STATE-OF-THE-ART PAPER
Heart Failure in Hispanics
Rey P. Vivo, MD*,*,
Selim R. Krim, MD*,
Cihan Cevik, MD* and
Ronald M. Witteles, MD
* Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas
Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California
Manuscript received September 11, 2008;
revised manuscript received October 31, 2008,
accepted December 1, 2008.
* Reprint requests and correspondence: Dr. Rey P. Vivo, Texas Tech University Health Sciences Center, Department of Internal Medicine, 3601 4th Street STOP 9410, Lubbock, Texas 79430. (Email: rpvivo_upsilon{at}yahoo.com).
 |
Abstract
|
|---|
Although large-scale heart failure (HF) studies in Hispanic Americans are lacking, some compelling data indicate that they are a particularly vulnerable population and underscore the need for further research. Hispanics comprise the largest and fastest-growing ethnic group in the U.S., in whom the impact of this burgeoning public health problem may be magnified. Current data show that Hispanics with HF are more likely to be younger and underinsured than non-Hispanic whites. They have higher rates of readmissions but have lower in-hospital and short-term mortality rates. Epidemiologic studies demonstrate that Hispanics have excessive rates of diabetes, obesity, dyslipidemia, and metabolic syndrome. Although hypertension and ischemic heart disease are established risk factors in this ethnic group, it may be considered that insulin resistance plays a significant role in the pathogenesis of HF in Hispanics, accounting for their inordinate cardiometabolic risk burden and the growing evidence of novel metabolic risk factors for HF. Hispanics encounter multiple barriers to health care influenced by socioeconomic, linguistic, and cultural factors that, in turn, have an adverse impact on disease prognosis. Recognition of predominant risk factors and health care disparities in this population is crucial to tailoring appropriate management strategies. This review summarizes epidemiologic and clinical data on Hispanics with HF, details risk factors and health care impediments, and presents an agenda for future investigation.
Key Words: heart failure • Hispanic • insulin resistance • cardiomyopathy • ethnic disparity
|
Abbreviations and Acronyms
| | CAD = coronary artery disease | | HF = heart failure | | LV = left ventricle |
|
By midcentury, minorities are projected to become the majority in the U.S. Playing a central role in this demographic shift are Hispanic Americans who lead all ethnic groups in the U.S. in number and rate of population growth. Presently, 45.5 million Hispanics live in the U.S., comprising 15% of the total population. Spurred by higher birth rates and immigration, this number is expected to nearly triple to over 130 million by 2050, when it is projected that 1 of 3 U.S. residents will be Hispanic (1). As the public health burden of heart failure (HF) continues to increase in the general population with its health care-related cost amounting to nearly $30 billion (2), its consequences are expected to be magnified among Hispanics for 3 key reasons. Foremost, the remarkable growth in the Hispanic population is expected to present a challenge to the health care system. Second, Hispanics have a disproportionate cardiometabolic risk burden (3), making them an important population to elucidate the association between novel metabolic risk factors and HF outcomes. Finally, they are significantly and unfavorably affected by health care disparities shaped by multiple socioeconomic, contextual, and cultural factors (4,5).
|
Epidemiology
|
|---|
Between 2000 and 2006, the Hispanic population grew almost 4 times faster (24.3%) than the total U.S. population (6.1%). Approximately 1 of every 2 persons added to the national population between 2005 and 2006 was Hispanic, thereby accounting for nearly one-half of the population growth during that period. The majority of Hispanics in the U.S. are of Mexican origin (64%); Puerto Ricans (9%), Cubans (3.4%), and Dominicans (2.8%) constitute other major national groups. Although the largest number of Hispanics resides in California, Texas, Florida, New York, and Illinois, the highest Hispanic growth rate has been reported in the Southeast, particularly in the states of Arkansas, Georgia, South Carolina, Tennessee, and North Carolina (Fig. 1). Mexicans comprise nearly one-third of the population in Texas and California; approximately one-half of the nation's Dominicans live in New York City, and about one-half of the nation's Cubans reside in Miami-Dade County, Florida. More than 90% of Hispanics reside in metropolitan regions—a trend strongly driven by migration from rural farm jobs to urban city occupations that began in the 1950s (1).
View larger version (51K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1 Percent Change in Population by State 2000 to 2006 Hispanic or Latino
Geographic differences in population growth of Hispanics in the U.S. Reprinted, with permission, from the U.S. Census Bureau (1).
|
|
Race, ethnicity, "Hispanic" clarified.
Current federal standards describe 5 racial categories: 1) white; 2) black or African American; 3) American Indian or Alaska native; 4) Asian; and 5) native Hawaiian or other Pacific islander. Meanwhile, ethnic categories are defined as either "Hispanic or Latino" or "not Hispanic or Latino" (6).
It must be emphasized that Hispanics make up the only ethnic group defined not by geographic origin but rather by common language (7). "Hispanic" in health literature broadly refers to a heterogeneous group of populations ancestrally linked to Spain and the Spanish-speaking nations of the Caribbean and Central and South America (1,3,8). Subcategorizing the population according to national origin provides a more precise albeit imperfect classification that may inadequately explain variables that impact health outcomes (e.g., acculturation) (8). National origin will be cited in this review according to specificity of available data.
Demographic and clinical features of HF patients.
Pertinent literature on HF in Hispanics remains scarce due to their under-representation in HF trials; this results in limited data primarily restricted to retrospective subgroup analyses. This was confounded by dichotomous (i.e., white and black) race/ethnicity coding in older medical databases, as illustrated by the 1994 expansion of Medicare data to include Hispanics and other minorities (9).
