and central adiposity

In Singapore, Indians are at a higher risk for heart disease with CHD rates among Indian men aged 30 – 69 years being 3.8 times those for Chinese and 1.9 times those for Malays (Hughes, Lun, & Yeo, 1990) However, these high rates remain unexplained by traditional risk factors such as cigarette smoking, hypertension, or increased low-density lipoprotein cholesterol (Hughes et al, 1997), which have been found to show no important ethnic differences

A prospective study, the Singapore Cardiovascular Cohort Study (Lee et al., 2001), investigated the relationship between established coronary risk factors with incident CHD for Chinese, Malay, and Indian males Indians were found to have an increased risk of CHD compared to the other ethnic groups All the risk factors examined (hypertension, high low-density lipoprotein cholesterol, smoking, diabetes, obesity) were found to play varying

roles, with hypertension, diabetes and obesity emerging as the most important risk factors among this Asian cohort Research thus points to the fact that variations in CHD may in fact be explained in some part by traditional risk factors but the exact relationships vary across populations and ethnic groups For instance, Hughes and colleagues found

non-insulin dependent diabetes mellitus (NIDDM) was highest among Indians, then Malays and Chinese in Singapore (Hughes et al (1990) Those with NIDDM also had higher mean body mass indices, waist hip ratio and abdominal diameters, prevalence of hypertension and higher levels of serum triglycerides (Hughes, Choo, Kuperan, Ong, &

Aw, 1998) Although the higher rates of CHD in Indians are partly explained by central obesity, insulin resistance and metabolic syndrome (Hughes et al., 1997), these traditional risk factors have not been able to fully explain ethnic and sex differences in incidence and progression of CHD

We continue with examining some of the other explanations that have been put forth to describe and understand differences in CHD across ethnicity and sex To arrive at specific research questions for investigating the roles of ethnicity and sex in explaining risk and incidence of CHD among Indians, the focus here lies on anger / hostility and migratory status as psychosocial risk factors modified by ethnicity and sex, their relationship to cardiovascular reactivity, and therefore, to CHD

Psychosocial Risk Related to Coronary Heart Disease

Ethnic variations in CHD may reflect the unique personal and historical

experiences as well as the current social conditions of ethnic groups The health behaviors and other risk factors for CHD should therefore be understood within the personal and social contexts that facilitate their initiation and maintenance (D.R.Williams & Rucker, 1996) Some researchers have thus looked at psychosocial factors that have been linked to CHD as possible explanations for ethnic differences in the disease Similarly, how these psychosocial factors affect men and women and therefore their cardiovascular health may

be different This highlights the need to look at both ethnic and sex differences as related to psychosocial risk for CHD

An expanding literature has documented associations between several

psychosocial factors and increased incidence of CHD The most prominent of the

identified factors include anger/hostility, psychological stress, depression and the lack of social support (Krantz & McCeney, 2002) All of these have been associated with clinical outcomes in CHD patients through mechanisms that involve physiological pathways as well as possible failure to adopt a healthy lifestyle These factors have also been found to have a close relationship with anger / hostility and are therefore briefly discussed here

Psychological stress has been implicated in the etiology of CHD, both with

laboratory/experimental stressors as well as in real life/everyday stress situations

Exaggerated cardiovascular reactions to acute stress have been implicated in both the development and expression of cardiovascular disease (Schwartz et al., 2003; Lepore, Miles & Levy, 1997) Mental stress has been found to predict future blood pressure and hypertension in a study that recorded blood pressure at initial screening and during a mental stress task (Carroll et al., 2001) Examination of blood pressure status ten years later showed that both systolic blood pressure (SBP) and diastolic blood pressure (DBP) reactions to stress were predictive of hypertension at follow-up This suggests that

heightened blood pressure reactions to mental stress may contribute to the development of hypertension There is also emerging evidence that acute stress reactivity as examined in laboratory settings may not be independent of stressful life experiences (Carroll, Philips, Ring, Der, & Hunt, 2005) Individuals exposed to high impact life events may be less likely to engage with the minor challenges of acute stress tasks, or the mere exposure to stressful life events may desensitize the hemodynamic system of an individual, thus resulting in diminished reactivity

Depression has also been identified as a frequent precursor of CHD and may

impede recovery as well (Booth-Kewley & Friedman, 1987; Frasure-Smith, Lesperance,

& Talajic, 1993; 1995; Lesperance, Frasure-Smith, Juneau, & Theroux, 2000) There is consistent evidence that depression affects organic disease processes and subsequent morbidity and mortality among individuals having cardiovascular disease (Krantz &

McCeney, 2002) Behavioral and physiological mechanisms associating depression and cardiovascular disease suggest that depressed individuals are likely to indulge in

risk-related behaviors such as smoking or lack of physical activity (Carney, Freedland, Rich, & Jaffe, 1995) However, after controlling for such traditional risk factors and

related behaviors, depression remains associated with poor cardiac outcomes (Glassman

