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Zocor - Is there a generic in the works

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General fitness, health and nutrition
Published
26 October 2003
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13 November 2003
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Pat
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  1. What's the story on Zocor. I heard years ago that it was set to be approved
    for generics at lower prices, or has the FDA and the pols been paid
    convinced otherwise?

  2. simvastatin....... Zocor generic

    Merck Frosst no longer exists..... the generic is available though

    "Pat" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    What's the story on Zocor. I heard years ago that it was set to be


    approved

    Quoted message said:

    for generics at lower prices, or has the FDA and the pols been paid
    convinced otherwise?

  3. I am assuming you are also aware of lovastatin, the first statin
    prescription drug made generic. It is less expensive if you obtain the
    80 mg tab and split in half for a 40 mg dose, which is the standard
    dose. Many pharmacies do not carry the 80 tab and will tell you 'it is
    not available', so ask around.

    As to non-prescription statins, there are some interesting compounds
    that act just like statins; policosanols and red-yeast-rice extracts.
    These are available online and in my experience have lowered LDL and
    increased HDL to goal for some patients. They can act as a 'booster'
    for lower dose prescription statins too. I find it interesting that
    red-yeast-rice, although used in Eurasia before written history, was
    banned by the FDA by the makers of the then patented lovastatin
    (Mevacor). Red-yeast-rice has lovastatin-like compounds that made the
    pharmaceutical company making Mevacor nervous enough for profit that
    they pushed the 'patented' issue until RYR was banned (I wonder how
    much of the cost of lobbying efforts were passed on to the consumers
    at the time) even though RYR had been on the market before Mevacor was
    offered.

    http://www.wholehealthmd.com/news/viewarticle/1,1513,29,00.html

    hope this helps. pb

  4. "Tiger Lily" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    simvastatin....... Zocor generic

    I entered the generic name into the input field and got the following.

    http://www.drugstore.com/pharmacy/prices/drugprice.asp?ndc=00006074082&trx=1Z5006

  5. "Patrick Blanchard, M.D., A.B.F.P." <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    I am assuming you are also aware of lovastatin, the first statin
    prescription drug made generic. It is less expensive if you obtain the
    80 mg tab and split in half for a 40 mg dose, which is the standard
    dose. Many pharmacies do not carry the 80 tab and will tell you 'it is
    not available', so ask around.

    As to non-prescription statins, there are some interesting compounds
    that act just like statins; policosanols and red-yeast-rice extracts.
    These are available online and in my experience have lowered LDL and
    increased HDL to goal for some patients. They can act as a 'booster'
    for lower dose prescription statins too. I find it interesting that
    red-yeast-rice, although used in Eurasia before written history, was
    banned by the FDA by the makers of the then patented lovastatin
    (Mevacor). Red-yeast-rice has lovastatin-like compounds that made the
    pharmaceutical company making Mevacor nervous enough for profit that
    they pushed the 'patented' issue until RYR was banned (I wonder how
    much of the cost of lobbying efforts were passed on to the consumers
    at the time) even though RYR had been on the market before Mevacor was
    offered.

    http://www.wholehealthmd.com/news/viewarticle/1,1513,29,00.html

    hope this helps. pb

    I have tried alternatives but Zocor seems to work well. Also, they claim a
    study that brags about Zocor being more effective than the competitive meds.
    Is it true, or hype?

    http://www.zocor.com/simvastatin/zocor/consumer/heartprotectionstudy/study_results/index.jsp

  6. Pat said:


    "Patrick Blanchard, M.D., A.B.F.P." <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    I am assuming you are also aware of lovastatin, the first statin
    prescription drug made generic. It is less expensive if you obtain the
    80 mg tab and split in half for a 40 mg dose, which is the standard
    dose. Many pharmacies do not carry the 80 tab and will tell you 'it is
    not available', so ask around.

