Key Points
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Cardiovascular morbidity and mortality rates differ among diverse racial and ethnic groups in the United States.
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The major cardiac risk factors are the same in all ethnic and racial groups in the United States and worldwide; however, the demographics and relative weight attributed to each factor may differ.
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Chronic, subclinical inflammation appears to be one pathophysiologic mechanism explaining the increased risk of atherosclerotic disease regardless of the amount of obstruction produced by that coronary disease, and African Americans are more likely than white Americans to carry allelic variants demonstrated to increase production of inflammatory cytokines.
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Framingham risk calculation performs reasonably well for prediction of CHD events in all racial and ethnic groups; however, among Japanese American and Hispanic men and Native American women, the Framingham functions systematically overestimated the risk of 5-year CHD events.
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Different races respond differently to a variety of cardiovascular medications in terms of both efficacy and toxicity.
Cardiovascular Disease in Racial and Ethnic Minorities: Overview and Perspectives
Cardiovascular disease (CVD) is the leading cause of death in the United States and worldwide. In 2001, heart disease accounted for approximately 29% of deaths among U.S. residents; 17% of those deaths occurred among persons aged <65 years. From 1996 to 2006, death rates from CVD have decreased 29%; however, the decline has not been uniform for all populations. It is well documented that cardiovascular morbidity and mortality rates differ among diverse racial and ethnic groups in the United States.
Recent data from the Centers for Disease Control and Prevention reveal that African Americans have earlier and higher mortality rates from coronary heart disease (CHD) than those of whites, American Indian/Alaska Natives, Asian/Pacific Islanders, or Hispanics ( Fig. 23-1 ). Ethnic differences in the prevalence of complex diseases such as atherosclerosis are undoubtedly multifactorial. It is clear that there are social, environmental, biologic, genetic, and probably other determinants leading to the disparities in CHD.
Whereas earlier articles have explored many of these factors, ongoing large population-based and cohort studies are lending valuable insight. One of these studies, the Multi-Ethnic Study of Atherosclerosis (MESA), is adding important insights into CVD among various ethnic groups in the United States. MESA was initiated in July 2000 to investigate the prevalence, correlates, and progression of subclinical CVD in a population-based sample of 6814 men and women aged 45 to 84 years. The cohort was selected from six United States field centers and is approximately 38% white, 28% African American, 23% Hispanic, and 11% Asian (primarily of Chinese descent). Baseline measurements taken included measurement of coronary calcium by computed tomography, measurement of ventricular mass and function by cardiac magnetic resonance imaging, measurement of flow-mediated brachial artery endothelial vasodilation, carotid intima-media wall thickness, and measurement of peripheral vascular disease by ankle and brachial blood pressures. Assessments of demographic measures, standard CVD risk factors, sociodemographic factors, life habits, and psychosocial factors were also made. Blood samples were assayed for blood chemistries, lipids, inflammatory markers, and DNA.
The MESA cohort has been observed since 2000 for identification and characterization of CVD events, including acute myocardial infarction and other CHD, stroke, peripheral arterial disease, heart failure, therapeutic interventions for CVD, and mortality. Thus, MESA and other epidemiologic studies will lend invaluable insights into the role of race and ethnicity in CVD.
This chapter summarizes currently available data on ethnic differences in CVD, cardiac risk factors, vascular biology, genetic factors, and socioeconomic determinants of atherosclerosis, but it is important to keep in mind that ethnic populations are far from homogeneous with respect to many genetic and biologic traits. Nonetheless, investigation into variations among ethnic groups can be an important key to understanding the causes of complex genetic conditions like atherosclerosis. Such investigations can also lead to important research into pathophysiology and treatment, thus improving outcomes for all populations.
Epidemiology of Cardiovascular Risk Factors among Racial and Ethnic Populations in the United States
Considerable information has been gathered about cardiovascular risk factors in ethnic populations. The major cardiac risk factors are the same in all ethnic and racial groups in the United States and worldwide; however, the demographics and relative weight attributed to each factor may differ. Among African Americans, for example, some of the excess CHD may be accounted for by the excess prevalence of known complicating risk factors, such as hypertension, left ventricular hypertrophy, and diabetes mellitus. Differences in other risk factors, such as plasma lipoprotein profiles, may not completely explain disparities but may lend insight into ethnic differences in the biology of atherosclerosis.