& Shapiro, 1998)

Social support has been consistently linked to health outcomes and lack of social

support has emerged as a risk factor of considerable magnitude, not only for CHD, but also morbidity and mortality from all causes (Allan & Scheidt, 1996) Prospective studies have confirmed the association between low social support and risk of CHD (Kawachi, Sparrow, Spiro, Vokonas, & Weiss, 1996) and indicated an important role of low social support in mortality from pre-existing disease (Case, Moss, Case, McDermott & Eberly, 1992; R.B.Williams et al., 1992) In fact, both quantity and quality of social support may

be important predictors of health (Orth-Gomer, Rosengren, & Wilhelmsen, 1993; Krantz

& McCeney, 2002)

Anger / hostility has often been implicated as predisposing factors in coronary

heart disease as well as hypertension (Everson et al., 1997) Increasingly well designed prospective studies as well as quantitative reviews have found this association to hold true High levels of a tendency to experience anger have been found to be positively related to

resting blood pressure and development of hypertension (Jorgensen, Johnson, Kolodziej,

& Schreer, 1995; Suls, Wan & Costa, 1995) Previously a quantitative review came to the conclusion that anger / hostility and related behaviors are associated with an increase in CHD risk and premature mortality (Miller, Smith, Turner, Guijarro & Hallet, 1996) and later prospective studies confirm such associations (Chang, Ford, Meoni, Wang, & Klag, 2002; Gallacher, Yarnell, Sweetnam, Elwood, & Stansfeld, 1999) In addition there is growing evidence that anger and hostility are associated with psychological distress (Kopper & Epperson, 1996), lower levels of social support (Houston & Vavak, 1991), and depression (G.A Kaplan, 1995)

Clustering of Psychosocial Risk Factors

One significant development in research findings has been the realization that a person’s risk of developing CHD rarely depends on a single factor; in most cases risk is determined by a synergy between two or more risk factors, thus magnifying their effect

on CHD risk (R.B.Williams, 1999; R.B.Williams, Barefoot, & Schneiderman, 2003) Psychosocial factors such as anger, hostility, stress, depression, anxiety and social support

do not occur in isolation, but tend to cluster in the same individuals and groups

Benotsch, Christensen and McKelvey (1997) have shown that individuals with high levels

of anger / hostility also show greater levels of interpersonal stress in their daily lives, less social support, and higher mean SBP Similarly, R.B.Williams et al (1997) identified

potential mediators of job strain effects on health among working women, reporting increased levels of negative emotions like anxiety, anger, depression and hostility, as well

as reduced levels of social support Such findings clearly indicate that the

health-damaging psychosocial factors considered, tend to cluster in certain individuals, and when such psychosocial factors do co-occur, their impact on mortality is further compounded

Contrada (1994) points out that the relationship between anger and stress can be explained through the three components of exposure, problem representation, and

response generation Exposure refers to the fact that individuals high in trait anger also report frequent episodes of experiencing anger and respond with anger to a wider range of provocations (Deffenbacher, 1992) As an individual shapes his or her own environment, anger prone individuals are likely to find themselves in more stressful situations and then react with greater anger to such situations In terms of problem representation, people high in anger tend to appraise situations as threatening and thus experience escalating levels of frustration and antagonism Finally, in responding to stressful situations, anger prone people frequently let out their frustrations through physical or verbal expression of their anger

Expressing anger in a frustrating, uncontrolled manner is likely to lead other persons to believe that these anger prone individuals are less likeable people to be around

during social interactions This undermines an angry or hostile individual’s potential sources of social support as friends and acquaintances tend to avoid them Such

individuals also avoid seeking or accepting social support and may thus perceive

themselves as having less social support during a stressful situation Individuals

displaying high levels of hostility, as reflected through cynical mistrust, and with a

tendency of suppressing their anger, have been found to report receiving less family

support and having less trusting relationships (Greenglass, 1996) Such social isolation is also likely to lead to feelings of rejection, loneliness and depression Thus we find that not only is anger / hostility directly related to CHD but is also likely to play a role in the effects of other psychosocial factors linked to cardiovascular disorders

Social support is also affected by anger / hostility among individuals when

examined in relation to health behaviors Although hostility and social support have

typically been examined as separate factors related to CHD, some findings suggest that when considered in combination they account for cardiovascular outcomes above and beyond their separate main effects (Knox et al., 2000) Complex interactions in the effects

of anger / hostility and social support have also been well demonstrated in a study by Brownley, Light and Anderson (1996) The effects of hostility and social support on clinic, work and home SBP and DBP were evaluated in African American and Caucasian

