Management of patients with statin-induced myalgia

The No. 1 reason why patients with dyslipidemia are referred to us is intolerance to lipid-lowering medication. As described in a previous post, many patients prescribed statins experience side effects and discontinue therapy. Observational studies estimate that muscle side effects such as aches, cramps and/or weakness may occur in 5% to 10% of patients on statin therapy. The prevalence in some practices, including my own, may be higher. Fortunately, the much more serious adverse event of rhabdomyolysis is very rare.

The first thing I do when someone reports muscle symptoms is evaluate for other possible explanations. Does the patient have hypothyroidism, severe vitamin D deficiency, polymyositis or another medical reason to have muscle pain and/or weakness? Did he or she recently engage in intense physical activity or have an acute viral or other illness? Is he or she on other medications such as gemfibrozil or certain antibiotics which could interact with the statin and increase the risk for muscle side effects?

If I am not sure whether the statin is the culprit, I stop the statin temporarily to evaluate for causality. If the muscle symptoms are severe I also order a creatinine kinase test. However, remember that not all creatinine kinase elevations are due to statin, and many patients with statin-induced myalgia do not have abnormal creatinine kinase. Sometimes, despite holding the statin, the symptoms do not improve and the patient admits to having had symptoms even before the statin was initiated. Although statins can certainly cause muscle side effects, never forget to evaluate for other possible causes.

In patients who do appear to have myalgia from the statin, there are several options. Some patients swear that coenzyme Q10 (CoQ10) allows them to tolerate a statin, which would not be possible otherwise. Some research has suggested that patients with statin-induced myalgia have lower levels of CoQ10 compared with those without. CoQ10 is synthesized by the same pathway as cholesterol, and it is necessary for normal mitochondria respiration. The problem is that the few studies evaluating the effects of CoQ10 on statin-induced myalgia had mixed results — similar to my own clinical experience. Nevertheless, there is no evidence that CoQ10 is harmful; thus, if a patient is able to tolerate statin by taking CoQ10, I do not discourage it.

We should never give up on all statins because a patient has had side effects from one statin. Many patients who are not able to tolerate one statin may be able to tolerate another. Others are able to tolerate a lower dose of the same or different statin. Fluvastatin (Lescol XL, Novartis) is not prescribed frequently because it does not lower LDL to the degree of other statins, but it appears to have the lowest reported rate of myalgia. I occasionally prescribe a long-acting statin such as rosuvastatin (Crestor, AstraZeneca) to be taken every other day or once a week. Although the LDL lowering may not be as much as with a higher-dose statin taken daily, I would rather have my patients be on whatever dose of statin they can tolerate than no statin at all.

The most important aspect of managing patients with statin-induced myalgia is taking the patient’s symptoms seriously and involving him or her in decision-making regarding their care. I explain why statins are important for cardiovascular risk reduction and what our options are. I ask patients how they would like to proceed. There is not one best way to manage a patient who has side effects due to medication; everyone is unique. What works in one patient may not be successful in another.

If the muscle symptoms are mild and self-limited, sometimes we choose to continue with close monitoring. In others we will try some or all of the options described above. There are some patients, however, in whom no strategy is successful. If all else fails, we may have no choice but to try non-statin therapies.

For more information:

Smiley WH. Management of the Statin-Intolerant Patient. Current Treatment Options in Cardiovascular Medicine. 2009;11:263–271.