American Heart Association 2008 statistics revealed that the prevalence of HF was lowest in the Mexican-American subgroup, followed by non-Hispanic whites and African Americans (3). The annual prevalence rates for men were 2.1% in Mexican Americans, 2.8% in non-Hispanic whites, and 2.7% in African Americans. For women in the same populations, the prevalence rates were 1.9%, 2.1%, and 3.3%, respectively (Table 1). A study of elderly patients in Florida, on the other hand, revealed that the prevalence of self-reported HF was highest in Hispanic Cubans compared with non-Hispanic whites and African Americans; moreover, Hispanic Cuban women had the greatest HF prevalence rate on sex-adjusted analysis (10). A recent report from MESA (Multi-Ethnic Study of Atherosclerosis) documented that the incidence rate of HF was greater in African Americans (4.6 per 1,000 person-years) and Hispanics (3.5) than in non-Hispanic whites (2.4) (11). African-American and Hispanic subjects had higher incident HF with no interim myocardial infarction than non-Hispanic whites did, whereas a greater increase in HF risk was noted among Hispanics and non-Hispanic whites for any given increase in left ventricular (LV) mass index.
Retrospective and observational studies have largely documented that compared with non-Hispanic whites, Hispanics with HF are more likely to be younger (12–14), underinsured (12), and to have higher rates of diabetes, dyslipidemia, and kidney disease (12–15). In addition, Hispanics have a relatively higher prevalence of abnormal LV ejection fraction (13,14,16)—usually implying worse prognosis in HF. An observational analysis from the ADHERE (Acute Decompensated Heart Failure Registry) registry reported that age and rates of renal insufficiency and ischemic cardiomyopathy of Hispanics were intermediate between non-Hispanic whites and African Americans (15).
|
Risk Factors for HF
|
|---|
Hispanics are uniformly affected by excessive rates of diabetes, overweight and obesity, atherogenic dyslipidemia, metabolic syndrome, and poorly controlled hypertension (3) (Table 2). The conglomeration of these conditions, including related pathophysiologic components that are emerging as novel risk factors for HF (17,18), is expected to amplify the risk of this ethnic group for HF.
Diabetes.
Hispanics are nearly twice as likely to have diabetes as age-matched non-Hispanic whites (19). Moreover, the increase in diabetes prevalence from 2005 to 2050 is expected to be highest among Hispanics (20). The high prevalence of diabetes in this ethnic population has been attributed to higher rates of obesity (21), highly atherogenic diet consumption (22), and genetic susceptibility (23,24). Diabetes-related microvascular complications and mortality are higher in Hispanics than in non-Hispanic whites (25,26). In addition, diabetic Mexican Americans less frequently self-monitor their blood glucose and have poorer glycemic control than non-Hispanic whites (27). Although data have shown that low socioeconomic and educational status, poor medical care access, and inability to speak English do not predict worse glycemic control in Hispanics (27–29), a recent study reported that modifiable self-management behaviors, particularly higher diabetes-specific emotional distress, contribute to uncontrolled hyperglycemia in this population (30).
Poorly controlled diabetes predicts a higher risk of HF. The UKPDS (United Kingdom Prospective Diabetes Study) documented that every 1% incremental rise in glycated hemoglobin increased the risk for nonfatal HF by 16% (31). There is growing recognition of a "diabetic cardiomyopathy" that accounts for the increased risk of developing HF among diabetics in the absence of coronary artery disease (CAD), hypertension, or other known structural heart disease (32). Data from MESA indicating ethnic differences in diabetes-associated LV abnormalities, wherein increased LV mass and wall thickness were completely attributable to subclinical atherosclerosis and hypertension in non-Hispanic whites but not in Hispanics, suggest a greater contribution from diabetes in the latter group (33).
Obesity.
More Mexican-American men are overweight than their non-Hispanic white and African-American counterparts (3). They also have a higher proportion of abdominal fat than women (34). Among women, a higher percentage of Mexican Americans are overweight and obese than non-Hispanic whites. Hispanic adults (47.6%) are less likely than African Americans (51.3%) and non-Hispanic whites (66.1%) to engage in leisure-time physical activity (3).
The risk of HF progressively increases 5% in men and 7% in women for every point increase in body mass index without any apparent threshold (35). Mechanistic, pathologic, and animal studies provide evidence for an "obesity cardiomyopathy" (likely related to "diabetic cardiomyopathy" or "insulin-resistant cardiomyopathy") (36–39). Extensive data have shown, however, that a higher body mass index predicts paradoxically better survival after the onset of HF in patients with stable disease and among those with varying levels of functional impairment (40–44). Proposed explanations for the obesity paradox include earlier detection (due to more symptoms for the same degree of LV dysfunction), a protective effect from lipoprotein-mediated down-regulation of cytokines (40,41), and a greater metabolic reserve to surmount the catabolic and inflammatory stresses of cardiac cachexia (42,45).
Hypertension.
Although Mexican Americans are nearly as likely to have hypertension as non-Hispanic whites (3), their level of blood pressure control is poorer (46). In addition, only 35% of hypertensive Mexican Americans receive treatment and an even lower 14% achieved control compared with 24% in non-Hispanic whites (47).
By itself, hypertension more than triples the risk of HF (48). The prevalence of hypertension is increased in patients with diabetes, and hypertensive diabetics have worse LV function than normotensive diabetics (49). In addition, hypertension frequently coexists with obesity and is a recognized component of metabolic syndrome.
Dyslipidemia.
In contrast to non-Hispanic whites, Hispanics have higher triglyceride and lower high-density lipoprotein levels (50); Mexican Americans, in particular, have more elevated small, dense low-density lipoprotein particles (51), a pattern with a high prevalence in type 2 diabetics (52).
Although dyslipidemia is a predisposing risk factor for HF (53), a number of studies have documented that, after the onset of HF, there is an inverse association between total cholesterol levels and survival among HF patients (54–56). While this paradoxical association has been explained by the anti-inflammatory effects of cholesterol (57), some investigators propose that lower cholesterol levels—like lower body mass index in cardiac cachexia—may merely reflect the severity of HF (58). Cholesterol reduction with statin use has been shown to decrease incident HF in patients with CAD (59). However, 2 recently completed randomized, placebo-controlled trials demonstrated that statin therapy did not confer significant survival benefit among patients with ischemic or nonischemic HF and those with either reduced or preserved systolic LV function (60,61).