    As to non-prescription statins, there are some interesting compounds
    that act just like statins; policosanols and red-yeast-rice extracts.
    These are available online and in my experience have lowered LDL and
    increased HDL to goal for some patients. They can act as a 'booster'
    for lower dose prescription statins too. I find it interesting that
    red-yeast-rice, although used in Eurasia before written history, was
    banned by the FDA by the makers of the then patented lovastatin
    (Mevacor). Red-yeast-rice has lovastatin-like compounds that made the
    pharmaceutical company making Mevacor nervous enough for profit that
    they pushed the 'patented' issue until RYR was banned (I wonder how
    much of the cost of lobbying efforts were passed on to the consumers
    at the time) even though RYR had been on the market before Mevacor was
    offered.

    http://www.wholehealthmd.com/news/viewarticle/1,1513,29,00.html

    hope this helps. pb

    I have tried alternatives but Zocor seems to work well. Also, they claim
    a
    study that brags about Zocor being more effective than the competitive
    meds.
    Is it true, or hype?

    http://www.zocor.com/simvastatin/zocor/consumer/heartprotectionstudy/study_results/index.jsp

    You are asking "do statins have a class effect?", or "are all statins equal
    in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be more
    important than the first. You might want to check out the CIMT thead too.

    Hope this helps.
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  7. "Patrick Blanchard, M.D. >>" <tag" <[email hidden]***remove> wrote in
    message news:[email hidden]...

    Quoted message said:

    You are asking "do statins have a class effect?", or "are all statins


    equal

    Quoted message said:

    in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be more
    important than the first. You might want to check out the CIMT thead too.

    Hope this helps.
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

    I suspect that all statins are a family that have common benefits and work
    in similar ways. However, the fact that doctors recommend one vs. the other
    has me wondering if its because of the pharmaceutical reps convincing them
    about their preferences or that some patients react differently and/or
    register higher or lower cholesterol rates when taking more than one statin.
    Have you seen data to corroborate this?

  8. Pat said:


    "Patrick Blanchard, M.D. >>" <tag" <[email hidden]***remove> wrote in
    message news:[email hidden]...

    Quoted message said:

    You are asking "do statins have a class effect?", or "are all statins


    equal

    Quoted message said:

    in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be
    more
    important than the first. You might want to check out the CIMT thead
    too.

    Hope this helps.
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

    I suspect that all statins are a family that have common benefits and
    work
    in similar ways. However, the fact that doctors recommend one vs. the
    other
    has me wondering if its because of the pharmaceutical reps convincing
    them
    about their preferences or that some patients react differently and/or
    register higher or lower cholesterol rates when taking more than one
    statin.
    Have you seen data to corroborate this?

    Yes, there is plenty to be found on prescribing practices at www.pubmed.gov
    I refused to see pharm. reps 6 or 7 years ago because of this issue. It is
    not uncommon to see a "hot" new drug prescribed in groups of physicians
    when an inexpensive generic is just as good if not better.
    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  9. M.D. said:


    You are asking "do statins have a class effect?", or "are all statins equal
    in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be more
    important than the first. You might want to check out the CIMT thead too.

    My intuition agrees with you but eventually it's "data talk, [censored]
    walks"

    Are there good surrogate or direct clinical markers for "stabilizing
    vulnerable plaques" as opposed to blood lipids?

    Were these tested in either

    a) registrational
    b) post-approval

    clinical studies by the pharmaceutical companies, or by other
    sponsors?

  10. Dr Chaos said:
    M.D. said:


    You are asking "do statins have a class effect?", or "are all statins
    equal in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be
    more important than the first. You might want to check out the CIMT
    thead too.

    My intuition agrees with you but eventually it's "data talk, [censored]
    walks"

    Are there good surrogate or direct clinical markers for "stabilizing
    vulnerable plaques" as opposed to blood lipids?

    A vulnerable plaque is commonly defined as a collection of 'guel' within
    the intima-media complex with a fragile fibrous, or outer coating. The
    intima, once supple and pliable has been replaced with fibrous like cells
    that are stiffer. This guel under a thin and sickly fibrous cap is still
    metabolically active, expressing certain proteins on the surface that
    normally are not present on healthy intima. High resolution CIMT can
    visualize fibrous capping when there is a vulnerable plaque present in the
    carotid arterial beds, and is an added bonus of understanding with CIMT.
    However, the abscence of plaque in the carotid beds do not preclude plaque
    in the coronary or other arterial beds.