American men and women Importantly among the high hostile participants, across

ethnicity and sex, high appraisal of social support was related to lower overall BP while

no buffering effect was evident among the low hostile individuals

Raynor, Pogue-Geile, Kamark, McCaffery and Manuck (2002) argue that

depression, hostility and social support should be interrelated, as depressed persons may view the world in a cynically hostile manner A hostile individual may be less likely to perceive social support or may drive away sources of social support, thereby increasing risk of depression Brummett et al (1998) found that social support was independently and negatively associated with depression, and hostility predicted depression, by way of its negative relation with social support These results are just one example of the

complex effects of social support in the presence versus absence of hostility with regards

to CHD related health behaviors

To sum up, anger / hostility emerges as an important psychosocial risk factor related to CHD, not only as an independent factor but also related strongly to other

psychosocial factors that have been found to show negative effects on cardiovascular health The present study focuses on anger as an underlying risk factor to examine its contribution to CHD related risk

Anger / Hostility

The deleterious effects of anger / hostility on cardiovascular health are

increasingly gaining attention in the research literature with evidence for an anger-CHD

association derived from studies using different measures of anger and different CHD end points Hostility is generally referred to as a multifaceted cognitive phenomenon

(Spielberger, Jacobs, Russell, & Crane, 1983) consisting of negative beliefs about others and an endorsement of statements that other people are untrustworthy, undeserving, or even immoral (Barefoot, 1992) It thus carries a negative connotation of attitudes such as cynicism, mistrust and suspicion These beliefs may produce attribution biases that make

it more likely for the behaviors of others to be interpreted as antagonistic or threatening Anger on the other hand, refers to an affect experienced by an individual facing

frustration or irritation The experience of anger varies in intensity from mild irritation or annoyance, to fury and rage, (Speilberger et al., 1983) and is usually accompanied by

physiological arousal, characteristic facial expressions and activation of action tendencies Anger can be experienced as a situationally determined transient emotional state (T.W Smith, 1994), or as an enduring trait predisposing an individual to experience frequent

and pronounced episodes of anger across a number of situations

Studies have shown that hostility as measured by the Cook and Medley Hostility Scale (Cook & Medley, 1954) is moderately correlated with some measures of anger

(Bishop & Quah, 1998; T.W & Frohm, 1985) High hostile individuals also tend to

experience excessive anger over a wide variety of situations (T.W Smith, Pope, Sanders, Allred, & O’Keeffe, 1988) and such anger arousals tend to be high in terms of frequency,

intensity and duration Hence, hostility and anger appear to share a common denominator, with hostility reflecting negative worldviews and beliefs about other people, and anger arousal forming the means of translating such beliefs and outlooks into affective and/or behavioral responses Hostility can thus be seen as an underlying attribute in the

expression and experience of anger As such, it becomes difficult to operationally tease out these two concepts, even though they remain conceptually distinct (Miller, Smith, Turner, Guijarro, & Hallet, 1996) For the present study we are focusing on anger as the presumed pathway by which hostility exerts its effect

A number of prospective studies have consistently demonstrated the relation between anger / hostility and risk for major coronary events and mortality (T.W Smith, 1992; Miller et al., 1996) whether taken as a personality characteristic (a trait) or as an episode (a state) It has been suggested that persons with high trait anger, merely with their propensity towards anger and longer exposure to its physiological effects might be more susceptible to CHD (J E Williams et al., 2000) as intense anger has been associated with increased risk of acute myocardial infarction (Mittleman et al., 1995) and angina pectoris (Kawachi et al., 1996) as well as progression of coronary arthrosclerosis (Angerer et al., 2000)

Chang et al (2002) performed a prospective study of 1055 men followed up for 32

to 48 years to examine the risk of premature and total cardiovascular disease associated

with anger responses to stress during early adult life During a median follow-up of 36 years, 205 men developed cardiovascular disease, 77 of whom developed premature disease (defined as events before 55 years of age) Information on reactions to stress was obtained through self reports on the Habits of Nervous Tension Questionnaire (Thomas,

1977 as cited in Chang et al., 2002) The highest level of anger (defined as self report of all

3 possible reactions to stress – expressed or concealed anger, gripe sessions, and

irritability) was associated with an increased risk of premature CHD (relative risk, 3.5; 95%

CI, 1.1-11.8) and premature myocardial infarction (relative risk, 6.4; 95% CI, 1.8 - 22.3) compared to lower levels of anger Evidence also suggests that hostility is more highly associated with cardiovascular outcomes in younger individuals (Miller et al., 1996)

In Kawachi et al.’s (1996) study, 1303 men who were free of diagnosed coronary disease completed a trait anger questionnaire (MMPI-2 derived Anger Content scale) After a 7-year follow-up, there were 50 cases of documented CHD and 60 cases of angina pectoris Compared to men with low anger content scores, the adjusted relative risk among men with high scores on this trait-anger scale was 3.15 for documented CHD and 2.66 for all coronary events including angina pectoris