Hypertension
Worldwide, hypertension is known to account for considerable cardiovascular risk. The INTERHEART trial highlighted this risk. In the INTERHEART study, a standardized case-control study that screened all patients admitted to the coronary care unit or equivalent cardiology ward for a first myocardial infarction at 262 participating centers in 52 countries throughout Africa, Asia, Australia, Europe, the Middle East, and North and South America, hypertension was thought to account for 23.4% of the population-attributed risk for a myocardial infarction.
Compared with all other ethnic groups in the United States, hypertension in African Americans is more common, begins earlier, is more severe, and causes more target organ damage. Relative to hypertensive whites, African Americans with hypertension demonstrate delayed sodium excretion, plasma volume expansion, lower plasma renin activity, elevated intracellular sodium concentration, and altered numbers and activities of sodium transporters (Na + -H + antiporter, Na + ,K + -ATPase, and Na + -K + -Cl − cotransporter). Many of these differences may have a genetic basis.
To possibly explain the greater prevalence and severity of hypertension in African Americans, several candidate genes have been explored. Genes encoding components of epithelial sodium channels, the renin-angiotensin-aldosterone system, alpha- and beta-adrenergic receptors, endothelin, kallikrein, natriuretic peptides, and the nitric oxide pathway have been investigated. To date, few convincing genetic explanations for ethnic differences have emerged.
Hypertension in part increases CHD risk by predisposing to left ventricular hypertrophy. Left ventricular hypertrophy increases cardiac risk up to fourfold and is more common in African Americans, even after adjustment for blood pressure. The mechanisms by which left ventricular hypertrophy increases risk are poorly understood but likely include predisposition to ischemia and arrhythmias.
The MESA has given us valuable insight into the prevalence, treatment, and control of hypertension in the United States. Whereas most prior studies investigating the association between ethnicity and hypertension in the United States focused on differences between African Americans and whites and did not include other racial and ethnic groups such as Chinese or Hispanics, a paper by Kramer and colleagues used MESA data to examine the association between ethnicity and hypertension and hypertension treatment among white, African American, Chinese, and Hispanic ethnic groups. These authors found that the prevalence of hypertension, defined as systolic blood pressure ≤140 mm Hg and/or diastolic blood pressure ≤90 mm Hg or self-reported treatment for hypertension, was significantly higher in African Americans compared with whites (60% versus 38%; P < 0.0001), whereas prevalence in Hispanic (42%) and Chinese participants (39%) did not differ significantly from that in whites. After adjustment for age, body mass index (BMI), prevalence of diabetes mellitus, and smoking, African American ethnicity (OR, 2.21; 95% CI, 1.91-2.56) and Chinese ethnicity (OR, 1.30; 95% CI, 1.07-1.56) were significantly associated with hypertension compared with whites. They further found that among hypertensive MESA participants, the percentage of treated but uncontrolled hypertension in whites (24%) was significantly lower than that in African Americans (35%; P < 0.0001), Chinese (33%; P = 0.003), and Hispanics (32%; P = 0.0005), but only African American race and ethnicity remained significantly associated with treated but uncontrolled hypertension after control for socioeconomic factors (OR, 1.35; 95% CI, 1.07-1.71).
Dyslipidemia
The epidemiologic relationship between serum cholesterol levels and the risk of CHD is well documented. Across cultures, cholesterol is linearly related to CHD mortality, and despite differences in the prevalence of CHD between various populations, the relative increase in CHD mortality rates for a given cholesterol increase is remarkably consistent. There is a complex interplay between genetic and environmental factors that influences the expression of lipoprotein levels in individuals and between groups of people, and differences in plasma lipoprotein levels have been reported between various ethnic groups.
African Americans have one of the highest CHD event rates of any ethnic or racial group in the United States. Despite this fact, epidemiologic studies have consistently shown that plasma lipoprotein concentrations appear more favorable in African Americans than in white Americans.
African Americans have been shown to have higher high-density lipoprotein cholesterol (HDL-C) levels than white populations. This is likely due, at least in part, to the lower activity of hepatic lipase in African Americans. Hepatic lipase is an enzyme involved in HDL-C catabolism; thus, the lower the hepatic lipase activity, the higher the HDL-C level. Hepatic lipase activity has been found to be lower in African American men than in white men by Vega and colleagues, in part because of increased prevalence of a hepatic lipase allele (514T) that is associated with reduced hepatic lipase activity.
