LETTER TO THE EDITOR
Apolipoprotein E genotype and coronary heart disease: Reply
Kwame O. Akosah, MD, FACCa
a Gundersen Lutheran Heart Center, 1836 South Avenue, La Cross, Wisconsin 54601, USA
We appreciate the comments of Batalla et al. concerning our paper on premature coronary artery disease (CAD). The authors share with us their data on young adults admitted with acute coronary syndrome. They also provide follow-up information in the subgroup with normal cholesterol compared to those with abnormal cholesterol levels as defined by the ratio of total cholesterol to high density lipoprotein levels. There are some similarities between their data and ours; however, major differences exist. Similar features include the fact that both studies evaluated young adults age 50 years or younger. Second, both populations were high risk, with high rates of categorical risk factors. For instance, the rate of smoking was 73% in their study compared to 75% in our group. The rate of hypertension was 36% and diabetes mellitus was 9% in Batalla et al., which is similar to the 39% and 12% in our study for those two conditions, respectively.
Hypercholesterolemia was 77% in their report. The rate of hypercholesterolemia was 46% in our report, but the two studies used different definitions. A comparison between the two studies is limited by major differences in methodology and incomplete data provided by the authors. First, their report involves exclusively male subjects, whereas as many as 30% of our population were young women. Second, their analysis was done by comparing two groups based on cholesterol levels. We, in contrast, compared two groups based on irrefutable evidence of significant CAD. Furthermore, they do not specify the time period over which the data was collected. For this reason we do not know the frequency of admissions for premature CAD. Next, what percent does this represent for admissions of acute coronary syndrome?
We commend the authors for providing follow-up information on outcomes. In their report, after 32 months’ follow-up there were no differences in outcome between those with abnormal compared to normal cholesterol. They conclude that the absence of differences in outcomes represents a lack of benefit of low cholesterol in young adults with high rates of smoking. This interpretation is similar to an earlier report by Jee et al. (1) in subjects without previous CAD. The suggestion that low cholesterol does not confer a benefit for secondary prevention in young adults has important clinical implications. There are, however, other possible explanations. This was an observational study that did not consider the effect of treatment. It is possible that the lack of outcome differences may be attributable to some treatment benefit in the group with high cholesterol who were treated according to current guidelines. This actually proves the merit of guidelines for secondary prevention.
Finally, a secondary explanation concerns the small sample size. With a small sample size in each group it is possible that one would need a much longer duration of follow-up to appreciate differences. We do agree that, in young adults with multiple cardiovascular risk factors, the best strategy to reduce recurrent events in the short term should be based on managing all modifiable risk factors, including smoking and cholesterol abnormalities.
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References
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1. Jee SH, Suh IL, Soon IL, Appel LJ. Smoking and atherosclerotic cardiovascular disease in men with low levels of serum cholesterol. JAMA. 1999;282:2149–2155[Abstract/Free Full Text]
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