A meta-analysis of studies has shown that this association between anger and coronary disease remains significant when other risk factors are statistically controlled (Miller, et al., 1996) and is at least as strong as the relationship between coronary disease

and traditional risk factors such as smoking and cholesterol (T.W Smith, 1992) In fact, Everson et al (1997) found that the association between anger / hostility and an increased risk of a coronary event was mediated through other behavioral factors – suggesting that individuals high on anger / hostility might have a psychological profile that makes them more vulnerable to coronary disease Mittleman et al (1995) found that intense episodes of anger expressed outwardly served as significant triggers for acute myocardial infarctions Compared to a control period, the relative risk for experiencing such an event in two hours following an episode of intense anger was 2.3

Mechanism Linking Psychosocial Risk Factors to CHD

Despite the evidence linking psychosocial factors to CHD risk, mechanisms underlying this association still remain to be fully understood Two sets of pathways have been proposed One is the behavioral pathway, whereby health behaviors such as smoking, diet, physical activity or alcohol consumption are influenced by psychosocial factors which

in turn modify CHD risk (Stansfeld & Marmot, 2002) The second is the

psychophysiological pathway and involves more direct effects on the biological functions relevant to CHD

The dynamic associations between psychological factors and biological responses represent the psycho-physiological processes These processes are defined as the

pathways through which psychosocial factors influence physiological systems via the

central nervous system activation of autonomic, neuroendocrine, and immunological responses (Steptoe & Brydon, 2005) Research in this area has greatly contributed to the understanding of possible ways in which psychosocial factors increase risk of CHD and/or trigger cardiac events in people with diagnosed CHD, although the strongest evidence in its favor still comes from animal studies (Kaplan & Manuck, 1999; McCabe

et al., 2000) In proposing some potential avenues for research, R.B Williams (1994) suggested that the impact of correlates of hostility such as high cholesterol and increased catecholamines reactivity on macrophage activation could accelerate atherogenesis Furthermore, the biobehavioral characteristics of hostile individuals could in fact be due

to diminished brain serotonin function; thus making anger / hostility a pathogenic factor for CHD

In understanding the link between psychosocial factors and coronary disease, stress emerges as a crucial factor to be examined It is known to produce hemodynamic,

endocrine, and/or immunological changes that plausibly effect the development or

progression of heart disease in human beings Hemodynamic and neuroendocrine

responses to stress are typically characterized by release of catecholamines and

corticosteroids, increases in heart rate, cardiac output, and blood pressure (Krantz & Manuck, 1984) as well as changes in processes relevant to clotting, such as coronary vasoconstriction, platelet aggregation, or plaque rupture (Patterson, Krantz, & Jochum,

1995) In exploring the effect of stress on CHD it is also important to note and clarify the distinction between chronic and acute risk factors Krantz and McCeney (2002) point out that chronic risk factors refers to factors that exert their influence over long periods of time such as smoking, elevated levels of cholesterol, hypertension, and so on An acute risk factor, on the other hand, is a transient pathophysiologic change that is a result of exposure

to external physical or psychological factors The primary concern here is with regards to psychosocial effects of acute stress and anger

Two aspects of physiological responses elicited in an individual – reactivity

(magnitude of change elicited) and recovery (time taken to reach initial levels of response before change was elicited) have been linked to CHD related risk For most physiological indicators, high reactivity and delayed recovery are considered pathogenic and suggestive

of dysfunction in the physiological regulatory processes (Steptoe, 1998) Cardiovascular reactivity is defined as changes in physiological parameters (such as heart rate, blood pressure, etc.) in response to behavioral or psychological stressors or challenges (Krantz

& Manuck, 1984) It is suggested in many current psychosomatic models that repeated, severe and/or prolonged episodes of stress related CVR contribute to the development of CHD (T.W Smith & Christensen, 1992) when occurring in combination with other

psychosocial factors

One proposed pathway suggests that cardiovascular reactivity is a stable

individual difference variable The reactivity hypothesis states that certain individuals are dispositionally high reactors to stressful situations and such exaggerated responses have a harmful effect on the cardiovascular system, which increases risk of subsequent CHD (Christenfeld, Glynn, Kulik, & Gerin, 1998), while others being low reactors remain at a lower risk of developing heart disease A complementary hypothesis in the cardiovascular reactivity-CHD link presents cardiovascular reactivity as a possible mediating variable between psychosocial risk factors and heart disease (Anderson & Lawler, 1995)

