Pediatric Risk Factors Predict CAD in Adults
ABSTRACT & COMMENTARY
Synopsis: Offspring of CAD parents were consistently overweight beginning in childhood. Over time, the risk factors of cholesterol, glucose, and insulin increased at a rate higher than those offspring whose parents did not have CAD.
Source: Bao W, et al. JAMA 1997;278:1749-1754.
There is not a significant amount of information on the development and progression of risk factors from childhood to adulthood in offspring of parents with coronary artery disease (CAD). This prompted Bao and colleagues to look at 271 patients with clinically verified parental history of CAD and compared those to 1253 who did not have parents with CAD. The mean age of CAD event was 50 years old for fathers and 52 years old for mothers. They looked at body mass index, skin folds, blood pressure, cholesterol and cholesterol subfractions, and glucose and insulin levels.
By comparing the two groups, they were able to discern that, beginning in youth, the offspring of parents with CAD were consistently overweight. This prevalence was 35% in subjects with parental history of CAD compared with 26% in subjects without parental history of CAD.
By performing a step-wise logistic progression analysis, they discovered that elevations in cholesterol and subfractions such as LDL-C and plasma glucose and insulin would reach P-value of significance at older ages. This was due to a high rate of increase in these factors over time.
They found two other interesting facts: 1) that parental CAD history was related to LDL-C in the adult whites (especially males) and 2) this was only correlated with insulin levels in the young adult black offspring.
COMMENT BY LEN SCARPINATO, DO
There have been great strides in the world of coronary artery disease over the last 20 or 30 years, but what about the need to prevent CAD? What better way to do it than to identify at-risk individuals early in life? Surprisingly, this has not been the focus of significant amounts of research.
We know from Korean War veterans with traumatic injuries that fatty streaks occur in the aorta as early as 18 years of age. This lifelong disease reaches clinical significance depending on other risk factors and genetics, yet there wasn’t much research.
Wouldn’t it be wonderful if we could recognize when and where and what individuals would be at risk for coronary artery disease? We could counsel, institute significant risk factor modification programs, and put all of our efforts into those at-risk individuals, as opposed to the entire population. It would save time and be more cost-effective.
Bao et al’s study has pointed us in the right direction. By finding that there is a higher prevalence of childhood obesity in offspring in early CAD patients, they were able to point out one significant risk factor. With the horrible results of weight loss programs in adults, it is not surprising that these are worrisome data. Can we modify the risk factor profile by reducing the weight in these patients and in the children of these patients as they get older? We don’t know. Also, finding out that risk factor profiles worsened at a quicker rate points us in another direction. We could certainly identify the at-risk individuals and, as their other risk factors become abnormal or even before they become abnormal, we can institute therapies that would reduce their risk factors overall.
In an editorial in the same issue of JAMA, Van Horn and Greenland called for improved communication between adult and pediatric medical providers.1 We need to be aware of these findings and aggressive in exploring risk factor modification in the offspring of adults with CAD.
Reference
1. Van Horn L, Greenland P. JAMA 1997;278:1779-1780.
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