CoQ10 and L-carnitine for Statin Myalgia?

James J DiNicolantonio

Disclosures

Expert Rev Cardiovasc Ther. 2012;10(10):1329-1333. 

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Expert Commentary

Ruling out drug interactions, especially medications that inhibit intestinal and liver CYP enzymes, is a reasonable approach in order to determine the cause of statin myalgia. Simply lowering the dose of a statin or introducing it again slowly may also help with these side effects. If someone is experiencing muscle pain on a statin, a CK level should be checked to make sure that the statin does not need to be immediately ceased. When the CK level is elevated (>10,000 U/l), it may indicate rhabdomyolysis (muscle breakdown), which can lead to renal and respiratory failure, pancreatitis and hepatotoxicity.[6]

Informing patients to hold their statin before they perform extreme physical activity may be another alternative for treating statin myalgia. Patients performing endurance exercise on a statin have a significantly increased total CK and CK myoglobin levels compared with patients not on a statin (p = 0.03 and p < 0.05, respectively), suggesting that statins increase exercise-related muscle injury.[19] Patients who have familial hypercholesterolemia who cannot tolerate statins due to myalgia (despite all efforts) may need to consider LDL-apheresis. Drug holidays or every other day rosuvastatin dosing may help to achieve LDL goals and reduce the severity of statin myalgia. However, every other day statin dosing has never been shown to reduce CV events and is currently not an evidence-based recommendation.

When considering the addition of another cholesterol-lowering medication on top, or in place of a statin, fenofibrate seems to be an appropriate choice, especially when compared with gemfibrozil. Gemfibrozil can increase the AUC of almost every statin, accept for fluvastatin, by approximately twofold, and gemfibrozil has a 15-fold increased risk of rhabdomyolysis compared with concomitant statin–fenofibrate.[20] Moreover, fenofibrate has been shown to reduce the risk of CV events in patients with diabetes in the FIELD trial. When average use of statins (16% placebo, 7.5% fenofibrate; p < 0.0001) was adjusted, fenofibrate showed a significant reduction in the primary end point (19% reduction in coronary heart disease [p = 0.01]).[21] Furthermore, fenofibrate prevents amputations, retinopathy, progression to albuminuria, macular edema and worsening of renal function (glomerular filtration rate decline of 6.9 vs 1.94 ml/min, placebo vs fenofibrate, respectively) in diabetic patients.[22] Thus, fenofibrate seems to offer both macro- and micro-vascular protection in patients with diabetes, a combined benefit not seen with many other CV medications. Other evidence-based CV medications such as cholestyramine and niacin can be tried in patients with or at high risk of CV disease who are in tolerant to statins.

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