Compared with 1999–2000, the estimated 10-year UKPDS risk for developing CHD among people with diagnosed diabetes was 22% lower by 2007–2008. The estimated risk for CHD decreased significantly among men, women, whites, African Americans, and Mexican Americans. Improvements in concentrations of HbA1c, systolic blood pressure, and the ratio of TC/HDLC mostly accounted for the decreased risk.
The mortality rate of CHD in the U.S. population has decreased tremendously since the 1960s (9
). Medical treatments of CHD and favorable trends in key risk factors for CHD have contributed roughly equally to this decline (10
). Whether the incidence of CHD also demonstrated favorable secular trends has been less clear. Although trends in the incidence of CHD among people with diabetes remain unknown, people with diabetes have experienced decreases in the mortality rate from cardiovascular disease (11
). One study (12
) showed that the mortality rate from cardiovascular disease decreased substantially among men but decreased little among women with diabetes. In the FHS, however, men and women experienced similar reductions in mortality from cardiovascular disease (13
). The results of the current study showed that risk declined significantly to a similar extent among both men and women. Because the UKPDS risk engine used fatal and nonfatal myocardial infarction or sudden death as its end point, it is possible that changes in mortality between men and women could differ even if changes in incidence were similar because of differences in the case-fatality rate. Therefore, surveillance for the incidence of cardiovascular disease and the case-fatality rate among people with diabetes is of critical importance to understanding the dynamics of this diabetes complication.
The difference in estimated UKPDS risk between men and women is partially a function of the UKPDS risk equation because the sex coefficient assigns a lower risk to women. The difference in the estimated risk for CHD among the three major racial or ethnic groups can be attributed to differences in the coefficient for race or ethnicity in the UKPDS risk engine as well as to the more favorable lipid profile in African Americans than the other groups because the UKPDS risk engine assigns a great deal of weight to the coefficient for the ratio of TC/HDLC. The coefficient for the race or ethnicity variable in the ARIC study risk equations also indicates a lower risk for African Americans. Thus, both the UKPDS and ARIC study risk equations predict that the risk for developing CHD is lower among African Americans than whites when values for the risk factors are the same.
The UKPDS and FHS risk estimates suggested that favorable developments in the risk for developing CHD extended to all three major racial or ethnic groups. The estimated UKPDS risk during 2007–2008 was 43% lower among African Americans, 22% lower among Mexican Americans, and 20% lower among whites compared with 1999–2000. However, the ARIC study risk estimates did not show a significant decrease in the risk for CHD among African Americans, and the FHS risk estimates for Mexican Americans showed a reduction in risk over time that was of borderline significance. Because analyses stratified by race or ethnicity failed to demonstrate significant reductions in several risk factors, reducing smoking, HbA1c, and blood pressure among whites; smoking among African Americans; and blood pressure and TC among Mexican Americans is critical to further reducing the future risk for CHD in these groups.
Population studies in the U.S. have shown increased treatment for and control of hypercholesterolemia and hypertension (3
). Increased uptake of medications to lower blood glucose, systolic blood pressure, and TC by people with diabetes likely contributed to the improvements in these risk factors (4
). Less clear is the role of lifestyle behaviors, such as physical activity and diet (saturated fat, polyunsaturated fat, trans
fats, dietary cholesterol, salt, and fruits and vegetables), in affecting the observed trends. Although an anthropometric measure is not part of any of the three risk engines used in the current study, excess weight promotes increased blood pressure and dyslipidemias. Thus, weight management is critical to optimizing levels of blood pressure and lipids that are important components of the UKPDS risk engine and to estimating cardiovascular risk.
The present analysis suggests that reducing TC to <200 mg/dL and raising HDLC to at least 40 mg/dL in men and 50 mg/dL in women would result in the largest reduction in risk. In part, the size of the potential risk reduction was governed by the high prevalence of dyslipidemias of 69.5%. Optimizing medical management and promoting behavioral change, such as increasing physical activity (keeping in mind medical limitations), improving dietary quality, and weight management, can contribute to lowering concentrations of HbA1c, blood pressure, and concentrations of lipids. Smoking is an important risk factor for CHD. Therefore, the absence of a meaningful decrease in the prevalence of smoking in diabetic adults during the 10-year study period suggests that this behavior contributed little to the observed trends in the estimated risk for CHD. Had all diabetic participants who were current smokers not smoked, the estimated risk would have been ~4% lower in 1999–2000 and in 2007–2008.