Metabolic syndrome and insulin resistance.
Mexican Americans lead all race/ethnic groups in the age-adjusted prevalence of metabolic syndrome (62). A genetic linkage of increased susceptibility to insulin resistance in the Hispanic population has been reported (63,64).
A distinct insulin-resistant cardiomyopathy, supported by basic science and clinical evidence, was recently postulated as a dominant cause of nonischemic HF (65). Furthermore, human data have demonstrated that metabolic syndrome is a significant predictor of LV dysfunction and incident HF, independent of blood pressure or intervening myocardial infarction (66,67).
|
Other Etiologic Conditions of HF
|
|---|
A few traditional and less conventional etiologies of HF are relevant to Hispanic patients.
CAD.
In contrast to non-Hispanic whites, some data have shown that Hispanics have a lower atherosclerotic burden demonstrated by lower prevalence of obstructive CAD, abnormal coronary artery calcium score (68), and common carotid artery intima-media thickening (69), even after adjusting for risk factor differences. Further evidence demonstrating an unexpectedly lower cardiovascular mortality among Hispanics despite their high cardiometabolic risk have indicated a "Hispanic paradox" (70–73). Contrary to this concept, more recent studies that prospectively ascertained vital status information have reported similar or higher all-cause and cardiovascular death rates in Mexican Americans than in non-Hispanic whites (74,75). Among women with acute coronary syndrome, Hispanics and non-Hispanic whites have been found to have similar in-hospital risk-adjusted mortality (76).
Rheumatic heart disease.
The national incidence of rheumatic fever and rheumatic heart disease has declined substantially but remains high in a few populations including Hispanics, particularly Mexican Americans (3,77). One study reported that the age-adjusted mortality rates for rheumatic heart disease in New Mexico over a 25-year period were higher in Hispanics than in non-Hispanic whites (77). Another study of patients presenting for mitral valve surgery revealed that Hispanics were younger and had higher prevalence of rheumatic disease and HF than non-Hispanic adults (78). These observations have been attributed to poorer economic status and access to public health services in this group (77,78).
Chagas' disease.
First described in Brazil and etiologically linked to the parasite Trypanosoma cruzi by Carlos Chagas (79), American trypanosomiasis or Chagas' disease is an important cause of HF in endemic regions including Mexico and Central and South America, where approximately 16 to 18 million people are infected (80). Although previously considered rare in the U.S., an estimated 50,000 to >350,000 Hispanic immigrants may have chronic, asymptomatic T. cruzi infection (80,81) with a 20% likelihood of progression to chronic cardiomyopathy in this population (82). Chagas' disease in the U.S. is principally driven by immigration, yet disease transmission can also occur via blood transfusion or organ transplant, or congenitally in pregnant women (80). Apart from HF, Chagas' heart disease may present as angina, fatal arrhythmias, or sudden death (83). Misdiagnosis of idiopathic dilated cardiomyopathy or CAD is common due to poor disease recognition in both patients and medical professionals, especially in nonendemic areas (81).
|
Diagnostic and Treatment Patterns
|
|---|
A study of Medicare beneficiaries examining ethnic disparities in quality of HF care reported that compared with non-Hispanic whites and African Americans, Hispanics were least likely to have an assessment of LV ejection fraction and to be discharged on angiotensin-converting enzyme inhibitor treatment (84). The OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) study showed that Hispanic ethnicity was an independent predictor for nondelivery of complete discharge instructions, even among hospitals serving the highest proportion of this population (85). Data from the GWTG-HF (Get With the Guidelines–Heart Failure) program demonstrated that the percentages of Hispanic patients receiving 2 HF performance measures (discharge instructions and angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker therapy) were intermediate between African Americans and non-Hispanic whites. For 2 GWTG-HF quality indicators (aldosterone antagonist therapy for LV systolic dysfunction and lipid lowering therapy), the percentages of Hispanics receiving them were higher than either subgroup (86).
|
Outcomes
|
|---|
Existing data indicate that despite their higher rates of hospitalization (87) and readmission (12) than non-Hispanic whites, Hispanics with HF have lower in-hospital (87) and short-term mortality rates (12) (Table 3), even after adjustment for age and sex. Furthermore, Hispanic patients were most likely to be discharged home and least likely to be discharged to a skilled nursing facility (87).
The ADHERE registry analysis documented that in-hospital mortality and length of stay of Hispanics were intermediate between non-Hispanic whites and African Americans (15). A multicenter study demonstrated more significant improvement in health-related quality of life over time in Hispanics with HF than in other ethnic groups after controlling for demographic, clinical, and treatment differences (88).
|
Barriers to Health Care
|
|---|
Although eliminating racial/ethnic health disparities is a major goal of the Healthy People 2010 national public health agenda (89), there are insufficient strategies that address numerous health care barriers in Hispanics (4,90). Across populations, Hispanics have the poorest health insurance access: over one-third of them have no medical insurance (91). In addition, they are most likely to have no usual place of care (92) and to have the most difficulty paying for medical care, irrespective of insurance status (93). Among different Hispanic subgroups, Mexican Americans are least likely to be insured and to use preventive health services (92). Cuban Americans more frequently have insurance coverage as a result of employment benefit or higher incomes, whereas Puerto Ricans are more likely to be covered by Medicaid (5,92).