Cardiovascular reactivity in relation to CHD has been investigated using both of the above-mentioned pathways Some studies have examined the hypothesis suggesting that CVR is an individual difference variable For instance, Light, Sherwood & Turner (1992) studied a sample of 51 men from 1988 to 1989 who had participated in an earlier study conducted between 1974 and 1978 At this 10 to 15 year follow-up, high reactivity for a reaction time task predicted higher blood pressure (BP) and heart rate (HR) levels Reactivity predicting higher resting BP shows a relationship between hyper-reactivity under stress and higher resting BP levels that increase the likelihood of developing

hypertension, which is an established risk factor for heart disease The Kuopio Ischemic Heart Disease study of Eastern Finnish men, also demonstrated that a hyper-reactive cardiovascular response is predictive of increased CHD risk (Kamarck et al., 1997) From an initial sample of 2682 men (1984-1989), 1038 volunteered for a follow-up

(1991-1993) Testing at the initial phase involved assessing participants’ blood pressure and HR reactivity during a series of tasks Results showed that during follow-up, BP and

HR reactivity were significantly related to various indices of atherosclerosis (e.g

intima-medial thickness - IMT and plaque height) For instance, DBP responses were associated with mean IMT, maximum IMT and mean plaque height, while SBP reactivity was found to be associated only with mean IMT

Similarly, other studies have explored CVR as a mediating variable in the

psychosocial risk – CHD link In support of the psychophysiological reactivity hypothesis, hostile individuals have been shown to exhibit exaggerated blood pressure responses when provoked, with higher cardiovascular reactivity and lowered parasympathetic functions (Suls & Wan, 1993) Everson, McKey and Lovallo (1995) assessed trait hostility (Type A structured interview, using the Potential for Hostility scores) for 48 Caucasian men and categorized them as high and low on hostility based on a median split of 6.5 scores on the Type A structured interview The participants did two sessions of a mental arithmetic task, during the second of which they were harassed Results showed that harassment increased SBP, DBP, HR and rate pressure product more for high hostile participants than low hostile individuals The two hostility groups had similar responses to an affectively neutral task, pointing to comparable physiological reactivity However, greater reactivity of high-hostile men after provocation suggests a psychological basis for it, that is, if hostile men were

simply more reactive to any challenge, then they would have shown greater reactivity even for the affectively neutral task

The physiological mechanisms underlying cardiovascular reactivity are briefly outlined here Exposure to psychosocial stress has been found to be associated with increased activity of the Hypothalamic-Pituitary-Adrenocortical Axis (HPA axis) and the Sympatho-Adreno-Medullary system (SAM) (Kemeny, 2003) The HPA axis involves the hypothalamus, pituitary, and cortex of the adrenal glands The axis gets activated by release of the corticotrophin releasing factor (CRF) from the hypothalamus, which then travels to the pituitary leading to subsequent release of adrenocorticotropic hormone (ACTH) In addition to CRF, vasopressin is also released from the hypothalamus and participates in stimulating secretion of ACTH Once ACTH reaches the adrenal cortex, it leads to synthesis and release of corticosteroids – specifically cortisol Elevations in cortisol as a response to psychological stress restore heightened immune activation

induced by stress and thus prevent harmful effects of unchecked immune response

However, persistently elevated levels of cortisol in response to chronic or acute stress or negative emotion may lead to multiple cardiovascular problems

The SAM involves both central-hypothalamic and peripheral aspects The

sympathetic nervous system (SNS) in conjunction with the parasympathetic nervous system (PNS) has an essential role to play in the fight-flight response to stress The SNS

controls activity of cardiac muscles by secreting norepinephrine (NE) which enhances the rate and force of contraction of the cardiac muscles Sympathetic preganglionic fibres in the adrenal medulla secrete acetylcholine causing the adrenal medulla to release

epinephrine and NE into the circulation The brain stem regulates catecholamine release during emotional activation When this system is activated it causes the release of NE which facilitates a heightened state of attention leading to increased anxiety These

responses may be further enhanced during experience of anger or intense emotional states

Anger and Cardiovascular Reactivity

The social psycho-physiological reactivity model suggests that psychosocial factors such as anger / hostility contribute to heart disease through their association with heightened cardiovascular and neuroendocrine reactivity (T.W Smith & Gerin, 1998) Also, people high on anger / hostility tend to exhibit greater physiological arousal with greater frequency than others, thus increasing risk of heart disease Anger has specific physiological effects whereby it has been associated with heightened levels of CVR A hyper-reactive physiological response to stress, such as that exhibited through anger has been found to predict hypertension (Light et al., 1992) and is hypothesized as a potential risk factor for development of atherosclerosis and CHD (Manuck, 1994)

Individuals high in anger / hostility tend to show exaggerated psychophysiological reactivity (T.W Smith, 1992) especially under conditions of social challenges such as

harassment, debate or recall of anger-provoking events (Suls & Wan, 1993) Such

associations of anger / hostility and heightened reactivity to stressful situations have been

found in the laboratory (T.W Smith & Gallo, 1999; Suarez, Kuhn, Schanberg, Williams, & Zimmermann, 1998) as well as during daily activities (Benotsch, Christensen, &