Two other polymorphisms that cause amino acid substitutions in hepatic lipase (N193S and L334F) have since been found that are also associated with lower hepatic lipase activity and are also much more common in African Americans than in whites. This higher HDL-C level, however, may not protect African Americans from CHD, as one might expect. In an analysis of the Veterans Affairs HDL Intervention Trial (VA-HIT), Rubins and colleagues found that the African American participants, all of whom had CHD, had low-density lipoprotein cholesterol (LDL-C) levels similar to those of the white men with CHD in the study but substantially higher HDL-C levels. Furthermore, compared with whites, African Americans have been found to have similar or slightly lower total cholesterol levels, lower LDL-C levels, and lower triglyceride levels, thus giving African Americans what would appear to be a more favorable lipoprotein profile.
Small, dense LDL-C particles are associated with an atherogenic lipoprotein phenotype that increases risk of myocardial infarction up to three times. In a study by Kral and colleagues, racial differences in the prevalence of small, dense LDL-C were studied. They investigated 159 African American and 477 white siblings of persons with premature CHD (CHD occurring at <60 years). Multiple logistic regression analysis demonstrated that white race ( P = 0.009), triglyceride level ( P = 0.0001), and diabetes ( P = 0.02) were independent predictors of the likelihood of having small, dense LDL-C particles. White individuals had more small, dense LDL-C particles than African Americans did despite comparable levels of total cholesterol and LDL-C.
Lipoprotein(a) is structurally similar to LDL-C, with an additional disulfide-linked glycoprotein termed apolipoprotein(a). Apolipoprotein(a) shares extensive structural homology with plasminogen but varies in size, which is due to the variation in the number of kringle 4–like domains (type 2 repeats) of plasminogen. Because of the size heterogeneity, apolipoprotein(a) exhibits a genetic size polymorphism with apparent molecular masses of isoforms ranging from 300 to 800 kDa.
There are considerable differences in the mean of plasma lipoprotein(a) concentrations between different populations and ethnic groups. Many although not all epidemiologic and case-control studies have shown that when lipoprotein(a) is present in high level in the plasma, it is an independent risk factor for CHD. In addition to high lipoprotein(a) levels, the presence of small apolipoprotein(a) isoforms (with fewer kringle 4 type 2 repeats) has been associated with CHD in whites. Interestingly, although mean lipoprotein(a) levels are more than twice as high in African Americans as in whites, some studies have failed to establish a significant association between elevated lipoprotein(a) levels and CHD among African Americans. The reason for this may be that the majority of whites with high lipoprotein(a) levels possess at least one small apolipoprotein(a) isoform; however, the majority of African Americans with high lipoprotein(a) levels have no small apolipoprotein(a) isoforms.
The major Hispanic subgroups are Mexican Americans, Central and South Americans, Puerto Ricans, and Cuban Americans, with Mexican Americans making up the largest single Hispanic group. Native Mexicans have lipids characterized by low HDL-C and elevated triglyceride levels. In a survey done in 417 Mexican cities, information on lipid levels was obtained for 15,607 subjects, 20 to 69 years of age. Mean total cholesterol concentration in this cohort was 185 mg/dL; mean triglyceride level was 212 mg/dL; mean HDL-C level was 40 mg/dL; and mean LDL-C concentration was 118 mg/dL. The most prevalent lipoprotein abnormality in this cohort was low HDL-C (HDL-C levels below 35 mg/dL), which occurred in 46% of men and 29% of women.
Hypertriglyceridemia (triglyceride levels ≥200 mg/dL) was the second most prevalent abnormality, occurring in 24.3% of participants, with severe hypertriglyceridemia (≥1000 mg/dL) being observed in 0.42% of this population. Half of the subjects with hypertriglyceridemia had a mixed dyslipidemia with low HDL-C levels as well. Insulin resistance was found to be prevalent in this population, being found in 59% of the subjects. Thus, the prevalence of dyslipidemia in urban Mexican adults is very high, with much of this likely due to insulin resistance.
This pattern of dyslipidemia has also been seen in Mexican American adults and children living in the United States. When Hispanics of different ancestry are studied, similar results are seen as well. Bermudez and colleagues studied 490 Hispanics of Caribbean origin (Puerto Rico and the Dominican Republic) and 163 non-Hispanic whites. They found that concentrations of total cholesterol, HDL-C, and apolipoprotein A-I were significantly lower among Hispanic women than among non-Hispanic white women. Although LDL-C concentrations are not higher in Hispanics, there appears to be a higher incidence of small, dense LDL-C.