Acculturation, a measure of integration of a group into a dominant culture (92), has been documented as a direct correlate of cardiovascular disease screening adherence among Mexican Americans (94). A study reported that shorter U.S. residence predicts fewer ambulatory or emergency care visits and lower likelihood to have any prescription medications (5). In the U.S., Hispanics have the lowest level of education (93), an important correlate of health risk. Another significant variable of acculturation and health care impediment for many Hispanics is the language barrier. About 8 million Hispanics in the U.S. do not speak English fluently (95). Monolingual Spanish speakers have a higher prevalence of cardiovascular risk factors and poorer recognition of coronary symptoms (96). In turn, exclusively English-speaking physicians engage Hispanic patients less effectively in their medical care than do bilingual physicians (97). Additionally, providers may contribute to disparities through clinical uncertainty and stereotyping of health behaviors related to minority patients (98).
Improving the cultural competency of providers requires awareness of health beliefs inherent to Hispanic culture. Values such as trust (confianza) and personalized care (personalismo), essential in the physician-patient relationship, may drive Hispanics to consult with family, friends, or traditional healers before seeking an empathic provider. Delays in medical treatment may also be ascribed to customs including fatalism and submission to the will of God (99). Data showing that Hispanics were more likely to consider hypertension as an expected and untreatable consequence of aging indicate that specific health attitudes may contribute to underuse of preventive services (100). Other cultural factors including unique disease perception, spirituality, stronger social support, and coping mechanisms, however, have been shown to positively impact health-related quality of life in Hispanic HF patients (88).
An important barrier to expanding the knowledge on Hispanics is limited research representation. A review of multiethnic clinical trials conducted in the U.S. between 1995 and 1999 noted that Hispanic subjects constituted only 3% of participants, which was far lower than their representation in the national population (101). Among patients enrolled in 83 trials from the Veterans Affairs Cooperative Studies Program (1975 to 2000), 76%, 20%, and 4% were non-Hispanic whites, African Americans, and Hispanics, respectively. Trials involving an invasive intervention enrolled even fewer ethnic minorities (102). Data showing that Hispanics are as willing as non-Hispanic whites to participate in health research suggest that their under-representation in research studies is less likely a result of reluctance to enroll but rather inadequate access provided by investigators/funding organizations (103). Other factors limiting minority participation in research include poor information dissemination, geographic inaccessibility of study sites, language/cultural barriers (e.g., Spanish translation of recruitment, consent, protocol materials), insufficient reimbursement of travel cost, and legal apprehensions of undocumented immigrants (103–105).
|
Conclusions and Future Directions
|
|---|
Whereas the validity of studying diseases on the basis of race/ethnicity has been occasionally fraught with skepticism, available data suggest that Hispanics with HF manifest demographic and clinical features, as well as health care challenges, distinct from other populations. Compelling evidence indicate that Hispanic ethnicity is marked by a disproportionate cardiometabolic risk burden, largely due to exceedingly high rates of insulin resistance. Therefore, we hypothesize that the central concept of insulin resistance—compounded by inflammation and neuroendocrine overactivity—may be a predominant etiologic factor for cardiomyopathy in Hispanics. We propose the following agenda for further investigation (Table 4):- • Adequate representation of Hispanics in HF registries and trials is paramount to expand the database and to construct significant data comparisons across other racial/ethnic populations. Subgroup analyses between Hispanic nationalities should reflect the ethnic diversity of the population.
- • It is imperative to evaluate the magnitude and mechanisms by which health care barriers affect HF presentation and outcomes in Hispanics. The paradox of higher hospitalization rates and lower mortality may be partly driven by poorer access to quality outpatient care, highlighting the importance of accounting for health care access variables when examining clinical end points (12).
- • Cardiometabolic risk biomarkers, subclinical disease parameters, and clinical end points should be examined thoroughly. Risk factor control (e.g., glycated hemoglobin, medication adherence) should also be assessed. Prospective studies with sufficiently long follow-up should help determine whether the reverse epidemiology shown by the obesity and cholesterol paradoxes are based on true association, survival bias, or reverse causation (45).
- • Our hypothesis intuitively invites the possibility of specific therapeutic targets and strategies for populations with strong cardiometabolic risk. The efficacy of newer pharmacologic options for cardiometabolic risk reduction, such as inhibitors of the poly(adenosine diphosphate-ribose) polymerase (32) and the cannabinoid-1 receptor (106), should be investigated.
|
Acknowledgments
|
|---|
The authors would like to acknowledge Lynn Bickley, MD, Sharma Prabhakar, MD, Kenneth Nugent, MD, and Michael Phy, DO, for their critique of the paper.
