Re: Statins and side effects......Statin Chest Pains


"listener" <listener@xxxxxxxxxx> wrote in message
news:Xns976227371282some1outthere@xxxxxxxxxxxxxxxxxx
You're a chronic cherry picker

Which of these studies do you consider to be cherries?

CHEST PAIN & STATINS
Frequently Asked Question: Chest pain, that my cardiologist cannot explain
via angiogram, stress test, EEG or EKG, is one of the side-effects I see is
reported by many people. Is there any information on chest pain associated
with statins?


Naturally, chest pain should be first evaluated by a cardiologist. If the
usual explanations for chest pain do not apply to you, and you believe that
statin adverse-effect may be the cause, here are some articles that may give
you some background, or may be useful to give to your doctor. Some are
specific to statins and cardiomyopathy, some are background on how statins
affect CoQ10 production and how a CoQ10 deficiency affects the cells.



Most of these research articles have been found via a search of the National
Institutes of Health website
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=&DB=PubMed , a repository
for hundreds of medical journals. In most cases, only the abstract is
available and the full article must be purchased. Many of the others can be
found via a Google or other net search, or were discovered via posts on the
Lipitor message boards.



See:

http://www.lipitor.com/pi/default.asp Pfizer's Physician's Info for
prescribing Lipitor, includes documented known adverse effects. Note "Body
as a Whole: Chest pain," the italics indicate that the incidence was > 2% in
original trials.



Phillips PS, Phillips CT, Sullivan MJ, Naviaux RK, Haas RH.

Statin myotoxicity is associated with changes in the cardiopulmonary
function.

Atherosclerosis. 2004 Nov;177(1):183-8.

PMID: 15488882 [PubMed - in process]

Scripps Mercy Clinical Research Center, Scripps Mercy Hospital, Cardiology
(Mer 74), Catheterization Laboratories, Scripps Mercy Hospital, 4077 Fifth
Avenue, San Diego, CA 92103, USA. phillips.paul@xxxxxxxxxxxxxxxxx

"The mechanism of the muscle toxicity associated with lipid-lowering therapy
remains obscure. Pathological and biochemical findings in patients with
statin myotoxicity suggest impaired fatty acid oxidation. Exhaled gas
analysis can be used to assess substrate utilization including fatty acid
oxidation. In order to determine if muscle toxicity due to lipid-lowering
therapy might be related to abnormalities in lipid oxidation, exhaled gas
analysis was performed in the fasted state on 11 patients subsequent to
statin-associated myositis reactions. Results were compared to those of 16
normal controls who were measured both on and off statin therapy.
Post-myositis patients showed a depressed anaerobic threshold (AT) (P=0.009)
compared to controls while age-adjusted maximal oxygen consumption (VO2max)
and ventilatory efficiency (VE/VCO2) were not significantly different. The
fasting respiratory exchange ratio (RER) of post-myositis patients off
statins was abnormally increased (P=0.00001) as was their S1-slope
(P=0.023). Controls demonstrated a significant increase in their RER while
taking statins consistent with decreased lipid oxidation (P <0.00001). These
findings suggest that abnormal lipid oxidation in certain patients may
predispose them to the myotoxicity caused by lipid-lowering therapies."



1: Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A.

Effect of atorvastatin on left ventricular diastolic function and ability
of coenzyme Q10 to reverse that dysfunction.

Am J Cardiol. 2004 Nov 15;94(10):1306-10.

PMID: 15541254 [PubMed - indexed for MEDLINE]

"This study evaluated left ventricular diastolic function with Doppler
echocardiography before and after statin therapy. Statin therapy worsened
diastolic parameters in most patients; coenzyme Q(10) supplementation in
patients with worsening diastolic function with statin therapy improved
parameters of diastolic function."



2: Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A.

Statin cardiomyopathy? A potential role for Co-Enzyme Q10 therapy for

statin-induced changes in diastolic LV performance: description of a
clinical protocol.

Biofactors. 2003;18(1-4):125-7.

PMID: 14695927 [PubMed - indexed for MEDLINE]

"Lipid-lowering statins are thought to have a favorable safety profile.
Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase,
the rate-limiting step of mevalonate synthesis. Mevalonate is the substrate
for further synthesis of cholesterol and Co Enzyme Q10 (CoQ10). CoQ10 plays
an important role during oxidative phosphorylation in the myocardial cell.
Since myocardial diastolic function is a highly ATP dependent, we reasoned
that early changes of diastolic function may be an early marker of
ventricular dysfunction. METHODS: Patients who are to commence on statin
therapy will be enrolled in the trial. Baseline measurements of plasma
CoQ10, total cholesterol, LDL, HDL, CoQ10/LDL ratio, peak E, peak A
velocities, E/A ratio, deceleration time, isovolumetric relaxation time,
color M-mode propagation velocity will be performed and patients will then
begin to take Oral atorvastatin (Lipitor, Parke-Davis) 20 mg daily for three
to six months. All baseline measurement will be repeated after 3 to 6 months
of statin therapy. Those patients demonstrating > 1 measurement of diastolic
LV function that worsened during the 3 to 6 months of statin therapy will be
supplemented with CoQ10 300 mg. daily for 3 months. A followup
echocardiogram and blood CoQ10 level will be measured in patients who
received CoQ10 supplementation. RESULTS: Statistical analysis will be
performed using the paired t test to compare coenzyme levels and
echocardiographic indices at baseline and after treatment and after
supplementation."





3: Langsjoen PH, Langsjoen AM.

The clinical use of HMG CoA-reductase inhibitors and the associated
depletion of coenzyme Q10. A review of animal and human publications.

Biofactors. 2003;18(1-4):101-11. Review.

PMID: 14695925 [PubMed - indexed for MEDLINE]

"The depletion of the essential nutrient CoQ10 by the increasingly popular
cholesterol lowering drugs, HMG CoA reductase inhibitors (statins), has
grown from a level of concern to one of alarm. With ever higher statin
potencies and dosages, and with a steadily shrinking target LDL cholesterol,
the prevalence and severity of CoQ10 deficiency is increasing noticeably. An
estimated 36 million Americans are now candidates for statin drug therapy.
Statin-induced CoQ10 depletion is well documented in animal and human
studies with detrimental cardiac consequences in both animal models and
human trials. This drug-induced nutrient deficiency is dose related and more
notable in settings of pre-existing CoQ10 deficiency such as in the elderly
and in heart failure. Statin-induced CoQ10 deficiency is completely
preventable with supplemental CoQ10 with no adverse impact on the
cholesterol lowering or anti-inflammatory properties of the statin drugs. We
are currently in the midst of a congestive heart failure epidemic in the
United States, the cause or causes of which are unclear. As physicians, it
is our duty to be absolutely certain that we are not inadvertently doing
harm to our patients by creating a wide-spread deficiency of a nutrient
critically important for normal heart function."


.

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