(Circulation. 1999;99:3323D-3326.)
© 1999 American Heart Association, Inc.
Correspondence |
Beth Israel Deaconess Medical Center Harvard Medical School, Boston, Mass
Cardiology Division University of Connecticut Health Center, Farmington, Conn
To the Editor:
We read with interest the intriguing study by Frolkis et al1 regarding frequency of risk factor evaluation, lipid testing, and treatment of hypercholesterolemia in patients admitted to the coronary care unit of a large university hospital. We2 and others3 have recently reported similarly disappointing rates in outpatients that underscore the authors' sobering findings.1 The recognized limitations of their study notwithstanding, Frolkis et al have made an important contribution toward increasing awareness of the need for vigilance in coronary risk factor assessment and modification, and we applaud their efforts. We have, however, several comments that may be of value in clarifying the authors' findings.
In particular, we suggest a degree of caution regarding the authors' conclusions concerning appropriate evaluation and initiation of lipid-lowering therapy in the setting of an acute coronary event. The National Cholesterol Education ProgramAdult Treatment Panel II (NCEP-ATPII) guidelines offer recommendations for outpatient therapy that are longitudinal in nature and require serial evaluation of lipid profiles as patients move toward their goal. They emphasize repeated testing and a graded approach to therapy. As the authors recognize, the stress of an acute hospitalization may significantly decrease the serum cholesterol level for multiple reasons.4 5 Accordingly, we disagree with the authors' assertion that deferral of cholesterol testing during an acute hospitalization is necessarily a misguided approach. Longitudinal follow-up data would have been useful to accurately assess adequacy of compliance. In our series, nearly a third of patients whose cholesterol level was not initially controlled ultimately reached NCEP-ATPII targets.2
We are also curious to learn how the authors decided that male sex and age were so obvious as to warrant exclusion from their analysis, but premature menopausal status was not. Given the prevalence of coronary artery disease in men compared with women before the age of menopause and the inclusion of sex as a risk factor within the NCEP guidelines, might not the inclusion of male sex have increased the robustness of the authors findings?
References
Section of Preventative Cardiology, Cleveland Clinic Foundation, Cleveland, Ohio
Case Western Reserve School of Medicine
Department of Family Medicine Cleveland, Ohio
We appreciate the comments of Danias and Silverman concerning our article on physician noncompliance and welcome the opportunity to respond. They voice concern that application of the NCEP guidelines in an acute setting may violate the ambulatory and longitudinal intention of the recommendations. We submit that whether one uses the NCEP guidelines, the Framingham risk scores, or the framework suggested by the 27th Bethesda Conference, there is growing recognition of the value of risk stratification and the need to base treatment on the results of such an assessment. Since one of the main points of emphasis in NCEP-ATPII is the identification and aggressive treatment of those individuals with known coronary heart disease (CHD) (based in turn on the significantly increased risk of subsequent morbid and mortal events in this population), the use of the NCEP guidelines in a high-risk sample like the one we describe seems quite appropriate.
Danias and Silverman point out that acute hospitalization can lower serum lipid levels, an issue we address explicitly in our article. At no point, however, do we state or imply that "deferral of cholesterol testing during an acute hospitalization is necessarily a misguided approach." In fact, we agree with others1 that to obtain a valid lipid panel in the acute setting, the specimen must be collected within 24 hours of admission. Our point was that even allowing for this effect, clinical decision making based on lipid values that may have been spuriously low remained strikingly inadequate. By lowering lipid levels, in other words, the effect of the "acute phase response" would have been, if anything, to inflate the measured physician performance; our results may have been even more discouraging if such a mechanism was not operating.
Finally, Danias and Silverman appear to have misunderstood our intent regarding the risk factors of sex (not just male sex, as they state) and age. One of the goals of the study was to evaluate how thoroughly physicians and nurses elicited key risk factors for CHD. Since gender was immediately observable and age automatically printed in the hospital chart, no independent effort was required for their ascertainment; hence, we excluded them when assessing screening performance. However, when we constructed the statistical algorithms that were used to judge compliance with NCEP guidelines, sex and age were both incorporated per NCEP criteria.
The comments of Danias and Silverman do point to an issue of considerable interest and importance. Precisely because of results like the ones we, they,2 and others3 report, there is an evolving consensus that in high-risk, secondary-prevention patients, lipid-lowering therapy should perhaps be started before hospital discharge. Although some authors would limit such an intervention to patients whose LDL levels exceed desirable (NCEP-based) cutpoints,4 others recommend treatment in this setting even without screening, because patients have demonstrated by their disease that their levels are too high.5 Until outpatient implementation of recommendations such as the NCEP-ATPII guidelines improves, this may emerge as a key hedge against physician noncompliance.
References
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