|
References
|
|---|
1. U.S. Census Bureau Population Estimates http://www.census.govAccessed August 27, 2008.2. Pleis JR, Lethbridge-Çejku M. Summary health statistics for U.S. adults: national health interview survey, 2005. National Center for Health Statistics. Vital Health Stat 10(232). 2006 [online publication] http://www.cdc.gov/nchs/data/series/sr_10/sr10_232.pdfAccessed October 24, 2008. 3. Rosamond W, Flegal K, Friday G, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart disease and stroke statistics—2008 update. A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117:e25-e146.[Free Full Text] 4. Mensah GA, Mokdad AH, Ford ES, Greenlund KJ, Croft JB. State of disparities in cardiovascular health in the United States Circulation 2005;111:1233-1241.[Abstract/Free Full Text] 5. Weinick RM, Jacobs EA, Stone LC, Ortega AN, Burstin H. Hispanic healthcare disparities: challenging the myth of a monolithic Hispanic population Med Care 2004;42:313-320.[CrossRef][Web of Science][Medline] 6. Office of Management and Budget Revisions to the Standards for the Classification of Federal Data on Race and Ethnicity. 2006 [online publication] http://www.whitehouse.gov/omb/fedreg/ombdir15.html 2004Accessed on April 2, 2008. 7. Taylor AL, Wright JT. Importance of race/ethnicity in clinical trials Circulation 2005;112:3654-3660.[Free Full Text] 8. Novello AC, Wise PH, Kleinman DV. Hispanic health: time for data, time for action JAMA 1991;265:253-255.[Abstract/Free Full Text] 9. Lauderdale DS, Goldberg J. The expanded racial and ethnic codes in the Medicare data files: their completeness of coverage and accuracy Am J Public Health 1996;86:712-716.[Web of Science][Medline] 10. Demirovic J, Prineas R, Rudolph M. Epidemiology of congestive heart failure in three ethnic groups Congest Heart Fail 2001;7:93-96.[Medline] 11. Bahrami H, Kronmal R, Bluemke DA, et al. Differences in the incidence of congestive heart failure by ethnicity Arch Intern Med 2008;168:2138-2145.[Abstract/Free Full Text] 12. Alexander M, Grumbach K, Remy L, Rowell R, Massie BM. Congestive heart failure hospitalizations and survival in California: patterns according to race/ethnicity Am Heart J 1999;137:919-927.[CrossRef][Web of Science][Medline] 13. Minutello RM, Chou ET, Hong MK, Wong SC. Impact of race and ethnicity on inhospital outcomes after percutaneous coronary intervention: report from the 2000–2001 New York State Angioplasty Registry Am Heart J 2006;151:164-167.[CrossRef][Web of Science][Medline] 14. Yeo KK, Li Z, Amsterdam E. Clinical characteristics and 30-day mortality among Caucasians, Hispanics, Asians and African-Americans in the 2003 California coronary artery bypass graft surgery outcomes reporting program Am J Cardiol 2007;100:59-63.[CrossRef][Web of Science][Medline] 15. Jimenez J, Osorio JM, Andrade S, Bauerlein J, Mallon S, Yancy C. Decompensated heart failure among Hispanic Americans: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) J Card Fail 2004;10(Suppl 1):S93. 16. Aronow WS, Ahn C, Kronzon I. Comparison of echocardiographic abnormalities in African-American, Hispanic, and White men and women aged >60 years Am J Cardiol 2001;87:1131-1133.[CrossRef][Web of Science][Medline] 17. Ingelsson E, Arnlov J, Sundstrom J, Zethelius B, Vessby B, Lind L. Novel metabolic risk factors for heart failure J Am Coll Cardiol 2005;46:2054-2060.[Abstract/Free Full Text] 18. Bahrami H, Bluemke DA, Kronmal R, et al. Novel metabolic risk factors for incident heart failure and their relationship with obesity: the MESA (Multi-Ethnic Study of Atherosclerosis) study J Am Coll Cardiol 2008;51:1775-1783.[Abstract/Free Full Text] 19. Centers for Disease Control and Prevention Prevalence of diabetes among Hispanics: selected areas, 1998–2002 MMWR Morb Mortal Wkly Rep 2004;53:941-944.[Medline] 20. Venkat Narayan KM, Boyle JP, Geiss LS, Saaddine JB, Thompson TJ. Impact of recent increase in incidence on future diabetes burden: U.S., 2005–2050 Diabetes Care 2006;29:2114-2116.[Free Full Text] 21. Ramachandran A, Snehalatha C, Viswanathan V, Viswanathan M, Haffner SM. Risk of noninsulin dependent diabetes mellitus conferred by obesity and central adiposity in different ethnic groups: a comparative analysis between Asian Indians, Mexican Americans and Whites Diabetes Res Clin Pract 1997;36:121-125.[CrossRef][Web of Science][Medline] 22. Haffner SM, Knapp JA, Hazuda HP, Stern MP, Young EA. Dietary intakes of macronutrients among Mexican Americans and Anglo Americans: the San Antonio Heart Study Am J Clin Nutr 1985;42:1266-1275.[Abstract/Free Full Text] 23. Mitchell BD, Kammerer CM, Blangero J, et al. Genetic and environmental contributions to cardiovascular risk factors in Mexican Americans. The San Antonio Family Heart Study. Circulation 1996;94:2159-2170.[Abstract/Free Full Text] 24. Lorenzo C, Serrano-Rios M, Martinez-Larrad MT, et al. Was the historic contribution of Spain to the Mexican gene pool partially responsible for the higher prevalence of type 2 diabetes in Mexican-origin populations? The Spanish Insulin Resistance Study Group, the San Antonio Heart Study, and the Mexico City Diabetes Study Diabetes Care 2001;24:2059-2064.[Abstract/Free Full Text] 25. Stern MP, Haffner SM. Type II diabetes and its complications in Mexican Americans Diabetes Metab Rev 1990;6:29-45.[Web of Science][Medline] 26. Carter JS, Pugh JA, Monterrosa A. Non-insulin-dependent diabetes mellitus in minorities in the United States Ann Intern Med 1996;125:221-232.[Abstract/Free Full Text] 27. Harris MI, Eastman RC, Cowie CC, Flegal KM, Eberhardt MS. Racial and ethnic differences in glycemic control of adults with type 2 diabetes Diabetes Care 1999;22:403-408.