Differences in Cardiac Structure and Function Between Black and White Patients: Another Step in the Evaluation of Cardiovascular Risk in Chronic Kidney Disease

Black Americans have the highest incidence of heart failure (HF) among racial groups in the United States, HF affecting 3% of all African American adults. This reflects a 50% greater incidence of HF among African Americans than seen in the remaining population.1 These observations have fueled interest in exploring the differences in left ventricular (LV) mass (LVM) and geometry between Blacks and Whites, because it is well known that LV hypertrophy (LVH) and related abnormalities of LV diastolic function may precede and predict subsequent HF.2,3 Indeed, several lines of evidence,4–8 with some exceptions,9 support the notion of a strong association between Black ethnicity and increased LVM and relative wall thickness. There is indisputable evidence that LVH is not only harbinger of HF, but carries incremental prognostic value beyond that afforded by traditional cardiovascular factors,2,3 being also independently associated with an enhanced risk for myocardial infarction, cardiac sudden death, and stroke in the general population, as well as in patients with systemic hypertension, coronary heart disease, chronic kidney disease (CKD), and atrial fibrillation. In a large cohort of Blacks, LVH proved to be an even more powerful predictor of mortality than coronary artery disease and LV ejection fraction.3 Compared with Whites, Blacks have more clustering of cardiovascular risk factors, including hypertension, obesity, and insulin resistance, but less severe lipid abnormality and lower waist girth for comparable levels of body mass index,4–9 possibly because of the racial differences in body composition. These differences may potentially explain the greater prevalence of LVH observed in Blacks as compared to Whites. However, it is important to note that in most studies exploring the ethnic differences regarding LVM, the positive relationships between Black ethnicity and LVH held even taking into account the effect of these and other potential confounding factors and regardless of the method used to assess LVH, that is EKG, echocardiogram or cardiac magnetic resonance imaging (MRI). In the HyperGEN network study,7 Kizer et al. reported that LVM remained greater in 1,060 hypertensive Black individuals than in 580 White participants, even after adjusting for sex, body dimensions, blood pressure, diabetes, duration of hypertension, and antihypertensive treatment. Drazner et al., in the Dallas Heart Study, analyzed also socioeconomic factors as additional confounders for ethnicity-related LVM differences.4 This further analysis is justified because differences in socioeconomic status are able to track different distributions of risk factors and behavior in their management. However, also considerations of socioeconomic factors did not change the influence of ethnicity on prevalence of LVH, that in this study was detected by cardiac MRI.4 Similar results were obtained in more recent studies.8 The Coronary Artery Risk Development in Young Adults (CARDIA) study is a large multicenter community-based population study, sponsored by the National Institutes of Health/National Heart, Lung, and Blood Institute and designed to investigate the development and determinants of coronary disease risk factors in young adults.8 Participants with echocardiographic examination at the year-25 examination (n = 3320; 44% men, 46% African American) were recently assessed in order to investigate race–ethnic and sex-specific relationships of LV structure and function. African American men have the highest values of LVM among the 4 race/sex groups in the CARDIA study, after adjustment for demographics and cardiovascular risk factors at year-25.8 Importantly, although these studies support an independent association between Black ethnicity and higher LVM and concentric LVH, ethnicity by itself only explains a small proportion of the variance in LVH and environmental influences appear more relevant. It is interesting to note that in the CARDIA study, Blacks showed worse diastolic function compared with Whites, which remained significant after adjustment for antihypertensive medications and other potentially confounding factors.8 These results are in agreement with the findings of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), composed of hypertensive patients without evidence of HF, and where LV structure and function were measured in 509 patients using conventional and tissue Doppler echocardiography.9 In African-Caribbean patients, tissue Doppler early diastolic velocity E’ was significantly lower and the ratio of this and the transmitral early filling velocity E (E/E’) was significantly higher. After adjustment for age, gender, systolic blood pressure, pulse pressure, cholesterol, smoking, ejection fraction, LVM index, and diabetes mellitus, the effect of African-Caribbean ethnicity on diastolic function remained highly significant.9 This suggests that Blacks may have an increased susceptibility to diastolic dysfunction in response to similar blood pressure levels and even in absence of LVH. In the current issue Ahmad et al.10 conducted a cross-sectional analysis of the Chronic Renal Insufficiency Cohort Study (CRIC) to compare the prevalence of different types of left ventricular remodeling (concentric hypertrophy, eccentric hypertrophy, and concentric remodeling) by race/ethnicity. LVH is associated with shorter cardiovascular event-free survival, higher risk of incident HF, and higher risk of death in patients with CKD.11–14 The very high prevalence of LVH15–18 in CKD, in large part responsible for diastolic dysfunction, plays a fundamental role in the development of HF with preserved ejection fraction and contributes to considering CKD as a major risk factor for the development of HF.19,20 In the study of Ahmad et al., the prevalence of LVH (61.6% in non-Hispanic Blacks and 38.7% in non-Hispanic Whites) was very high especially in the Black population with a overwhelming preponderance of concentric geometry and, consequently, an higher prevalence of diastolic dysfunction (76.5% in non-Hispanic Blacks and 65.9% in non-Hispanic Whites) that must be considered a critical precursor of HF with preserved ejection fraction.5,13 The fundamental problem is that since structural (LVH) and functional (LV-dysfunction) alterations are evident, a therapeutic efficacy in order to modify the natural history and improve prognosis is limited. We think that in all patients with CKD, especially in the Black population, an echocardiographic examination with a complete study of diastolic function (better yet including Tissue Doppler Imaging) should be carried out in order to obtain a better prognostic definition and to begin an early treatment that could lead to prevent HF. The authors declared no conflict of interest.