Clinical trials, especially the more recent ones, have generated considerable controversy concerning the effect of glycemic control, particularly rigorous glycemic control, on all-cause mortality (15
). Therefore, the hypothetical reductions in risk for CHD attributable to glycemic control discussed above should be viewed with considerable caution. Meta-analyses of clinical trials in people with diabetes demonstrated that treating patients with hypertension or elevated concentrations of LDL cholesterol improves cardiovascular outcomes (16
), and, therefore, the control of these two risk factors is clearly vital in reducing the risk for CHD in people with diabetes. Furthermore, comprehensive management of major cardiovascular risk factors in people with diabetes greatly reduces cardiovascular disease (18
The number of risk prediction algorithms to calculate the risk for CHD or cardiovascular disease has increased substantially since the emergence of risk prediction for CHD. Because the FHS and other risk prediction algorithms may not adequately assess the risk for CHD among people with diabetes (19
), two additional risk prediction algorithms, the UKPDS and ARIC study risk prediction algorithms that were developed using samples of diabetic participants, were used in the current study. The UKPDS risk prediction algorithm, however, was developed using data from a cohort of participants with diabetes who did not have a recent history of myocardial infarction, angina, or heart failure. Thus, this risk prediction algorithm may underestimate the risk for developing CHD in studies, such as the present one that include participants with such histories of myocardial infarction, angina, or heart failure. The predictive ability of several risk prediction algorithms among people with diabetes has been compared with observed outcomes in a number of prospective studies (19
). The FHS risk prediction algorithm underestimated the observed risk for CHD in some studies (19
) and overestimated the risk in others (22
). The UKPDS risk prediction algorithm also overestimated the risk in some studies (21
). A comparison of risk functions in New Zealand showed that the 5-year UKPDS risk estimates were lower than the FHS risk estimates (25
). Thus, considerable uncertainty exists about how best to estimate the risk for cardiovascular disease in people with diabetes.
Several limitations deserve mention. First, diagnosed diabetes was based on self-reported information and is thus subject to some degree of erroneous reporting and misclassification. However, self-reported diabetes generally has good sensitivity and specificity. Second, the number of participants with diagnosed diabetes was too small to calculate reasonably stable estimates of risk for CHD by several levels of stratification of the study variables. Third, estimates of 10-year risk were calculated for the three major racial or ethnic groups. The UKPDS and ARIC study participants included participants of African heritage, and, therefore, the use of these two sets of risk equations among African Americans in the current study appears reasonable, although limited experience exists concerning the use of these risk equations in African American populations. Furthermore, the validity of applying these equations to samples of participants of Hispanic heritage remains to be established. Furthermore, estimates for only three major racial or ethnic groups were calculated because data for other races or ethnicities were not available or had inadequate sample size. Thus, studies focused on other races or ethnicities will be helpful to examine the totality of the dynamics of CHD among people with diabetes. Finally, the laboratories and methods for measuring HbA1c and lipids changed during the 10-year period. Crossover studies were performed to examine the possible effects of these changes, and equations were developed to bridge any differences. The changes in the methodology for measuring concentrations of HDLC may have partially led to the increase in the means of HDLC from 1999 to 2006, particularly after all specimens were analyzed by using the direct method of measuring HDLC starting in 2003. Therefore, it is possible that this artifact may have been responsible for some small proportion of the favorable trend in the risk for CHD that was observed.
In conclusion, recent favorable trends in several major risk factors for CHD, namely HbA1c, systolic blood pressure, and the ratio of TC/HDLC, have resulted in an encouraging reduction in the estimated risk for CHD among adults with diagnosed diabetes in the U.S. The estimates from the current study also suggest that continuing declines in the mortality rate from CHD among people with diabetes can be anticipated going forward. Sustained efforts in targeting these three risk factors as well as an additional focus on reducing smoking in the diabetic population should further benefit the cardiovascular health of people with diabetes. Because the most recent data did not indicate that the decrease in the estimated risk for CHD from 1999–2000 to 2005–2006 continued into 2007–2008, future monitoring will be essential to determine whether this possible interruption in the trend is a temporary phenomenon that may represent sampling variation or represents a real change in the direction of the trend.