Coronary heart disease symptoms and conditions

Cholesterol slightly elevated Dr. recommended 10mg dosage. Began experiencing neck and shoulder pain, dizziness, nausea, foot stiffness and leg numbness up to the lower thigh. Voluntarily stopped the medication after four months. All noticed side effects disappeared except for the foot stiffness and leg numbness. It has been 2 1/2 years and these remaining side effects are constant. Not optimistic for recovery. Anyone else with similar symptoms?

Taking high dose of statin (generic zocor 80mg/day), I was short of breath, severe fatigue and couldn't get out of bead for long. The following information saved me. The article was published in 2002 by a Board Cerified Cardiologist:

"July 8, 2002
STATIN-INDUCED CARDIOMYOPATHY
INTRODUCTION TO THE CITIZEN’S PETITION ON STATINS
By Peter H. Langsjoen, MD
The medical profession has, after more than 30 years of excellent propaganda, successfully created the wholly iatrogenic - "pseudo-disease" dubbed "hypercholesterolemia" and the associated malady "cholesterol neurosis". After decades of dismal failure to cure this "disease" of numbers with low fat diets and a host of cholesterol lowering drugs, the medical profession stumbled upon the magic bullet, the cure for this dreaded artificial disease - statins (HMG-CoA reductase inhibitors). First released on the US market in 1987, statins have rapidly grown into one of the most widely prescribed class of drugs in history. Statins do three things:
1. They block the body's ability to make cholesterol, thus lowering the blood level of cholesterol, thereby curing cholesterol neurosis. Doctors and patients equally neurotic have immediate gratification. The "evil" high cholesterol has been dramatically lowered and the future is bright and promising. So far...so good.
2. Unrelated to their cholesterol lowering, statins have been found to have anti-inflammatory, plaque-stabilizing properties which have a slight benefit in coronary heart disease.
3. Statins kill people - lots of people - and they wound many, many more. All patients taking statins become depleted in Coenzyme Q10 (CoQ10), eventually - those patients who start with a relatively low CoQ10 levels (the elderly and patients with heart failure) begin to manifest signs/symptoms of CoQ10 deficiency relatively rapidly - in 6 to 12 months. Younger, healthier people who's only "illness" is the non-illness "hypercholesterolemia" can tolerate statins for several years before getting into trouble with fatigue, muscle weakness and soreness (usually with normal muscle enzyme CPK tests) and most ominously - heart failure.
In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, "statin cardiomyopathy". Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with "normal" cholesterol levels. We are in the midst of a CHF epidemic in the US with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes. We are now in a position to witness the unfolding of the greatest medical tragedy of all time - never before in history has the medical establishment knowingly (Merck & Co., Inc. has two 1990 patents combining CoQ10 with statins to prevent CoQ10 depletion and attendant side effects) created a life threatening nutrient deficiency in millions of otherwise healthy people, only to then sit back with arrogance and horrific irresponsibility and watch to see what happens - as I see two to three new statin cardiomyopathies per week in my practice, I cannot help but view my once great profession with a mixture of sorrow and contempt.
Statin-induced CoQ10 depletion is the topic of a recent petition to the FDA requesting that this drug/nutrient interaction be identified in a black box warning as part of statin package insert information. A comprehensive review of animal and human trials addressing this issue has been submitted to the FDA as a supporting document. We, of course, do not expect any response from the FDA, but 10 years from now when the full extent of statin toxicity becomes painfully evident, at least we can, in good conscience, know that we tried and who knows, sometimes small sparks may spread in dry grass.

See Also:
Cholesterol Drugs And The Depletion Of Coenzyme Q10: A Review Of Human And Animal Data.
By Peter H. Langsjoen, MD
Citizen Petition: Needed - A Change In The Labeling Of All Statin Drugs"

I'm 58 years old and I've been on 10 mg Simvastatin for 14 months since I was diagnosed with Diabetes 2. Also Metformin and Glipiside as my bs got up to 499 at diagnosis with high cholesterol.

I had NO IDEA that my suffering the past year could possibly be tied to one of the drugs I've been prescribed. In the first three months after diagnosis, my Diabetes was controlled and I've even backed off some of the meds. My cholesterol also came down beautifully. However, the debilitating weakness and muscle aches (which has increased over the 14 mos.) has become so bad (especially this last week) that I came to the Internet looking for possible reasons for 'body ache'.

And get this: I take a packet of vitamins every day which includes a daily dose of Q10... BUT I haven't been able to take them for about a week and this last week I felt like I was ready for a wheel chair~!!! Worse than it's ever been, knees and feet in horrible condition, hands and wrists unable to open a water bottle. Total body aches so severe it made me want to research something, anything to see what might be the problem.... before seeing the doctor about it!

