The comments,here presented,brings us back to the big argument:Are medications good for you?.Medications are altered molecules,introduced into the body,for it to benefit from.Being foriegn to the body,the body reacts.These are the side effects that damage and ,sometimes,kill the body.When it happen we say:"Ouch.I am sorry".Well it does not have to be that way.There are a lot of alternative medication that not only do a good job,but,as it is not a foreign body,the body does not react against it.

In the case of Cardiovsculr Diseases,we have the Statins,claimed to be a "Smart bomb",but it ain't!.It is a "Cluster bomb".We are witnessing a repetetive "Ouch".

What is the alternative? Niacin.Pure Niacin,immediate release,supervised by U.S.P.No side effects except the Flush.Too much noise about the Flush,scares everyboby.With minimal education Flush stops to be an issue.Who says that LDL is the target.Maybe the HDL?(HDL,the good,the bad and the ugly).

It is about time that Niacin will stop being:An Orphane Drug to many Non-Orphane diseases.

It is difficult to practice medicine and carry so many:"Black boxes"

Considering the low frequency of statin induced myopathy and the low risk imparted by this complication when appropriate CPK measurements are undertaken, I don't see a genetic test for statin myopathy risk being of any real clinical value.  In 28 years of clinical experience, I have seen one case of significant myopathy resulting in hospitilization but with a good outcome relatable to the use of statin (in this case the inappropriate concuurent use with  cyclosporin).

 Perhaps a niche for this test would be in relatives of patients who exeperienced myopathy with statins. 

I concur with the below comment regarding the low risk of biochemically evident myopathy. I personally avoid simvastatin 80 due to a higher risk suggested in the A to Z trial. I would like a reference regarding the HPS and the gene-myopathy connection. I do think validation in the case of other statins would be helpful. I am skeptical regarding routine use of this test unless its discriminatory value for myopathy (ROC curves) is demonstrated for simva 40, atorva 40, and/or rova20/40 is established.

On a related issue, I am interested in your opinion regarding the already marketed KIF6 genotyping.

I also concur with the last 2 comments on the extremely low risk of myopathy with statins. Translational medicine has not really made an impact on clinical lipidology to this point. Although a fascinating field to academics, such as Dr Topol, it just is not making much impact on the day to day practice of clinical medicine. I treat 400-600 patients for lipids monthly and I have maybe 1-2 patients/year who cannot tolerate statins due to myopathy. It just isn't the big problem its made out to be by talking heads who don't see patients on a daily basis.

Some important comments here. ApoA1  must have some unusual patients since mucle aches/pain is the most common side effect of statins, and in fact set up the ezetimibe market.  I have treated patients with statins for over 20 years and the incidence of this side ffect becoming an issue for patients is at least 5-10%, many stimate much higher. This is not an academic issue. Ceruvastatin (Baychol) was taken off the market since it induced rhabdomyolysis and deaths---likely indexed to the same gene. The story is not just about marked CK rise 10 fold or greater. There are series of patients who have muscle biopsy proven myositis without CK blood level excess.

Agree with D. Powell that we need more data on all statins. I think the KIF6 story in intriguing but we need more info on that marker as well. The reference in NEJM July 31 has all the related HPS info.

The amioadorone-statin interaction is yet another example of the problem, with many clinicians not aware of the need to go to lower statin doses when using amiodarone concurrently.  Learning the pathway for this myopathy unintended yet frequent effect sets up the potential to prevent it in the future.

My patient population is probably not as wealthy as yours since you practice in beautiful La Jolla and I practice in the inner city of Atlanta. But the 5-10% that complain of muscle pain like my toe hurts or my knee aches with normal CPK and no improvement with withdrawal of statins, I do not consider clinically significant. And I don't nor do I know of any guidelines that require one to preform a muscle biopsy to rule out myositis in patients who have muscle pain with a statin. If you just switch many of these patients to a differant statin or actually look at their med list to see if the statin metabolism was interfered with like the amiodarone example you have your answer. Also many of the market leaders metabolism is through P450 3A4 (atorvastatin) which results in alot of drug/drug interaction. In fact the majority of Rhabdo cases with cerivastatin was because it was combined with lopid. The only statin that doesn't interact with lopid is fluvastatin. In fact in a recent study patients deemed intolerant to statin were placed on Lescol up to 80mg without a problem in a majority of these patients. In that very very small group of patients that truely have clinically significant myopathy(symmetric large muscle pain with profound weakness with or without CPK elevation) I will consider KIF6. But again this is 1-2 patients/year. Now if guidelines change and I must  do muscle biopsy to rule out myositis this may change. But I doubt I will live long enough to see this happen. 

ApoA1,

 Dr. Topol was not recommending muscle biopsy. He was referring to the following series of studies:

 Ann Intern Med. 2002 Oct 1;137(7):581-5. Statin-associated myopathy with normal creatine kinase levels.

Genetic risk factors associated with lipid-lowering drug-induced myopathies. Muscle Nerve. 2006 Aug;34(2):153-62.

 Incidentally, I would echo the 5-10% risk of significant myalgias from everyday clinical practice.

In many cases alternative modes of lipid lowering therapy are available to address both the advantages of statins and the potential, low risk, disadvantages of statins. These include bile acid sequestrants, particularily, colsevelam, which is a more tolerable bas, niacin, and a multitude of  supplements which have shown to reduce levels of low density lipoproteins. 

These other medicines can be employed alone, or in combination with the statin. If the higher doses of statins are your concern add a non-systemic agent such as colsevelam to your existing low dose statin regimen.

 

I'm not a doctor but a user of statins.  All of my family memebers take them in one form or another because we have very high cholesterol levels in our family.  My doctor told me about the KIF6 test today and I am going to have it done.  All of my family members deal with muscle pain from the statins.  We just don't make a big deal about it to our doctors because we've all been told that we absolutely have to be on the statins or risk serious heart disease.  You learn to put up with the muscle pain and digestive side affects (zetia).  So maybe some doctors don't hear a lot of complaints about muscle pain, but it's there.  I'm hoping this test will help my doctor decide if I really need to be on statins and how much and what kind.  I am 66 and have a lot of living yet to do!  But the muscle pain I experience is almost overwhelming.  Any help I can get will improve my daily life so that I can enjoy my golden years!  Thanks for listening.