Seth S. Martin, MD; Roger S. Blumenthal, MD
Financial Support: Dr. Martin is supported by the Pollin Cardiovascular Prevention Fellowship and the Marie-Josée and Henry R. Kravis endowed fellowship. Dr. Blumenthal is supported by the Kenneth Jay Pollin Professorship in Cardiology.
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M13-2805.
Requests for Single Reprints: Roger S. Blumenthal, MD, Johns Hopkins Hospital, 1800 Orleans Street, Blalock 524C, Baltimore, MD 21287; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. Martin and Blumenthal: Johns Hopkins Hospital, 1800 Orleans Street, Blalock 524C, Baltimore, MD 21287.
Author Contributions: Conception and design: S.S. Martin, R.S. Blumenthal.
Analysis and interpretation of the data: R.S. Blumenthal.
Drafting of the article: S.S. Martin.
Critical revision of the article for important intellectual content: S.S. Martin, R.S. Blumenthal.
Final approval of the article: S.S. Martin, R.S. Blumenthal.
Table. The 5 Ps
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David L. Keller, MD, MS, FACP
March 5, 2014
Should we be measuring statin blood concentrations?
Patients who are at risk of adverse events due to atherosclerotic vascular disease (ASVD) are treated with statins, which have been well-proved to reduce these risks. Until now, physicians were told to treat these patients to goals based on blood levels of LDL cholesterol. Now, we are told that the evidence does not support treating to LDL goals, but rather dictates that certain doses of statin be administered, based on the doses which were used in clinical trials.
All medications work by some pharmacological effect. Prior guidelines were based on the assumption that lowering the LDL cholesterol concentration in the blood was the beneficial mechanism. This hypothesis implied that other types of medications should be as effective as statins at reducing adverse ASVD event rates, for equal degrees of LDL-lowering. If this has been disproved, then the new guidelines are reasonable to emphasize statin dose rather than LDL level as the treatment goal.
However, we can and should strive to quantify and normalize our statin treatment for each patient. If the pharmacological benefit of statin therapy is caused by the concentration of the statin in the blood, rather than by blood LDL levels, we should be measuring and monitoring statin levels now, instead of LDL levels. Otherwise, we are treating patients blindly.
A given dose of a statin will result in very different blood concentrations of that statin in different individuals, depending on their renal and hepatic functions, their body mass, their cytochrome genetics, and on other factors. To account for these differences in each unique patient, blood statin concentrations would seem to be required to most precisely maximize the benefits and minimize the risks for each patient.
Martin SS, Blumenthal RS. Concepts and Controversies: The 2013 American College of Cardiology/American Heart Association Risk Assessment and Cholesterol Treatment Guidelines. Ann Intern Med. ;160:356–358. doi: 10.7326/M13-2805
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Published: Ann Intern Med. 2014;160(5):356-358.
Cardiology, Coronary Risk Factors, Dyslipidemia, Endocrine and Metabolism.
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