My shock at seeing my medication here listed with the horrible side effects I'm experiencing has been a revelation~!! I am going to stop the Simvastatinn and see what happens. BTW, I've been an active person all my life, was a 2nd Degree Black Belt and taught Tang Soo Do and know what muscle aches and pains are, know my body (at least I did) and pretty much thought my active life was over.....

Not now~!!! I'm FURIOUS!!

Can Statins Cause Chronic Low-Grade Myopathy?
Statins (hydroxymethyl glutaryl coenzyme A reductase
inhibitors) are highly effective drugs for reducing serum
cholesterol and low-density lipoprotein cholesterol levels.
Clinical trials have shown that they also reduce risk for
coronary heart disease events, coronary procedures, and
stroke by about one third (1). Millions of people in the
United States and worldwide are being treated with statins.
In clinical trials and in clinical practice, statins have proved
to be remarkably safe.
The one notable side effect of statin therapy is myopathy.
A small fraction of patients who are treated with
statins will develop severe myopathy (2). In the worst cases,
severe myoglobinuria, acute renal failure, and even death
can occur. The incidence of severe myopathy is low, perhaps
1 in 1000 patients (2). Predisposing factors for severe
myopathy appear to include advanced age, relatively low
body weight, female sex, certain medications, use of multiple
medications, multisystem disease, and acute illnesses
or major surgery (3). If statins were avoided or used in low
doses in these circumstances, it is likely that the incidence
of severe myopathy could be greatly reduced.
Less severe forms of myopathy undoubtedly occur. In
some patients, fatigue and muscle pain and weakness develop
with moderately high serum creatine kinase levels
but not acute renal failure. In these cases, the myopathy
resolves when statin therapy is discontinued.
Still more patients report various muscle symptoms—
fatigue, pain, and muscle weakness—but have normal creatine
kinase levels. These symptoms probably are unrelated
to statin therapy in many patients. In middle-aged and
older people, muscle, joint, and tendon symptoms are very
common. Naturally, if a patient takes a medication that is
believed to produce muscle problems, symptoms are often
attributed to the medication. On the other hand, the major
controlled clinical trials have not detected a higher prevalence
of muscle symptoms during statin therapy versus placebo
(1). This failure of detection has generally led clinical
trialists to conclude that statin-associated myopathy with
normal creatine kinase levels essentially does not exist or
that, if it does exist, it cannot be detected above the “background
noise” of muscle symptoms in the general clinicaltrial
population.
Many physicians in clinical practice nonetheless believe
that they can identify a subset of statin-treated patients
who have a unique set of statin-related muscle symptoms.
Some patients clearly relate the onset of muscle
symptoms to initiation of statin therapy. These symptoms
may abate after discontinuation of therapy, only to reappear
when statin therapy is restarted. The number of such
patients is not large, and thus it may have been impossible
to identify them in large clinical trials.
In this issue, Phillips and colleagues (4) report on a set
of studies in four patients who had muscle symptoms during
statin therapy that resolved during placebo use. Quantitatively
measured muscle weakness also resolved during
placebo use. Muscle biopsies were performed in three patients
during statin therapy and then during placebo use.
Several pathologic changes were seen on biopsy specimens
obtained during statin therapy: increased lipid content of
mitochondria, fibers that did not stain for cytochrome oxidase
activity, and ragged red fibers. The authors suggest
that these patients had statin-associated myopathy with
normal serum creatine kinase levels.
Despite the study’s small size, we cannot dismiss these
observations as random variation in muscle structure.
However, these highly suggestive results are clearly preliminary.
The number of patients was small, and all appropriate
controls were not used. Nonetheless, this study is novel
because it used quantitative measures of muscle strength
and muscle biopsy to address the question of myopathy
with normal creatine kinase levels during statin therapy.
To be confirmed, the current data would have to be
extended to many more patients in whom muscle symptoms
are closely correlated with statin use. Reproducibility
of symptoms during therapy and symptom resolution after
discontinuation of statin therapy would be necessary. A
definitive study would have to be carefully designed and
executed. It would need to be double-blinded and placebocontrolled
and include sufficient numbers of patients to
provide a valid statistical comparison. In addition, investigators
would have to carefully consider the appropriate
selection of patients. The development of a registry of candidate
patients at multiple sites could facilitate a multicenter
study.
Is a carefully controlled, sizable study of this type
worth the investment of time and effort? To date, no evidence
indicates that prolonged statin therapy leads to permanent
muscle damage or progressive myopathy in patients
with normal creatine kinase levels. Controlled
clinical trials attest to the general safety of statins, and
symptomatic side effects appear to be limited to a relatively
small proportion of treated patients. In addition, no therapy
prevents or treats statin-induced myopathy, short of
withholding the drug. On the other hand, statins are being
prescribed to millions of people, and are usually continued
throughout the patient’s lifetime. It is certain that statins
cause myopathy in some patients. For these reasons, a valid
argument can be made for a more extensive study of lowgrade
myopathy in patients treated with statins.
In the meantime, physicians should recognize the great
benefit of statin therapy in high-risk patients and their
documented safety for most patients. For high-risk persons,
the proven efficacy for preventing cardiovascular disease
outweighs the unlikely possibility of permanent muscle
damage. Phillips and colleagues’ preliminary results
certainly do not provide adequate information on the spec-
Editorial
www.annals.org 1 October 2002 Annals of Internal Medicine Volume 137 • Number 7 617
trum, scope, or prognosis of myopathy with normal creatine
kinase levels during statin therapy. For these reasons,
prescription of statins for eligible patients should continue
despite the current results. Moreover, before discontinuing
therapy, physicians should carefully evaluate any patient
receiving statins who reports muscle symptoms. In most
cases, the symptoms will be found not to be consistent
with chronic myopathy, and often they will not be related
temporally to statin treatment. High-risk patients in particular
should not be deprived of major cardiovascular risk
reduction just because they display symptoms not clearly
documented to be closely related to statin therapy.
Despite these comments, the actions of statin on muscle
metabolism and structure deserve further investigation
to clarify the confusing area of low-grade myopathy apparently
associated with statin use in a few patients.
Scott M. Grundy, MD, PhD
University of Texas Southwestern Medical Center at Dallas
Dallas, TX 75390-9052
Current Author Address: Scott M. Grundy, MD, PhD, Center for
Human Nutrition and the Departments of Clinical Nutrition and Internal
Medicine, University of Texas Southwestern Medical Center at Dallas,
5323 Harry Hines Boulevard, Y3.206, Dallas, TX 75390-9052.
Potential Financial Conflicts of Interest: Honoraria (from Merck &
Co.; Pfizer, Inc.; Bristol-Myers Squibb; and Bayer); Grants (from Merck
& Co. and Pfizer, Inc.)
Ann Intern Med. 2002;137:617-618.
References
1. Executive Summary of The Third Report of The National Cholesterol Education
Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment
of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001;
285:2486-97.
2. Staffa JA, Chang J, Green L. Cerivastatin and reports of fatal rhabdomyolysis
. N Engl J Med. 2002;346:539-40.
3. Pasternak RC, Smith SC, Bairey-Merz CN, Grundy SM, Cleeman JI, Lenfant
C. ACC/AHA/NHLBI clinical advisory on the use and safety of statins (1)
(2). J Am Coll Cardiol. 2002;40:567-72.
4. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al.
Statin-associated myopathy with normal creatine kinase levels. The Scripps Mercy
Clinical Research Center. Ann Intern Med. 2002;137:581-5.
© 2002 American College of Physicians–American Society of Internal
Medicine
Editorial Statins and Low-Grade Myopathy
618 1 October 2002 Annals of Internal Medicine Volume 137 • Number 7 www.annals.org