[Abstract] 28. Haffner SM, Hazuda HP, Stern MP, Patterson JK, Van Heuven WAJ, Fong D. Effect of socioeconomic status on hyperglycemia and retinopathy levels in Mexican Americans with NIDDM Diabetes Care 1989;12:128-134.[CrossRef][Web of Science][Medline] 29. Lasater LM, Davidson AJ, Steiner JF, Mehler PS. Glycemic control in English- vs Spanish-speaking Hispanic patients with type 2 diabetes mellitus Arch Intern Med 2001;161:77-82.[Abstract/Free Full Text] 30. Heisler M, Faul JD, Hayward RA, Langa KM, Blaum C, Weir D. Mechanisms for racial and ethnic disparities in glycemic control in middle-aged and older Americans in the health and retirement study Arch Intern Med 2007;167:1853-1860.[Abstract/Free Full Text] 31. Stratton IM, Adler AI, Neil HAW, et al. U.K. Prospective Diabetes Study Group Association of glycaemia with microvascular and macrovascular complications of type 2 diabetes (UKPDS 35): prospective observational study BMJ 2000;321:405-412.[Abstract/Free Full Text] 32. Hayat SA, Patel B, Khattar RS, Malik RA. Diabetic cardiomyopathy: mechanisms, diagnosis and treatment Clin Sci 2004;107:539-557.[CrossRef][Web of Science][Medline] 33. Bertoni AG, Goff Jr. DC, D'Agostino Jr. RB, et al. Diabetic cardiomyopathy and subclinical cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis (MESA) Diabetes Care 2006;29:588-594.[Abstract/Free Full Text] 34. Pawson IG, Martorell R, Mendoza FE. Prevalence of overweight and obesity in U.S. Hispanic populations Am J Clin Nutr 1991;53(Suppl):1522S-1528S.[Medline] 35. Kenchaiah S, Evans JC, Levy D, et al. Obesity and risk of heart failure N Engl J Med 2002;347:305-313.[CrossRef][Web of Science][Medline] 36. Grassi G, Seravalle G, Quarti-Trevano F, et al. Excessive sympathetic activation in heart failure with obesity and metabolic syndrome. Characteristics and mechanisms. Hypertension 2007;49;:535-541.[Abstract/Free Full Text] 37. Vasan RS, Sullivan LM, Roubenoff R, et al. , on behalf of the Framingham Heart Study Investigators. Inflammatory markers and risk of heart failure in elderly subjects without prior myocardial infarction: the Framingham Heart Study. Circulation 2003;107:1486-1491.[Abstract/Free Full Text] 38. Alpert MA, Lambert CR, Panayiotou H, et al. Relation of duration of morbid obesity to left ventricular mass, systolic function, and diastolic filling, and effect of weight loss Am J Cardiol 1995;76:1194-1197.[CrossRef][Web of Science][Medline] 39. Poirier P, Giles TD, Bray GA, et al. , on behalf of American Heart Association and Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association scientific statement on obesity and heart disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Circulation 2006;113:898-918.[Abstract/Free Full Text] 40. Curtis JP, Selter JG, Wang Y, et al. The obesity paradox: body mass index and outcomes in patients with heart failure Arch Intern Med 2005;165:55-61.[Abstract/Free Full Text] 41. Horwich TB, Fonarow GC, Hamilton MA, MacLellan WR, Woo MA, Tillisch JH. The relationship between obesity and mortality in patients with heart failure J Am Coll Cardiol 2001;38:789-795.[Abstract/Free Full Text] 42. Davos CH, Doehner W, Rauchhaus M, et al. Body mass and survival in patients with chronic heart failure without cachexia: the importance of obesity J Card Fail 2003;9:29-35.[CrossRef][Web of Science][Medline] 43. Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition prognosis in chronic systolic heart failure: the obesity paradox Am J Cardiol 2003;91:891-894.[CrossRef][Web of Science][Medline] 44. Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA. Body mass index and mortality in heart failure: a meta-analysis Am Heart J 2008;156:13-22.[CrossRef][Web of Science][Medline] 45. Kalantar-Zadeh K, Block G, Horwich T, Fonarow GC. Reverse epidemiology of conventional cardiovascular risk factors in patients with chronic heart failure J Am Coll Cardiol 2004;43:1439-1444.[Abstract/Free Full Text] 46. Haffner SM, Morales PA, Hazuda HP, Stern MP. Level of control of hypertension in Mexican Americans and non-Hispanic whites Hypertension 1993;21:83-88.[Abstract/Free Full Text] 47. Burt VL, Whelton P, Roccella EJ, et al. Prevalence of hypertension in the U.S. adult population: results from the Third National Health and Nutrition Examination Survey, 1988–1991 Hypertension 1995;25:305-313.[Abstract/Free Full Text] 48. Kannel WB. Blood pressure as a cardiovascular risk factor: prevention and treatment JAMA 1996;275:1571-1576.[Abstract/Free Full Text] 49. Kamalesh M. Heart failure in diabetes and related conditions J Card Fail 2007;13:861-873.[CrossRef][Web of Science][Medline] 50. Haffner SM, Stern MP, Hazuda HP, Rosenthal M, Knapp JA. The role of behavioral variables and fat patterning in explaining ethnic differences in serum lipids and lipoproteins Am J Epidemiol 1986;123:830-839.[Abstract/Free Full Text] 51. Haffner SM, Mykkänen L, Valdez RA, Paidi M, Stern MP, Howard BV. LDL size and subclass pattern in a biethnic population Arterioscler Thromb Vasc Biol 1993;13:1623-1630.[Abstract/Free Full Text] 52. Grundy SM. Small LDL, atherogenic dyslipidemia, and the metabolic syndrome Circulation 1997;95:1-4.[Free Full Text] 53. Kannel WB, Belanger AJ. Epidemiology of heart failure Am Heart J 1991;121:951-957.[CrossRef][Web of Science][Medline] 54. Horwich TB, Hamilton MA, MacLellan WR, Fonarow GC. Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure J Card Fail 2002;8:216-224.