Do a subject search within this 86 page PDF on studies of statin
adverse effects for cardiopulmonary, cardiovascular, etc. All these
studies can be accessed at www.pubmed.org by using the PMID number:

http://www.freewebs.com/stopped_our_statins/StatinFAQ_031305wTOCv4.pdf

Read here, and contact Dr. Golomb:
http://medicine.ucsd.edu/SES/index.htm

Ask here to receive responses from several hundred others injured by
statins:
http://groups.yahoo.com/group/TakingLipitorAndHateIt/

Contact Dr. Phillips for his opinion. He is author of the study
following:
Atherosclerosis. 2004 Nov;177(1):183-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed
&list_uids=15488882&dopt=Abstract

Statin myotoxicity is associated with changes in the cardiopulmonary
function.
Phillips PS, Phillips CT, Sullivan MJ, Naviaux RK, Haas RH.

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@scrippshealth.org

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.

   PMID: 15488882 [PubMed - indexed for MEDLINE]

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Zee