    High sensitivity C-reactive protein hs.CRP and myeloperoxidase, or MPO are
    very promising markers for active inflammation and vulnerability for heart
    attack and stroke. I use hs.CRP to gauge progression of therapy in the
    short run (every few months) and CIMT for the long haul (annually).
    Unfortunately, MPO is still investigational.

    So yes, there are good markers for assesing plaque stability in my opinion.

    Quoted message said:


    Were these tested in either

    a) registrational b) post-approval

    clinical studies by the pharmaceutical companies, or by other
    sponsors?

    This is where I believe 'class effect' of most medications should be used.
    In other words, if company A underwrites a study of statin A showing rapid
    decrease in hs.CRP or MPO, and is the only one published then you have to
    be careful not to jump on the statin A bandwagon too quickly but hold
    company A's study up to the class effect studies and help the patient make
    the decision on their own. If someone asks me to decide, then I invariably
    stay with the 'class effect' model.

    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  11. Patrick said:
    Dr Chaos said:
    M.D. said:


    You are asking "do statins have a class effect?", or "are all statins
    equal in efficacy?".

    Yes, I believe all statins are equally effective, a also believe a
    phamaceutical rep can play physicians like parrots.

    Statins have at least 2 important roles; lowering cholesterol and
    stabilizing vulnerable plaques. Personally I believe the latter to be
    more important than the first. You might want to check out the CIMT
    thead too.

    My intuition agrees with you but eventually it's "data talk, [censored]
    walks"

    Are there good surrogate or direct clinical markers for "stabilizing
    vulnerable plaques" as opposed to blood lipids?

    A vulnerable plaque is commonly defined as a collection of 'guel' within
    the intima-media complex with a fragile fibrous, or outer coating. The
    intima, once supple and pliable has been replaced with fibrous like cells
    that are stiffer. This guel under a thin and sickly fibrous cap is still
    metabolically active, expressing certain proteins on the surface that
    normally are not present on healthy intima. High resolution CIMT can
    visualize fibrous capping when there is a vulnerable plaque present in the
    carotid arterial beds, and is an added bonus of understanding with CIMT.
    However, the abscence of plaque in the carotid beds do not preclude plaque
    in the coronary or other arterial beds.

    Nor vice versa (ie increased CIMT does not preclude significant coronary
    atherosclerotic disease).

    Quoted message said:


    High sensitivity C-reactive protein hs.CRP and myeloperoxidase, or MPO are
    very promising markers for active inflammation and vulnerability for heart
    attack and stroke. I use hs.CRP to gauge progression of therapy in the
    short run (every few months) and CIMT for the long haul (annually).
    Unfortunately, MPO is still investigational.

    What is unfortunate about investigation?

    Quoted message said:


    So yes, there are good markers for assesing plaque stability in my opinion.

    Neither CIMT nor hsCRP are good markers for assessing *coronary* plaque
    stability, imho.

    MPO might be based on the recent Cleveland Clinic study in NEJM.

    --
    Dr. Andrew B. Chung, MD/PhD
    Board-Certified Cardiologist
    http://www.heartmdphd.com/

  12. MD/PhD said:
    Patrick said:
    Dr Chaos said:

    On Tue, 28 Oct 2003 07:59:46 -0600, Patrick Blanchard, M.D. <> wrote:
    >
    > You are asking "do statins have a class effect?", or "are all statins
    > equal in efficacy?".
    >
    > Yes, I believe all statins are equally effective, a also believe a
    > phamaceutical rep can play physicians like parrots.
    >
    > Statins have at least 2 important roles; lowering cholesterol and
    > stabilizing vulnerable plaques. Personally I believe the latter to be
    > more important than the first. You might want to check out the CIMT
    > thead too.

    My intuition agrees with you but eventually it's "data talk, [censored]
    walks"

    Are there good surrogate or direct clinical markers for "stabilizing
    vulnerable plaques" as opposed to blood lipids?