[CrossRef][Web of Science][Medline] 55. Rauchhaus M, Clark AL, Doehner W, et al. The relationship between cholesterol and survival in patients with chronic heart failure J Am Coll Cardiol 2003;42:1933-1940.[Abstract/Free Full Text] 56. Christ M, Klima T, Grimm W, Mueller HH, Maisch B. Prognostic significance of serum cholesterol levels in patients with dilated cardiomyopathy Eur Heart J 2006;27:691-699.[Abstract/Free Full Text] 57. Rauchhaus M, Coats AJS, Anker SD. The endotoxin-lipoprotein hypothesis Lancet 2000;356:930-933.[CrossRef][Web of Science][Medline] 58. Cleland JGF, Loh H, Windram J, Goode K, Clark AL. Threats, opportunities, and statins in the modern management if heart failure Eur Heart J 2006;27:641-643.[Free Full Text] 59. Kjekshus J, Pedersen TR, Olsson AG, Faergeman O, Pyorala K. The effects of simvastatin on the incidence of heart failure in patients with coronary artery disease J Card Fail 1997;3:249-254.[CrossRef][Medline] 60. Kjekshus J, Apetrei E, Barrios V, et al. , for the CORONA Group. Rosuvastatin in older patients with systolic heart failure. N Engl J Med 2007;357:2248-2261.[CrossRef][Medline] 61. GISSI-HF Investigators Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial Lancet 2008;372:1231-1239.[CrossRef][Web of Science][Medline] 62. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among U.S. adults JAMA 2002;287:356-359.[Abstract/Free Full Text] 63. Langefeld CD, Wagenknecht LE, Rotter JI, et al. , on behalf of Insulin Resistance Atherosclerosis Study Family Study Investigators. Linkage of the metabolic syndrome to 1q23–q31 in Hispanic families: the Insulin Resistance Atherosclerosis Study Family Study. Diabetes 2004;53:1170-1174.[Abstract/Free Full Text] 64. Chandalia M, Grundy SM, Adams-Huet B, Abate N. Ethnic differences in the frequency of ENPP1/PC1 121Q genetic variant in the Dallas Heart Study cohort J Diabetes Complicat 2007;21:143-148.[CrossRef][Web of Science][Medline] 65. Witteles RM, Fowler MB. Insulin-resistant cardiomyopathy: clinical evidence, mechanisms, and treatment options J Am Coll Cardiol 2008;51:93-102.[Abstract/Free Full Text] 66. Sundstrom J, Arnlov J, Stolare K, Lind L. Blood pressure-independent relations of left ventricular geometry to the metabolic syndrome and insulin resistance: a population-based study Heart 2008;94:874-878.[Abstract/Free Full Text] 67. Ingelsson E, Arnlov J, Lind L, Sundstrom J. Metabolic syndrome and risk for heart failure in middle aged men Heart 2006;92:1409-1413.[Abstract/Free Full Text] 68. Budoff MJ, Yang TP, Shavelle RM, Lamont DH, Brundage BH. Ethnic differences in coronary atherosclerosis J Am Coll Cardiol 2002;39:408-412.[Abstract/Free Full Text] 69. D'Agostino Jr. RB, Burke G, O'Leary D, et al. Ethnic differences in carotid wall thickness: the Insulin Resistance Atherosclerosis Study Stroke 1996;27:1744-1749.[Abstract/Free Full Text] 70. Becker TM, Wiggins C, Key CR, Samet JM. Ischemic heart disease mortality in Hispanics, American Indians, and non-Hispanic whites in New Mexico, 1958–1982 Circulation 1988;78:302-309.[Abstract/Free Full Text] 71. Mitchell BD, Stern MP, Haffner SM, Hazuda HP, Patterson JK. Risk factors for cardiovascular mortality in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study Am J Epidemiol 1990;131:423-433.[Abstract/Free Full Text] 72. Liao Y, Cooper RS, Cao G, Kaufman JS, Long AE, McGee DL. Mortality from coronary heart disease and cardiovascular disease among adult U.S. Hispanics: findings from the National Health Interview Survey (1986 to 1994) J Am Coll Cardiol 1997;30:1200-1205.[Abstract] 73. Swenson CJ, Trepka MJ, Rewers MJ, Scarbro S, Hiatt WR, Hamman RF. Cardiovascular disease mortality in Hispanics and non-Hispanic Whites Am J Epidemiol 2002;156:919-928.[Abstract/Free Full Text] 74. Pandey DK, Labarthe DR, Goff DC, Chan W, Nichaman MZ. Community-wide coronary heart disease mortality in Mexican Americans equals or exceeds that in non-Hispanic whites: the Corpus Christi Heart Project Am J Med 2001;110:81-87.[Web of Science][Medline] 75. Hunt KJ, Resendez RG, Williams K, Haffner SM, Stern MP, Hazuda HP. All-cause and cardiovascular mortality among Mexican-American and non-Hispanic white older participants in the San Antonio Heart Study—evidence against the "Hispanic Paradox." Am J Epidemiol 2003;158:1048-1057.[Abstract/Free Full Text] 76. Shaw LJ, Shaw RE, Merz CN, et al. , for the American College of Cardiology-National Cardiovascular Data Registry Investigators. Impact of ethnicity and sex differences on angiographic coronary artery disease prevalence and in-hospital mortality in the American College of Cardiology-National Cardiovascular Data Registry. Circulation 2008;117:1787-1801.[Abstract/Free Full Text] 77. Becker TM, Wiggins CL, Key CR, Samet JM. Ethnic differences in mortality from acute rheumatic fever and chronic rheumatic heart disease in New Mexico, 1958–1982 West J Med 1989;150:46-50.[Web of Science][Medline] 78. DiGiorgi PL, Baumann FG, O'Leary AM, et al. Differences in mitral valve disease presentation and surgical treatment outcome between Hispanic and non-Hispanic patients Ethn Dis 2008;18:306-310.[Medline] 79. Hanford EJ, Zhan FB, Lu Y, Giordano A. Chagas disease in Texas: recognizing the significance and implications of evidence in the literature Soc Sci Med 2007;65:60-79.[CrossRef][Web of Science][Medline] 80. Leiby DA, Rentas FJ, Nelson KE, et al. Evidence of Trypanosoma cruzi infection (Chagas' disease) among patients undergoing cardiac surgery Circulation 2000;102:2978-2982.[Abstract/Free Full Text] 81. Schmunis GA. Epidemiology of Chagas disease in non-endemic countries: the role of international migration Mem Inst Oswaldo Cruz 2007;102Suppl:75–85. 