In the Insulin Resistance Atherosclerosis Study, Hispanics not only had lower HDL-C and higher triglyceride levels than non-Hispanic whites did but also a smaller LDL-C particle size. In regard to lipoprotein(a), available data suggest somewhat higher values in Hispanics compared with non-Hispanic whites. In a study by Chiu and associates, 390 non-Hispanic whites and 214 Hispanics from San Luis Valley, Colorado, were studied. Mean (±SD) and median lipoprotein(a) levels were 9.6 ± 12.5 mg/dL and 3.8 mg/dL, respectively, in non-Hispanic whites and 12.1 ± 15.6 mg/dL and 4.9 mg/dL, respectively, in Hispanics.
Asian Indians are known to be at increased risk for CHD. Rates of coronary artery disease in young Asian Indians younger than 40 years are 3 to 10 times higher than those in other populations, and some of this increased risk may be conferred by dyslipidemia. The typical lipid profile of Asian Indians living in Western societies is characterized by hypertriglyceridemia, low levels of HDL-C, and high levels of small, dense LDL-C. In a study by Hoogeveen and colleagues, Asian Indian subjects living in India and Asian Indians living in the United States were examined. Asian Indians living in the United States had higher plasma levels of triglyceride, total cholesterol, and LDL-C as well as lower HDL-C levels than did Asian Indians in India. Much of the dyslipidemia in Asian Indians also may at least in part be due to the greater prevalence of insulin resistance observed in this population.
Small, dense LDL-C is also found more commonly in Asian Indians than in whites. In a study of 78 subjects, the prevalence of small, dense LDL-C was significantly higher in Asian Indians compared with white subjects (44% versus 21%; P < 0.05). In this study, the increased prevalence of small, dense LDL-C type appeared to be due to the increased triglycerides.
Higher serum lipoprotein(a) concentrations have also been reported in Asian Indians. In a study of young Asian Indian patients (younger than 45 years) who had suffered a myocardial infarction, the mean lipoprotein(a) level was 22.3 ± 5.4 mg/dL in patients and 9.3 ± 22.6 mg/dL in controls.
These data on ethnic differences in lipoprotein levels are summarized in Table 23-1 . Of course, these general trends are based on population studies, and lipoprotein levels in a given individual may depart significantly. Nonetheless, knowledge of ethnic trends in plasma lipoprotein levels is useful for prognosis and treatment of CHD.
Ethnic Group | Total Cholesterol | LDL | % Small, Dense LDL | HDL | Triglyceride | Lipoprotein(a) |
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African American | ⇓ | ⇓ | ⇓ | ⇑ | ⇓ | ⇑⇑ |
Hispanic | ⇔ | ⇓ | ⇑ | ⇓ | ⇑ | ⇑ |
Asian Indian | ⇔ | ⇔ | ⇑ | ⇓ | ⇑ | ⇑ |
Insulin Resistance and Diabetes Mellitus
Type 2 diabetes varies considerably more by race and ethnicity as shown in Figure 23-2 . The highest rates in the United States are seen in African Americans, Hispanic Americans, American Indians, and Asian/Pacific Islanders.
In the Atherosclerosis Risk in Communities (ARIC) study, the incidence of diabetes was 2.4-fold greater in African American women and 1.5-fold greater in African American men than in their white counterparts. Excess adipose tissue accounted for almost half of the increased risk in African American women but little of the excess risk in African American men. African Americans with diabetes also have an increased risk of target organ damage, and several studies have documented a higher prevalence of insulin resistance in African Americans, even after correction for obesity and lifestyle factors.
In 2000, of the 30 million Hispanic Americans, about 2 million had been diagnosed with diabetes. Hispanic Americans are about twice as likely to have diabetes as are non-Hispanic whites of similar age. Diabetes is particularly common among middle-aged and older Hispanic Americans. For those aged 50 years or older, about 25% to 30% have either diagnosed or undiagnosed diabetes. Diabetes is twice as common in Mexican American and Puerto Rican adults as in non-Hispanic whites. The prevalence of diabetes in Cuban Americans is lower, but it is still higher than that of non-Hispanic whites.
Asian Americans are a diverse population composed of individuals of Chinese, Filipino, Asian Indian, Vietnamese, Korean, and Japanese descent and others with Asian ancestry, such as Pacific Islanders. Studies suggest that Asians are more likely to develop diabetes than are whites, even when they are less obese. For example, in the Honolulu Heart Study, the prevalence of physician-diagnosed plus newly diagnosed diabetes was 40% in Japanese American men older than 70 years compared with 19.2% in white men aged 75 years or older from the third National Health and Nutrition Examination Survey (NHANES III).