McKelvey, 1997; Linden, Chambers, Maurice, & Lenz, 1993) though underlying

mechanisms still remain to be fully explained Exaggerated SNS activity among

angry / hostile individuals may explain higher risk for CHD One specific feature of the SNS that has been specifically related to hostility is adrenergic receptor function Reduced β-adrenergic1 responsiveness has been implicated in the pathophysiology of hypertension

as well as a pre-clinical marker of CHD

Hughes, Sherwood, Blumenthal, Suarez and Hinderliter (2003) examined the

relationship between β-adrenergic receptor responsiveness and hostility and social support

in African American and Caucasian American men and women aged 25 to 45 years Hostility and social support were assessed using standardized self-report measures Results found hostility and social support unrelated to α-adrenergic receptor

responsiveness However, controlling for race, sex, age, SBP, and resting HR, hostility and social support predicted β-adrenergic receptor responses High hostility was associated with reduced β-adrenergic receptor function in both ethnic groups as was low levels of social support These results suggest that impaired β-adrenergic function may be a marker

of increased CHD risk among individuals high in hostility and low in social support

Elevated blood pressure responses to anger provocation in the laboratory settings have also been hypothesized as pointing to mechanisms explaining how the experience and/or expression of anger might lead to the development of CHD (Krantz & Manuck, 1984) For instance, individuals experiencing intense anger and expressing it overtly may exhibit exaggerated heart rate or blood pressure responses which in turn increase their risk for CHD (T.W Smith, 1992) al’Absi and Arnett (2000) suggest that chronic and repeated exposure to anger provoking stressful situations and frequent overt anger expression are associated with repeated bouts of HPA, SAM, and endogenous opioid system activity as well as interactions between these systems

It is of particular interest here that some researchers have found that exaggerated cardiovascular reactivity as a response to anger provoking and hostile situations is not uniform across different ethnic groups That is, mechanisms underlying cardiovascular reactivity due to anger and hostility may in fact vary between ethnic groups Finney, Stoney and Engebretson (2002) compared the relationships between hostility and anger

expression as well as cardiovascular and lipid reactivity between African Americans and European Americans, using a speech stressor Independent of ethnicity, those with a general tendency to either express or inhibit anger expression had higher triglyceride reactivity compared to those with a flexible style Also, African American men low in cynical hostility had greater BP reactivity to the stressors This effect appeared to be primarily due to low cynical men with high anger-in (inhibited anger expression) Thus low cynical hostility among African Americans appeared to result in detrimental health effects such as exaggerated stress reactivity of higher BP

In another study, Suchday and Larkin (2004) examined cultural differences in response to anger provocation among 20 Indian male immigrants in America and 40 White men The participants engaged in two interactions with a confederate and were instructed to suppress or express their anger Affective, cognitive, behavioral, and cardiovascular responses to these social confrontations were noted Results showed that Indian

participants used more introspective strategies of repression and rational-coping self statements to anger provocation than the White men The Indian participants also had a faster diastolic blood pressure recovery when allowed to inhibit anger, but delayed DBP recovery when asked to express anger before they were allowed to inhibit it White men showed heightened cardiac reactivity in response to anger provocation in comparison to Indian men who did not exhibit such a physiological response

Thus studies investigating ethnic differences in CHD in relation to anger and hostility have shown a positive relation between trait anger and cardiovascular reactivity among Caucasian and African Americans, but relatively few studies have been conducted

to investigate links between cardiovascular reactivity and anger related variables in other ethnic groups This creates a gap in the cross-cultural validity of the anger / hostility and cardiovascular reactivity link with regards to Asian societies as only a handful of studies have thus far addressed this issue in the Asian context (Bishop & Quah, 1998; Bishop & Robinson, 2000; Why et al., 2003, Enklemann et al., 2005) Ethnographic studies have found cross-cultural differences in the experience, regulation and expression of anger (Tanaka-Matsumi, 1995) as emotional displays are governed by varying socio-cultural rules (Drummond & Quah, 2001) This further highlights the importance and need to study the anger- cardiovascular reactivity link in a non-western culture such as that of Singapore

Cardiovascular Reactivity Across Ethnic Groups

There is interesting evidence related to ethnicity and differences in hemodynamic responses to stressors ( Saab et al., 1992; Sherwood, May, Siegel, & Blumenthal, 1995) A majority of the research examining ethnic differences in cardiovascular reactivity has looked at African Americans and Caucasian Americans (Murphy, Alpert, & Walker, 1992) with African Americans exhibiting responses that reflect a larger vasoconstrictive response than do Caucasian Americans (Light, Turner, Hinderliter, & Sherwood, 1993; Treiber et

al., 1990) This pattern of increased vasoconstrictive time responses among African American individuals has mostly been observed during the cold pressor task, a task that produces marked α-adrenergic vasoconstriction (Treiber et al., 1990) However, the reasons for heightened pressor response to stress in African Americans remain speculative

