There is risk on the order of 0.5% for complications.

At His service,

Andrew

--
Andrew B. Chung, MD/PhD
Board-Certified Cardiologist

**
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(2) http://makeashorterlink.com/?O2F325D1A
(3) http://makeashorterlink.com/?X1C62661A
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Hi Paul,

Re: I am a 33 year old male, fairly good health, have had high
cholesterol for some years now, and been on Lipitor which has knocked
it down a bit, but not entirely.

A few questions...
Has your Dr checked your homocysteine levels?
Are you taking Folic acid, B6 & B12?
What dosage of Lipitor are you taking?
Are you taking CoQ10 with Lipitor. Statins deplete CoQ10.
Your heart and brain need CoQ10.
You mention Lipitor knocked your levels down, but not entirely.....
Did your Dr increase the dosage around the time you had chest pains?

There are a couple of blood tests done when a heart attack is
suspected:
Troponin & CK [creatine kinase]

CK test is also one of the tests done when statin induced muscle damage
is suspected.

Is it possible that statins could actually cause both CK & Troponin to
elevate?
When someone is taking statins and cholesterol levels are not lowered
as expected, is the person taking said statins not able to metabolize
the drug and the statins are reaching toxic levels?
Just food for thought.....

Frankie

Possibly of interest to you:

Emerging, Noninvasive Surrogate Markers of Atherosclerosis
Samir N. Patel, MD, Venkataraman Rajaram, MD, Sanjay Pandya, MD,
Benjamin M. Fiedler, BA, Charlotte J. Bai, MD, Rachel Neems,
Matt Feinstein, Marshall Goldin, MD, and Steven B. Feinstein, MD

Address
Department of Medicine, Rush University Medical Center, 1653 West
Congress Parkway, Jelke 1015, Chicago, IL 60612, USA.

Current Atherosclerosis Reports 2004, 6:60-68
Current Science Inc. ISSN 1523-3804

Noninvasive surrogate markers of atherosclerosis allow the
physician to identify subclinical disease before the occurrence
of adverse cardiovascular events, thereby limiting the
need to perform invasive diagnostic procedures. Imaging
modalities, such as carotid artery ultrasound, two-dimensional
echocardiography, coronary artery calcium imaging,
cardiac magnetic resonance imaging, ankle-brachial indices,
brachial artery reactivity testing, and epicardial coronary
flow reserve measurements, provide information that may
improve the predictive value of a person's risk of developing
clinically significant atherosclerotic disease. Newer
imaging modalities have also emerged to bring insight into
the pathophysiology and treatment of atherosclerosis.

Conclusions
The use of c-IMT, EBCT, cMRI, ABI, brachial artery reactivity
testing, and epicardial coronary flow reserve measurements
has revolutionized the approach of
identifying individuals at high risk for developing
adverse cardiac events. The emergence of these noninvasive
imaging modalities gives the physician an alternative
to invasive procedures when assessing a patient's
atherosclerotic burden, thereby eliminating unnecessary
procedure-related complications.

These noninvasive surrogate markers of atherosclerosis
are integral in revealing subclinical disease and providing a
practical means of assessing its progression. In particular,
c-IMT has been directly correlated with myocardial infarction,
stroke, and death and has been extensively studied in
various clinical trials. Lipid-lowering therapy, ß-blockers,
and calcium antagonists have all shown beneficial effects
on c-IMT, thereby improving a patient's cardiovascular risk
profile. In addition, the use of computer-aided software
and FDA-approved contrast agents improve measurement
precision of c-IMT.

Newer, noninvasive modalities using radiolabeled
monoclonal antibodies targeted at vulnerable plaques
and 19F-fluorodeoxyglucose targeted at inflammation
are currently under development. Most recently, contrast-
enhanced ultrasound imaging permits direct visualization
of plaque neovascularization, thereby bringing
new insight into the pathophysiology and treatment of
atherosclerotic disease.