82. Milei J, Mautner B, Storino R, Sanchez JA, Ferrans VJ. Does Chagas' disease exist as an undiagnosed form of cardiomyopathy in the United States? Am Heart J 1992;123:1732-1735.[CrossRef][Web of Science][Medline] 83. Hagar JM, Rahimtoola SH. Chagas' heart disease in the United States N Engl J Med 1991;325:763-768.[Web of Science][Medline] 84. Correa-de-Araujo R, Stevens B, Moy E, Nilasena D, Chesley F, McDermott K. Gender differences across racial and ethnic groups in the quality of care for acute myocardial infarction and heart failure associated with comorbidities Womens Health Issues 2006;16:44-55.[CrossRef][Web of Science][Medline] 85. Albert NM, Fonarow GC, Abraham WT, et al. Predictors of delivery of hospital-based heart failure patient education: a report from OPTIMIZE-HF J Card Fail 2007;13:189-198.[CrossRef][Medline] 86. Yancy CW, Fonarow GC, LaBresh KA, et al. Disparate quality of care for black and Hispanic heart failure patients: a report from Get With the Guidelines–Heart Failure (GWTG-HF)(abstr) J Card Fail 2007;13(Suppl 2):S157. 87. Brown DW, Haldeman GA, Croft JB, Giles WH, Mensah GA. Racial or ethnic differences in hospitalization for heart failure among elderly adults: Medicare, 1990–2000 Am Heart J 2005;150:448-454.[CrossRef][Web of Science][Medline] 88. Riegel B, Moser DK, Rayens MK, et al. , on behalf of the Heart Failure Trialists Collaborators. Ethnic differences in quality of life in persons with heart failure. J Card Fail 2008;14:41-47.[CrossRef][Web of Science][Medline] 89. Department of Health and Human Services Healthy People 20102nd edition. Washington, DC: U.S. Government Printing Office; 2000. 90. Davis AM, Vinci LM, Okwuosa TM, Chase AR, Huang ES. Cardiovascular health disparities: a systematic review of health care interventions Med Care Res Rev 2007;64Suppl:29S–100S. 91. Trevino FM, Moyer ME, Valdez RB, Stroup-Benham CA. Health insurance coverage and utilization of health services by Mexican Americans, mainland Puerto Ricans, and Cuban Americans JAMA 1991;265:233-237.[Abstract/Free Full Text] 92. Solis JM, Marks G, Garcia M, Shelton D. Acculturation, access to care, and use of preventive services by Hispanics: findings from HHANES 1982–84 Am J Public Health 1990;80Suppl:11–9. 93. Bolen JC, Rhodes L, Powell-Griner EE, Bland SD, Holtzman D. State-specific prevalence of selected health behaviors, by race and ethnicity—Behavioral Risk Factor Surveillance System, 1997 MMWR CDC Surveill Summ 2000;49:1-60.[Medline] 94. Jurkowski JM, Johnson TP. Acculturation and cardiovascular disease screening practices among Mexican Americans living in Chicago Ethn Dis 2005;15:411-417.[Web of Science][Medline] 95. Institute of Medicine The health, health insurance and language status of racial and ethnic minority populationsIn: Smedley BD, Stith AY, Nelson AR, editors. Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care. Washington, DC: National Academes Press; 2003. pp. 88-89. 96. DuBard CA, Garrett J, Gizlice Z. Effect of language on heart attack and stroke awareness among U.S. Hispanics Am J Prev Med 2006;30:189-196.[CrossRef][Web of Science][Medline] 97. Seijo R, Gomez H, Freidenberg J. Language as a communication barrier in medical care for Hispanic patients Hisp J Behav Sci 1991;13:363-366.[Abstract] 98. Balsa AI, McGuire TG. Prejudice, clinical uncertainty and stereotyping as sources of health disparities J Health Econ 2003;22:89-116.[CrossRef][Web of Science][Medline] 99. Larkey LK, Hecht ML, Miller K, Alatorre C. Hispanic cultural norms for health-seeking behaviors in the face of symptoms Health Educ Behav 2001;28:65-80.[Abstract/Free Full Text] 100. Ontiveros JA, Black SA, Jakobi PL, Goodwin JS. Ethnic variation in attitudes toward hypertension in adults ages 75 and older Prev Med 1999;29:443-449.[CrossRef][Web of Science][Medline] 101. Evelyn B, Toigo T, Banks D, et al. Participation of racial/ethnic groups in clinical trials and race-related labeling: a review of new molecular entities approved 1995–1999 J Natl Med Assoc 2001;93Suppl:18S–24S. 102. Oddone EZ, Olsen MK, Lindquist JH, et al. Enrollment in clinical trials according to patients race: experience from the VA Cooperative Studies Program (1975–2000) Control Clin Trials 2004;25:378-387.[CrossRef][Web of Science][Medline] 103. Wendler D, Kington R, Madans J, et al. Are racial and ethnic minorities less willing to participate in health research? PLoS Med 2006;3:e19.[CrossRef][Medline] 104. Sabri AA, Qayyum MA. Increasing the participation: another factor PLoS Med 2006;3:e250.[CrossRef][Medline] 105. Davidson JA, Kannel WB, Lopez-Candales A, et al. Avoiding the looming Latino/Hispanic cardiovascular health crisis: a call to action J Cardiometab Syndr 2007;2:238-243.[CrossRef][Medline] 106. Jensen MD. What is the potential role of cannabinoid-1 receptor blockade in glucose and lipid management? Am J Med 2007;120Suppl 1:S25–32.
Related Article
-
Inside This Issue
J. Am. Coll. Cardiol. 2009 53: A25.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
L. W. Miller
Left Ventricular Assist Devices Are Underutilized
Circulation,
April 12, 2011;
123(14):
1552 - 1558.
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. W. Yancy, T. Y. Wang, H. O. Ventura, I. L. Pina, K. Vijayaraghavan, K. C. Ferdinand, L. L. Hall, and credo Advisory Group
The Coalition to Reduce Racial and Ethnic Disparities in Cardiovascular Disease Outcomes (credo): Why credo Matters to Cardiologists
J. Am. Coll. Cardiol.,
January 18, 2011;
57(3):
245 - 252.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Epidemiology