To determine the cardiac and vascular contributions of differences in blood

pressure reactivity across racial groups, Kelsey, Alpert, Paterson and Barnard (2000) evaluated BP, HR and impedance cardiographic measures of PEP and TPR in healthy African American and Caucasian American adolescents Results showed greater decreases

in PEP and increases in TPR in African Americans than Caucasian Americans during cold exposure, but no group differences during heat exposure These differences during cold reflect greater β-adrenergic cardiac reactivity and α-adrenergic vasoconstrictive reactivity

in African Americans Such variations in reactivity patterns across different races in America also point to the need for possible differences to be examined among racial sub-groups in the Asian context

Knox, Hausdorff and Markovitz (2002) explored the question of whether

cardiovascular reactivity to mental stress predicts subsequent ambulatory blood pressure differently across race subgroups Over 300 African American and Caucasian American men and women in the Coronary Artery Risk Development in Young Adults (CARDIA) Study were followed over a period of three years After controlling for age, baseline SBP,

familial history of hypertension, smoking, alcohol consumption, body mass index and exercise, SBP reactivity to star tracing and cold pressor stress were significantly associated with systolic ambulatory pressure in African American men and women three years later

HR reactivity to a video game challenge and to a star tracing task was also significantly predictive of subsequent ambulatory HR in African Americans and diastolic reactivity to star tracing was associated with ambulatory BP in African American women For the Caucasian participants, diastolic reactivity to both tasks was only predictive of ambulatory

BP in men This study points to hyper-responsivity to stress being a risk factor for

hypertension, and thereby one pathway leading to higher prevalence of hypertension in African Americans

Extending studies that have found differences in CVR across ethnic groups in the West, Enklemann, et al (2005) explored the relationship of hostility, negative affect and ethnicity to cardiovascular response in an ambulatory study in the Asian context of

Singapore The researchers hypothesized that ambulatory HR and BP would be higher only for individuals high in hostility when they experienced negative affect or social stress and this interaction would be stronger for Indians compared to Chinese and Malays Results supported the hypothesis such that those individuals high in hostility showed higher SBP when reporting negative affect This was not true for participants low in hostility Evidence for ethnic differences was obtained for DBP, mean arterial pressure (MAP) and HR

Firstly, a three-way interaction between ethnicity, hostility and social stress was noted for DBP For Indians with high hostility scores, DBP was a positive function of social stress, but for those low on hostility higher levels of social stress were related to lower DBP Such

an interaction was not seen among the Chinese or Malay participants Secondly, Indians showed an increase in mean arterial pressure (MAP) when angered, while MAP was negatively related to anger for Malays and unrelated for Chinese Finally, HR was found to

be an increasing function of negative affect for Chinese with high hostility scores and for Malays with low hostility scores For all other participants, HR was decreasing function of negative affect Indians in particular showed lower HR with increasing negative affect regardless of their hostility scores

Psychological and cardiovascular responses to experimental harassment have also been studied among Chinese and Indian men in Singapore to examine cardiovascular reactivity as a function of trait anger In a laboratory experiment, Bishop and Robinson (2000) obtained ratings of mood and measured HR and BP during computer tasks in which participants were either harassed or not harassed Chinese and Indian men, who differed in levels of dispositional anger, formed the subject pool Results showed greater systolic reactivity after harassment Interestingly, a race by dispositional anger by

harassment interaction effect was obtained for systolic reactivity, indicating different patterns of reactivity among Chinese and Indians Chinese participants showed low

systolic reactivity in the non-harassed situation irrespective of their level of dispositional anger, but higher reactivity during harassment On the other hand, for Indians, systolic reactivity increased as a function of dispositional anger for both harassed and

non-harassed conditions These findings indicate higher cardiovascular reactivity to stress among Indians with high trait anger as compared to Chinese men It also points to the undifferentiated patterns of blood pressure responses for high anger Indians irrespective

of task characteristics

To examine the underlying hemodynamic processes in cardiovascular reactivity Why, et al (2003) conducted an experiment involving 114 male patrol officers from the Singapore Police Force Participants performed tasks of mental arithmetic, number reading and anger recall and their BP and HR were taken along with other hemodynamic measures Across tasks, Indians high in hostility showed the most cardiac reactivity, while reactivity patterns for Malays and Chinese were not distinctive More specifically, across tasks hostility was positively related to cardiac output (CO) and negatively related to total peripheral resistance (TPR) reactivity for Indians This suggested that Indians who are high

in hostility are cardiac reactors, which may be related to their heightened risk of CHD (Sundin, Ohman, Palm, & Strom, 1995) As such, these patterns of hemodynamic

cardiovascular reactivity were consistent with the high rates of CHD among Indians in Singapore A lack of significant ethnicity by hostility by task interaction for CO and TPR

indices, also pointed to generalization of the ethnicity by hostility interaction across tasks The research team further noted that the three ethnic groups studied did not appear to show

a differential predisposition towards reactivity independent of hostility, as no main effect for ethnicity was obtained in the study Thus cardiovascular reactivity needs to be

investigated not only as a function of ethnicity but also underlying psychosocial factors such as anger / hostility that may play an important role in the observed cardiovascular reactivity

