I don't have cardiovascular disease but I experienced the pains you
describe when I was taking Lipitor and Baycol.
The standard liver function and nerve tests may not always show statin
damage. One needs to have muscle biopsies.
You may wish to take the following information to your father's
doctors. If you would like the full text PDF please e-mail me at the
address above. Search PUBMED for Dr. Paul S. Phillips work on statins,
statins and cardiopulmonary function, statin myopathy... . Zee
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Muscle Nerve. 2005 May;31(5):572-80.
Molecular clues into the pathogenesis of statin-mediated muscle
toxicity.
Baker SK.
Division of Physical Medicine and Rehabilitation, Department of
Medicine, McMaster University, McMaster University Medical Center, Room
4U4, Hamilton, Ontario, L8N 3Z5, Canada. bakersjj@hotmail.com
The pathophysiology of statin-mediated muscle dysfunction is poorly
defined. Reductions in skeletal muscle membrane cholesterol were
initially thought to account for the range of myopathic reactions,
e.g., myalgia, elevated serum creatine kinase, or rhabdomyolysis. This
assumption however, does not consider a potential role of the
isoprenoids in the pathophysiology of statin myopathy. The observation
that derangements in mevalonate kinase (MK), but not more distal
enzymes of cholesterologenesis, are associated with a skeletal myopathy
suggests a critical role for the isoprenoids in the maintenance of
muscle. Statins also deplete the isoprenoid pool by inhibiting the
enzyme, beta-hydroxy-beta-methylglutaryl coenzyme A reductase, which is
upstream of MK. Identifying candidate proteins that are both dependent
on isoprenoid-mediated modification and associated with muscle disease,
when genetically mutated, offers further insight into potential
mechanisms of statin myopathy. For example, lamin A/C, selenoprotein N,
alpha- and beta-dystroglycan, and cytoskeletal G-proteins all require
isoprenylation for optimal function. Understanding the pleiotropic
effects of protein prenylation, and the potential consequences of a
generalized insufficiency of this form of protein modification, may
help clarify the molecular pathogenesis of statin myopathy.
PMID: 15712281 [PubMed - in process]
> My Dad, 83 y/o, 12 years post-bypass and has had two MIs (most recent in
> 1993) and 2 angioplasties. Seems to be doing much better since advent of
[quoted text clipped - 16 lines]
>
> Larry E.
> My Dad, 83 y/o, 12 years post-bypass and has had two MIs (most recent in
> 1993) and 2 angioplasties. Seems to be doing much better since advent of
[quoted text clipped - 16 lines]
>
> Larry E.
Your father's neurologist should be qualified to spot any
contraindications for Neurontin.
Fwiw, coumadin anticoagulation does **not** obviate the need for aspirin
for secondary prevention of heart attacks and strokes.
In Christ's love and service,
Andrew
--
Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
**
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