Abnormalities in cholesterol metabolism have been associated with patient response to statin and ezetimibe therapy for LDL cholesterol (LDL-C) lowering.

Boston Heart’s exclusive Cholesterol Balance test directly measures the major production markers (lathosterol and desmosterol) and absorption markers (beta-sitosterol, campesterol and cholestanol) for circulating plasma cholesterol. The levels of these markers are indicators of LDL-C lowering response to treatments (e.g., statins or ezetimibe). This information enables healthcare providers to prescribe the most effective treatment strategy to lower LDL-C and help patients achieve their LDL-C goal.

For more than forty years, total circulating HDL cholesterol (HDL-C) has been used as a primary indicator of cardiovascular disease (CVD) risk. However, HDL is comprised of subpopulations of different sizes, composition and characteristics that impact cardiovascular risk in drastically different ways.

Data from the Framingham Heart Study, Framingham Offspring Study, Veterans Affairs HDL Cholesterol Intervention Trial (VA-HIT) and HDL-Atherosclerosis Treatment Study (HATS) have shown that HDL subpopulations are significantly better predictors of CVD risk than HDL-C values alone.

The Boston Heart HDL Map® is the only test available that quantifies the amount of apoA-I in the five most significant subpopulations, resulting in a deeper understanding of a patient’s CVD risk. This exclusive method provides healthcare providers with an accurate and consistent indication of reverse cholesterol transport by separating the larger, cardioprotective particles most associated with decreased CVD risk from the smaller HDL particles associated with increased risk. Healthcare providers can use this information to determine the most effective treatment strategy, as well as monitor response to therapy.

The SLCO1B1 gene is critical to the body’s uptake and metabolism of statins, drugs prescribed to reduce LDL-C levels for the prevention of heart attacks or strokes. Statin associated muscle symptoms (SAMS)—the onset of muscle aches, spasms, weakness and/or pain associated with statin therapy— are considered to be the most frequent adverse events associated with statins. 1-2

60% of patients who stopped taking a statin cited muscle pain as the primary reason for discontinuation.1 About 25% of people carry either one or two copies of the SLCO1B1 variant.3-5 This increases their risk up to 4.5-fold – or 17-fold respectively for developing significant statin induced myopathy (muscle aches, pains or weakness with significant creatine kinase elevation) due to statins.6 Research shows that patients who received SLCO1B1 genotype guided therapy were more likely to fill the statin prescription, take the medication and have a greater decrease in LDL cholesterol.7

The Boston Heart Statin Induced Myopathy (SLCO1B1) Genotype test identifies those patients who are at higher risk of developing statin induced myopathy due to a variation on their SLCO1B1 gene. This test helps healthcare providers identify patients who are at higher risk for such negative side effects and prescribe the right statin type and dose with the least probability of causing myopathy.

The SLCO1B1 genotype was identified by University of Oxford. Boston Heart holds the exclusive U.S. license for the SLCO1B1 genotype test.

References:

1. Wei MY, Ito MK, Cohen JD, Brinton EA, Jacobson TA. Predictors of statin adherence, switching, and discontinuation in the USAGE survey: understanding the use of statins in America and gaps in patient education. J Clin Lipidol. 7(5):472-483.
2. Stroes ES, Thompson PD, Corsini A, et al. Statin-associated muscle symptoms: impact on statin therapy—European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management. Eur Heart J. 2015;36(17):1012-1022.
3. Voora D, Shah SH, Spasojevic I, Ginsburg G. The SLCO1B1*5 genetic variant is associated with statin-induced side effects. J Am Coll Cardiol2009;54(17):1609-1616.
4. Akao H, Polisecki E, Kajinami K, Trompet S, Robertson M, Ford I, Jukema JW, de Craen AJ, Westendorp RG, Shepherd J, Packard C, Buckley BM, Schaefer EJ. Genetic Variation at the SLCO1B1 Gene Locus and Low Density Lipoprotein Cholesterol Lowering Response to Pravastatin in the Elderly. Atherosclerosis 2012;220(2):413-417.
5. Boston Heart Diagnostics. Database of over 240,000 samples.
6. SEARCH Collaborative Group. SLCO1B1 variants and statin-induced myopathy – a genomewide study. N Engl J Med 2008;359(8):789-799.
7. Li JH, Joy SV, Haga SB, et al. Genetically guided statin therapy on statin perceptions, adherence, and cholesterol lowering: a pilot implementation study in primary care patients. J Pers Med. 2014;4(2):147-162.