Excess weight, particularly central obesity, is recognized to be a major determinant of diabetes risk in all populations. Regardless of which measure of excess weight is used, the prevalence of diabetes is consistently higher among Asians than among whites at any given level of obesity. Because of this known heterogeneity of relationship between central obesity (waist circumference) and insulin resistance, race- and ethnic-specific cut points have been developed. Race-specific cut points for waist circumference in relation to insulin resistance risk are shown in Table 23-2 .
Population | Organization | Recommended Waist Circumference Threshold for Abdominal Obesity | |
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Men | Women | ||
United States | AHA/NHLBI (ATP III) | ≥102 cm | ≥88 cm |
Europid | IDF | ≥94 cm | ≥80 cm |
Middle East, Mediterranean | IDF | ≥94 cm | ≥80 cm |
Sub-Saharan African | IDF | ≥94 cm | ≥80 cm |
Ethnic Central and South American | IDF | ≥90 cm | ≥80 cm |
Asian | IDF | ≥90 cm | ≥80 cm |
It is clear that both genetic and environmental risk factors play critical roles in the development of type 2 diabetes; however, despite strong evidence of heritability, there has been little success in identification of specific genes. Numerous candidate genes have been investigated, and although some gene variants have been found that confer increased risk of type 2 diabetes, many others have not been verified. No genes that explain genetic differences have been established. Because of the considerable cardiovascular risk conferred by diabetes, further studies exploring ethnic differences are essential to reduce disparities.
Inflammation
It is now recognized that atherosclerosis is an inflammatory disease. Chronic, subclinical inflammation appears to be one pathophysiologic mechanism explaining the increased risk of atherosclerotic disease regardless of the amount of obstruction produced by that coronary disease. In the inflammatory model of atherosclerosis, it is the degree of inflammation, not the degree of obstruction, that causes acute coronary syndromes and increased CHD mortality.
Cytokines are key mediators of the inflammatory response and have been implicated in the development of atherosclerosis. Studies have shown that African Americans are more likely than white Americans to carry allelic variants demonstrated to increase production of inflammatory cytokines.
There is now accumulating evidence that markers of subclinical inflammation may indeed predict future CHD events. One of the most studied markers is C-reactive protein (CRP), and with use of a highly sensitive assay (hsCRP), elevation of hsCRP has been found to be associated with several major CHD risk factors and with unadjusted and age-adjusted projections of 10-year CHD risk in both men and women.
Levels of hsCRP have been shown to vary by race and ethnicity. In one study, with use of the NHANES data base, CRP levels were found to be highest among non-Hispanic black men and Mexican American women. According to multiple logistic regression analysis, cigarette smoking and increased age, BMI, and systolic blood pressure in men and BMI and diabetes in women were strongly associated with a greater likelihood of CRP levels ≥1.0 mg/dL ( P < 0.001).
Whereas hsCRP levels have been shown to be related to cardiovascular risk factors, public health approaches to modification of hsCRP levels have been less well studied. One study, however, addressed physical fitness and its relation to hsCRP by ethnicity. LaMonte and colleagues hypothesized that physical fitness might protect against high levels of hsCRP. They analyzed data from a subset of 44 African American women, 45 Native American women, and 46 white women who were part of the Cross-Cultural Activity Participation Study (CAPS) in the mid-1990s.
In CAPS, physical fitness was determined by exercise on a treadmill while both speed and incline were increased, and the women continued on the treadmill until they reached their point of exhaustion. Each woman’s treadmill time was adjusted for her age, and women in each of the three ethnic groups were divided into three levels of fitness (low, moderate, and high) on the basis of their treadmill tests. The researchers assessed CRP levels by race, fitness, obesity, and waist size. They found that CRP levels were 4.3 mg/L in African American women, 2.5 mg/L in Native American women, and 2.3 mg/L in white women. They also found that women with low fitness had significantly higher CRP levels (4.3 mg/L) than did those in the moderate (2.6 mg/L) and high (2.3 mg/L) fitness categories. They also reported that CRP was significantly elevated in women with the highest BMI. Women with BMI values from 18.5 to 24.9 had hsCRP levels of 1.9 mg/L, whereas overweight and obese women had hsCRP levels of 4.2 mg/L. Finally, they found that women whose waists measured more than 35 inches had CRP concentrations of 4.2 mg/L, whereas those with waist circumference of less than 35 inches had CRP levels of 2.5 mg/L. These data provide evidence of a key mechanism through which chronic stressors may accelerate atherosclerosis and may have important implications for certain racial and ethnic populations.
