This is the first population-based study to report ethnicity-related differences in the incidence of CHF among 4 major racial/ethnic groups in the United States. The incidence of CHF in our study was 3.1 per 1000 person-years, which is consistent with the estimated annual incidence of 1 to 5 in 1000 in the general population.3,4,10
Our results indicate that the incidence of CHF is greatest among African Americans, intermediate among whites and Hispanics, and lowest among Chinese Americans. We also demonstrate that these differences are in large part determined by higher prevalences of hypertension and diabetes mellitus among African Americans. Moreover, lower socioeconomic status and higher dietary caloric intake were also important factors in explaining racial/ethnic differences in the incidence of CHF. These findings suggest that the important determinants of this condition in the US are mainly environmental in nature. Finally, our study indicates that more than half of the cases of incident CHF among Americans without a history of cardiovascular diseases are not preceded by MI, and adjustment for interim infarction accentuates ethnic differences in the incidence of CHF between African Americans and whites.
As our knowledge of racial/ethnic disparities in cardiovascular diseases augments, there is growing interest in the causes of such disparities and whether they can be diminished by appropriate reduction of contributing factors. Racial/ethnic disparities in the incidence of other medical problems have been attributed to genetic and biological differences,28,29
the effects of various social and environmental factors across the lifespan,30,31
In the case of incident CHF, our results indicate that race- and ethnicity-related differences in the prevalences of hypertension and diabetes mellitus represent the main determinants of the greater incidence of CHF among African Americans. These differences are likely related to socioeconomic and behavioral characteristics, including disparities in access to and quality of health care, as documented by previous CHF morbidity and mortality studies12
as well as our own analyses. However, possible racial/ethnic differences in susceptibility to CHF owing to underlying genetic and biological factors cannot be completely excluded.33,34
There are a number of potential mechanisms to explain how racial differences in established risk factors such as hypertension and diabetes mellitus may determine differences in incident CHF. While biological differences in the incidence of hypertension and diabetes mellitus themselves may play a role, less optimal treatment and control of these risk factors (due to less access to health care) or poor compliance with medical treatment targeting these risk factors35,36
likely represent the main contributors. Although our study does not provide a direct and definitive answer to these questions, combining our findings with those of previous studies might be helpful in identifying the most likely determinants of CHF. In our study, lower household income and higher daily caloric intake were significant predictors, even when predisposing conditions such as diabetes mellitus, hypertension, and obesity were taken into account. The lack of health insurance was not a significant contributor to the ethnic disparities of incident CHF, and differences in medication use were attributable to differences in the prevalences of diabetes mellitus and hypertension. Although our study does not support a direct role of access and quality of health care in disparities in incident CHF, it is important to mention that previous studies on the prevalence and consequences of CHF have raised the issue of ethnic disparities in quality of care received for CHF.37-39
Of note, this notion has also been challenged more recently.40-42
Our study also demonstrates racial/ethnic differences in the relationships of incident CHF with more proximal predictors of CHF, ie, interim MI, subclinical CAD, and LV hypertrophy. African American participants had the highest incidence of CHF without prior MI, followed by Hispanic, white, and Chinese American participants. Moreover, adjustment for interim MI and subclinical CAD resulted in greater differences between African Americans and whites in incident CHF risk. These differences may also be at least partially owing to discrepancies in the prevalence and control of hypertension and diabetes mellitus among racial/ethnic groups. In our study, there were significant differences between African Americans and whites not only in the prevalence of hypertension and diabetes mellitus but also in the prevalence and magnitude of LV hypertrophy measured at baseline by both ECG and the gold standard method of MRI (). In addition, whereas baseline LVEF was significantly greater only among Chinese Americans, racial/ethnic differences in baseline myocardial contractile function measured by MRI tagging have been recently reported among MESA participants.43
Previous studies have also demonstrated that risk factors such as hypertension,44
cigarette smoking, diabetes mellitus,45
and subclinical atherosclerosis,46
are associated with myocardial dysfunction at study entry, defining what is known from basic studies34
as the typical protoplasm for CHF development.49
In this study, we demonstrate that the relationship between baseline LV mass and incident CHF varies by ethnicity. Moreover, although the incidence of MI was not statistically different among the 4 racial/ethnic groups, after developing an MI, African Americans were more likely to progress to CHF than whites. This observation supports previous research indicating that racial/ethnic differences play an important role in the progression from asymptomatic LV dysfunction to CHF. In the Studies of Left Ventricular Dysfunction (SOLVD), African Americans with mild to moderate LV systolic dysfunction were at higher risk for progression to CHF than whites.14
Our findings are also consistent with the results of the Vasodilator-Heart Failure Trials (V-HeFT) I and II.50
Indeed, previous studies have gone as far as suggesting different treatment strategies for CHF among different ethnic groups.51
In this regard, the accelerated disease progression to CHF from a proximal precursor such as MI among African Americans likely reflects differences in postinfarct remodeling induced by hypertension, diabetes mellitus, and other coexisting subclinical processes that are more prevalent among those who are poorer and have less access to quality medical care. Taken in combination, our findings suggest that incident CHF could be substantially reduced by aggressive control of hypertension and diabetes mellitus particularly among the poor, over and above efforts to reduce the incidence of MI and halt progression to CHF after infarction. Such efforts directed at primary prevention of incident CHF outside the clinical MI pathway should be particularly important to populations of different racial/ethnic backgrounds in the face of declining rates of coronary occlusion events. The efficacy of enhanced control of diabetes mellitus and hypertension in reducing racial/ethnic disparities in incident CHF requires further investigation.
This prospective large population-based study was performed in an ethnically diverse, asymptomatic population. The longitudinal design allowed us to measure the incidence of CHF rather than CHF prevalence, morbidity, or mortality. Nonetheless, there are limitations to this study that deserve discussion. Except for incident CHF and incident MI, all other variables were measured at baseline. Therefore, the study has limitations in making inferences regarding causal or temporal associations among baseline risk factors (eg, between household income and hypertension). Moreover, the median follow-up time was 4 years, and considering the low incidence of CHF, the results regarding relationships between incident MI and incident CHF should be interpreted cautiously. Conversely, the fact that differences between African American and white participants were significant during this relatively short follow-up period might also reflect the importance of these associations. Finally, while the diagnosis of CHF may be more challenging when compared with other cardiovascular events, we required that participants be symptomatic and have a physician-diagnosed CHF. This definition likely limited the inclusion of false-positive cases.