    A vulnerable plaque is commonly defined as a collection of 'guel' within
    the intima-media complex with a fragile fibrous, or outer coating. The
    intima, once supple and pliable has been replaced with fibrous like
    cells
    that are stiffer. This guel under a thin and sickly fibrous cap is still
    metabolically active, expressing certain proteins on the surface that
    normally are not present on healthy intima. High resolution CIMT can
    visualize fibrous capping when there is a vulnerable plaque present in
    the
    carotid arterial beds, and is an added bonus of understanding with CIMT.
    However, the abscence of plaque in the carotid beds do not preclude
    plaque
    in the coronary or other arterial beds.

    Nor vice versa (ie increased CIMT does not preclude significant coronary
    atherosclerotic disease).

    increased CIMT essentially predicts risk of increased IMT of the coronary
    bed. however, I do not know your reference point for 'significant' coronary
    atherosclerotic disease. please explain.

    Quoted message said:


    Quoted message said:


    High sensitivity C-reactive protein hs.CRP and myeloperoxidase, or MPO
    are
    very promising markers for active inflammation and vulnerability for
    heart
    attack and stroke. I use hs.CRP to gauge progression of therapy in the
    short run (every few months) and CIMT for the long haul (annually).
    Unfortunately, MPO is still investigational.

    What is unfortunate about investigation?


    there are no standards, or bell shaped curve to position therapy.

    Quoted message said:


    Quoted message said:


    So yes, there are good markers for assesing plaque stability in my
    opinion.

    Neither CIMT nor hsCRP are good markers for assessing *coronary* plaque
    stability, imho.


    'good' seems too subjective a word. can you be more specific?

    Thank you

    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  13. Patrick said:
    MD/PhD said:
    Patrick said:

    On Tue, 28 Oct 2003 18:05:08 +0000 (UTC), Dr Chaos
    <[email hidden]> wrote:

    > On Tue, 28 Oct 2003 07:59:46 -0600, Patrick Blanchard, M.D. <> wrote:
    >>
    >> You are asking "do statins have a class effect?", or "are all statins
    >> equal in efficacy?".
    >>
    >> Yes, I believe all statins are equally effective, a also believe a
    >> phamaceutical rep can play physicians like parrots.
    >>
    >> Statins have at least 2 important roles; lowering cholesterol and
    >> stabilizing vulnerable plaques. Personally I believe the latter to be
    >> more important than the first. You might want to check out the CIMT
    >> thead too.
    >
    > My intuition agrees with you but eventually it's "data talk, [censored]
    > walks"
    >
    > Are there good surrogate or direct clinical markers for "stabilizing
    > vulnerable plaques" as opposed to blood lipids?

    A vulnerable plaque is commonly defined as a collection of 'guel' within
    the intima-media complex with a fragile fibrous, or outer coating. The
    intima, once supple and pliable has been replaced with fibrous like
    cells
    that are stiffer. This guel under a thin and sickly fibrous cap is still
    metabolically active, expressing certain proteins on the surface that
    normally are not present on healthy intima. High resolution CIMT can
    visualize fibrous capping when there is a vulnerable plaque present in
    the
    carotid arterial beds, and is an added bonus of understanding with CIMT.
    However, the abscence of plaque in the carotid beds do not preclude
    plaque
    in the coronary or other arterial beds.

    Nor vice versa (ie increased CIMT does not preclude significant coronary
    atherosclerotic disease).

    increased CIMT essentially predicts risk of increased IMT of the coronary
    bed. however, I do not know your reference point for 'significant' coronary
    atherosclerotic disease. please explain.

    Preclude and predict risk are not synonymous.

    Quoted message said:
    Quoted message said:


    Quoted message said:


    High sensitivity C-reactive protein hs.CRP and myeloperoxidase, or MPO
    are
    very promising markers for active inflammation and vulnerability for
    heart
    attack and stroke. I use hs.CRP to gauge progression of therapy in the
    short run (every few months) and CIMT for the long haul (annually).
    Unfortunately, MPO is still investigational.

    What is unfortunate about investigation?


    there are no standards, or bell shaped curve to position therapy.

    Without investigation there will be no data.

    Quoted message said:
    Quoted message said:


    Quoted message said:


    So yes, there are good markers for assesing plaque stability in my
    opinion.