Sex Differences in Cardiovascular Reactivity

Many cross-sectional studies have compared cardiovascular responses to stressors

in men and women Results have confirmed consistently that men demonstrate greater systolic pressure increases than women to a variety of stressors (Stoney, Davies, &

Matthews, 1987; Saab, 1989) but diastolic pressure and HR response are not greater in males Women show lower average blood pressures and lesser prevalence of hypertension than do men until approximately age 50, when this trend reverses (Sherwood, 1993)

Burns and Katkin (1993) examined whether relationships between anger

expression, hostility, social evaluative anxiety and CVR to stress were moderated by stressful situation and gender Men and women performed a reaction time task in either harassment or social evaluation condition and their blood pressure and heart rate indices were recorded Anger expression was found to be related to CVR only among men in the

harassment condition Furthermore, hostile men who expressed their anger showed the greatest CVR across situations Neither of the traits assessed predicted CVR among women This study clearly suggested that psychological factors associated with CVR present themselves differently among men and women

In the past decade, several investigators have looked at the psychophysiological analysis of underlying hemodynamic patterns in relation to factors for hypertension such as sex In one such study (Girdler, Turner, Sherwood, & Light, 1990) women exhibited greater CO increases, whereas men showed greater vascular resistance responses across a series of stressful tasks Similarly, other studies also seem to support association of males with vascular reactivity and females with cardiac reactivity (Allen & Matthews, 1997), thereby suggesting that vascular reactivity may carry the greater epidemiological risk On the other hand, other research (Light et al., 1993; Lawler, Wilcox & Anderson, 1995; Lawler et al., 2001) has argued for a reverse association For instance, Lawler et al (2001) found no differential associations between sex and myocardial/vascular reactor group assignment during a math task nor were there any sex differences in magnitude of CO or TPR change However, during the anger recall interview, females were more likely to be classified as vascular reactors characterized by larger TPR increases, while males had larger CO increases characteristic of myocardial reactors Thus on balance, recent studies

of sex comparisons find males more myocardially reactive and females more vascularly reactive

Relatively less is known about associations between anger / hostility related variables and cardiovascular reactivity among women In an attempt to remedy this imbalance, Powch and Houston (1996) investigated relations between hostility-related variables (such as cynical hostility, aggressiveness, antagonism, anger-in) and CVR among White women under conditions of high versus low interpersonal stress

Participants higher in cynical hostility exhibited more SBP reactivity than those low in cynical hostility in the high interpersonal stress condition only and antagonism was positively related to heart rate reactivity across conditions Neither aggressiveness nor anger-in was related to reactivity in either condition Thus, cynicism and antagonism may predict risk for CHD among women whereas overt aggressive behaviors do not which is

in contrast to findings for male participants (Siegman, Anderson, Herbst, Boyle, &

Wilkinson, 1992; Deary, Fowkes, Donnan, & Housley, 1994)

Stoney et al (2002) examined responses of Asian Indian men and women to psychological stress as indexed by hemodynamic measures relative to European

Americans During a standard reactivity protocol involving two tasks (an impromptu video taped speech task and a mental arithmetic task), Asian Indians showed significantly smaller changes in SBP and MAP Asian Indian women showed a consistent pattern of

having significantly lower DBP and TPR reactivity, compared to European American men and women as well as Asian Indian men In addition, Asian Indian men and women showed significantly smaller SBP reactivity than their European American counterparts These results suggest an interactive influence of ethnicity and sex in vascular response to psychological stress Furthermore Asian Indian women may exhibit reduced

cardiovascular reactivity compared to men as well as their European American

counterparts With regards to studies conducted in the Asian context, none of the studies from Singapore included women as part of their study samples

With few studies of sex differences done in Asian populations and evidence to suggest that sex differences do in fact exist in hemodynamic patterns exhibited by men and women, there is a need to investigate these aspects in a multiethnic setting such as Singapore Sex differences may also emerge across different tasks such as subjective emotional tasks (anger recall interview) and more structured cognitive tasks such as the mental arithmetic task

Cardiovascular Reactivity Among Migrant / Minority Populations

The effects of migration on the risk factors and development of CHD presents distinct challenges due to the complex impact of cultural factors when people migrate from their native lands to a foreign land and culture Migration may be viewed as a

dynamic process that refers to a move from one place to another and, therefore, inherently