Lipitor NOT EFFECTIVE ON WOMEN!!

"Again and again, clinical studies have failed to show that the use of statins lowers cardiovascular risk in women who do not already have coronary heart disease or diabetes"

I am a 53 year old male on disability for a bad back and atributed a lot of my symptoms to my back. Leg pains, leg cramps, foot pains and extreme fatigue... Also occasional mental fogginess to depresion as I was on Prozac for depresion... When the side effects hit the hardest I was literally crippeled and barely able to get around on crutches although limited to one level of our split level home, the stairs were TOO MUCH. I had stopped the Lipitor immediately put that didn't help, the pain was overwhelming despite the Hydrocodone #10 I was taking 4-6 a day!! (I previously took 1 per day max) I found on the internet how statin drugs deplete the body of CoQ-10 and cause the muscles to atrophy.

For results of CoQ-10 see my other post...
I don't list website where I get mine because I don't want anyone to think I have anything to gain by making these posts. I am sharing what worked for me and got me out of a period of paid so intense. I only want to help others.
I had to find a cheaper place to buy because I'm on social security disabilty with kids and I don't get enough money to be able to buy it any where else so now maybe I can help them another way too. God Bless all who have been effected by this drug and may you have a complete recovery, if you refuse to quit taking it, supplement with coq-10 even drs and pharmacists agree (that know what they're talking about)