Abstract
A strange paradox haunts our attempts to prevent ischemic heart disease. Medicine has addressed the relation between serum lipids and atherosclerosis through a series of scientific triumphs. First, epidemiology demonstrated the association between abnormal cholesterol levels and coronary artery disease. Then, physiology and biochemistry elucidated the pivotal role of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase in the synthesis of lipoproteins. Next, pharmacology led to the development of new medications to target that enzyme without the often-unbearable side effects of earlier drugs. And finally, clinical researchers enrolled tens of thousands of patients at hundreds of centers worldwide to prove the efficacy of these treatments and help guide their use. Taken together, these steps represent one of the finest examples of the application of science to understand and ameliorate human disease. Article p 371 But shifting our focus from the successful laboratory or clinical trial site to the population reveals more disappointing data. We physicians fail to diagnose potentially dangerous lipid levels in up to a third of our patients with cardiovascular disease1,2; when the problem is identified, we often do not properly deploy the impressive arsenal of treatments that have been put in our hands. In the United States, fewer than half of those who would benefit from lipid-modifying treatment for coronary heart disease risk reduction are receiving it.3 And of those on therapy, just half of patients actually achieve their cholesterol goals.4 This results in part from poor persistence by physicians in monitoring lipid levels and adjusting therapy accordingly, as well as poor persistence by patients in staying with their prescribed regimens for both economic and noneconomic reasons.5 In summary, despite the wealth of tools available to diagnose and manage this common condition, only a fraction of people who have it are being adequately treated. The …
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