Obesity
Obesity is the most important cause of preventable death and the second leading cause of premature death in the United States. About 300,000 excess deaths are linked to obesity and its complications annually. Excessive adiposity is a major cause of hypertension, dyslipidemia, and type 2 diabetes mellitus. These clinical risk factors are known to be the primary precursors of CVD, and the obesity epidemic has the potential to reduce further gains in the U.S. life expectancy, largely through an effect on cardiovascular risk and mortality. As the prevalence of obesity and overweight in the United States increases, the CVD consequences may also be concurrently increasing.
The prevalence of obesity doubled in U.S. adults between 1980 and 2004. Although data from 2005 to 2006 have shown no statistically significant increase in the prevalence of obesity since 2004, more than one third of U.S. adults are now obese. According to NHANES data, the increase in prevalence of overweight and obesity has been similar across racial and ethnic groups in both men and women during the past three decades; however, there are racial differences in the prevalence of obesity as well as racial differences in the prevalence of health complications associated with obesity.
Data from Behavioral Risk Factor Surveillance System surveys conducted during 2006-2008 show that African American women had the greatest prevalence of obesity (39.2%), followed by African American men (31.6%), Hispanic women (29.4%), Hispanic men (27.8%), non-Hispanic white men (25.4%), and non-Hispanic white women (21.8%). According to these data, African Americans (35.7%) had 51% greater prevalence of obesity, and Hispanics (28.7%) had 21% greater prevalence, compared with non-Hispanic whites (23.7%). Other studies also have shown that the prevalence of obesity among Asian Americans has been much lower than the national average, but differences between different Asian groups are considerable, and the highest prevalence of obesity has been reported among native Hawaiians and Samoans.
Despite obesity’s disproportionately high prevalence in African Americans and Hispanic Americans, studies suggest that its adverse impact on cardiovascular risk and mortality may be reduced in some minority populations. For example, even though African Americans have a higher prevalence of hypertension, diabetes, and hypercholesterolemia than white Americans do, evidence suggests that the relationship of BMI to most CVD risk factors is steeper in whites, suggesting a stronger influence of obesity on risk factor levels in whites than in African Americans. Prior studies have suggested that for a given BMI category, rates of CVD death among African Americans are lower compared with whites.
This observation indicates that even with higher rates of risk factors in African Americans, risk factors are more strongly associated with increasing BMI in whites. These paradoxical observations might be explained by the higher rates of type 2 diabetes mellitus, hypertension, elevated LDL-C, and low HDL among African Americans than among whites in the normal weight group. Moreover, although the relative associations between BMI and cardiometabolic risk factors are stronger in whites than in African Americans, there is a strong association between increasing BMI and cardiometabolic risk factors in both groups.
Smoking
Smoking is an independent risk factor for CVD. There are a number of ways that smoking contributes to the pathogenesis of CVD. Smoking impairs lipoprotein metabolism, increases blood thrombogenicity, reduces the distensibility of blood vessel walls, and induces proinflammatory state. Smokers have higher serum levels of cholesterol and lower plasma concentrations of HDL-C. Also, cigarette smoking is associated with higher plasma concentrations of triglyceride.
According to the 2008 National Health Interview Survey, approximately 20.5% of adults are current smokers. Data from national surveys indicate broad disparities in cigarette smoking by race or ethnicity. Native Americans and Alaskan natives have the highest smoking prevalence (36.4%), followed by whites (21.4%), African Americans (25), Hispanics (19.8%), and Asians (13.3%). There are also large differences by ethnicity in receiving advice from providers to quit smoking. African Americans and Hispanics are significantly less likely to be offered assistance with cessation.
Nationally, only 21% of Hispanics report receiving regular care from a racially concordant physician, compared with 88% of whites and 23% of blacks. The lower frequency of smoking cessation advice among Hispanics and African American reflects disparities in health care providers’ perceptions of the need for or effectiveness of cessation advice in this ethnic subgroup.
Moreover, interest in quitting and attempts to quit differ in ethnic groups. Only 62% of Hispanic smokers reported wanting to quit compared with 71% of whites, 68% of African Americans, and 70% of Native Americans. The percentage of smokers who quit also varies sharply by ethnic group, with the highest level of success among whites (51%) and the lowest for African Americans (37%).