The article by Snow and colleagues, in this issue of JCR, analyzes the effects of cardiac rehabilitation and lipid medications on lipid levels in persons with known coronary heart disease (CHD).1 Lipid lowering to reduce risk of recurrent CHD is an important issue and clinical trials have convincingly shown that lipid therapy is effective in this setting.2,3 On the other hand, comprehensive cardiac rehabilitation (CR) has been shown to lower risk of cardiac mortality but not to reduce total mortality or nonfatal myocardial infarction.4

Lipid therapy in CHD survivors has become more and more common in recent years. For example, survey data that included a large physician group showed that persons with known CHD were not reaching their lipid goals in 2001, and Pearson et al5 estimated that approximately 18% of persons with CHD were at their low-density lipoprotein cholesterol (LDL-C) goals. However, LaBresh et al6 recently reported that a larger fraction of persons with CHD have been getting LDL-C measurements, and approximately 81% of persons with CHD had determinations during the follow-up phase of the 12-month study. In addition, the authors reported that referral to CR increased from 34% of participants at the beginning to 73% of the conclusion of the survey. If we focus on results for persons who did not change lipid medications during CR,1 it appears that the fraction of persons at LDL-C goal increased from 68.5% to 74.9% and the mean LDL-C declined from 90.6 to 86.4 mg/dL. These changes are not large but do represent effective additive lipid effects that can be reasonably attributed directly to CR following a CHD event.

Patients participating in an active exercise program may be more motivated to undertake therapeutic lifestyle changes and more adherent to take medications that have been prescribed. With this as background, it is admirable that Snow and colleagues have assiduously investigated the relative contributions of CR and lipid-lowering therapy on the achievement of lipid goals in the setting of a CR program.

Sorting out the relative effects of CR and lipid therapy can be difficult. Such programs typically advise changes in diet, exercise, smoking reduction, reduced alcohol intake, weight lowering, modification of cardiovascular prescriptions, and other changes.7,8 The authors of the current study appropriately utilized several tactics to focus on the lipid changes in the setting of CR. For example, all persons had been on lipid-lowering therapy for at least 4 weeks prior to enrolling in the CR program, and participants were stratified according to change in lipid medication during the course of CR.

In the current era, the degree of lipid improvement with medications depends upon the products and dosage. For example, statins typically lower LDL-C 30% or more and raise HDL-C levels 5% to 10%. Once the medication dose is stable, the LDL-C levels usually remain reduced.9 Lipid levels are also affected by lifestyle measures. Adoption of a 30% fat diet recommended as part of the ATP II guidelines has been shown to typically lead to a 10% reduction in LDL-C.

A meta-analysis of lipid effects related to exercise was undertaken by Tran and showed a 6.3% lowering in total cholesterol, 10.1% reduction in LDL-C, 13.4% lowering in the total cholesterol/high-density lipoprotein cholesterol (HDL-C) ratio, and 5% increase in HDL cholesterol.10 In that review article, the authors further investigated the effects of diet and exercise on lipoprotein cholesterol levels and concluded that an increase in HDL-C, typically about 5%, was the most common finding and that the LDL-C changes were much more variable, largely because dietary contents of cholesterol, fat, and carbohydrate have differential effects on LDL-C levels. A study by Kraus et al11 has further shown that the intensity of physical activity may affect both the amount of LDL-C change and the composition of the LDL particles, with more vigorous activity promoting a switch toward larger, more buoyant LDL particles.

It is encouraging that approximately 75% of the participants in the article by Snow, et al were at the currently recommended LDL-C goals at the start of the study. These are extremely high control levels and reflect the efforts of aggressive management early in the course of CR shortly following a CHD event. Such high control levels might not necessarily be found at a later time. It has been reported that lipid-lowering therapy may be continued in less than half of the candidates at an interval more than 6 months post myocardial infarction, and that the lower control rates may be attributable to several sources, including physician care, cost of prescriptions, and patient adherence. In that regard, future investigations by CR investigators over a longer term would be useful to identify whether the high proportion of lipid control described in the Snow paper can be successfully sustained beyond the interval of intensive cardiac rehabilitation.

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