    Neither CIMT nor hsCRP are good markers for assessing *coronary* plaque
    stability, imho.


    'good' seems too subjective a word. can you be more specific?

    Your word choice. Something good for me in this context would have proven
    clinical utility.

    Quoted message said:


    Thank you

    You're welome.

    --
    Dr. Andrew B. Chung, MD/PhD
    Board-Certified Cardiologist
    http://www.heartmdphd.com

  14. MD/PhD said:
    Patrick said:
    MD/PhD said:

    Patrick, Blanchard,, M.D., , >> wrote:

    > On Tue, 28 Oct 2003 18:05:08 +0000 (UTC), Dr Chaos
    > <[email hidden]> wrote:
    >
    > > On Tue, 28 Oct 2003 07:59:46 -0600, Patrick Blanchard, M.D. <>


    Quoted message said:

    > >>
    > >> You are asking "do statins have a class effect?", or "are all


    statins

    Quoted message said:

    > >> equal in efficacy?".
    > >>
    > >> Yes, I believe all statins are equally effective, a also believe a
    > >> phamaceutical rep can play physicians like parrots.
    > >>
    > >> Statins have at least 2 important roles; lowering cholesterol and
    > >> stabilizing vulnerable plaques. Personally I believe the latter to


    be

    Quoted message said:

    > >> more important than the first. You might want to check out the


    CIMT

    Quoted message said:

    > >> thead too.
    > >
    > > My intuition agrees with you but eventually it's "data talk,


    [censored]

    Quoted message said:

    > > walks"
    > >
    > > Are there good surrogate or direct clinical markers for


    "stabilizing

    Quoted message said:

    > > vulnerable plaques" as opposed to blood lipids?
    >
    > A vulnerable plaque is commonly defined as a collection of 'guel'


    within

    Quoted message said:

    > the intima-media complex with a fragile fibrous, or outer coating.


    The

    Quoted message said:

    > intima, once supple and pliable has been replaced with fibrous like
    > cells
    > that are stiffer. This guel under a thin and sickly fibrous cap is


    still

    Quoted message said:

    > metabolically active, expressing certain proteins on the surface that
    > normally are not present on healthy intima. High resolution CIMT can
    > visualize fibrous capping when there is a vulnerable plaque present


    in

    Quoted message said:

    > the
    > carotid arterial beds, and is an added bonus of understanding with


    CIMT.

    Quoted message said:

    > However, the abscence of plaque in the carotid beds do not preclude
    > plaque
    > in the coronary or other arterial beds.
    >

    Nor vice versa (ie increased CIMT does not preclude significant


    coronary

    Quoted message said:

    atherosclerotic disease).

    increased CIMT essentially predicts risk of increased IMT of the
    coronary
    bed. however, I do not know your reference point for 'significant'
    coronary
    atherosclerotic disease. please explain.

    Preclude and predict risk are not synonymous.

    I don't believe I said they were...

    Quoted message said:
    Quoted message said:
    Quoted message said:

    > However, the abscence of plaque in the carotid beds do not preclude
    > plaque
    > in the coronary or other arterial beds.

    (When carotid plaques are not present, it does not mean they are absent in
    the coronary and other arterial beds.)

    Quoted message said:
    Quoted message said:

    increased CIMT essentially predicts risk of increased IMT of the
    coronary
    bed.

    (If someone has increased carotid artery intima media thickness, there is a
    higher than normal risk of having increased coronary artery intima media
    thickness.)

    however, you have not addressed your reference point for 'significant
    coronary atherosclerotic disease'.

    predict (verb)

    predict, forecast, make a prediction, prognosticate, make a prognosis
    foretell, prophesy, vaticinate, forebode, bode, augur, spell
    foretoken, presage, portend
    foreshow, foreshadow, prefigure, shadow forth, forerun, herald, harbinger,
    usher in, come before
    point to, betoken, typify, signify, indicate
    announce, give notice, notify, advertise
    forewarn, give warning, warn
    look black, look ominous, lower, menace, threaten
    promise, augur well, bode well, bid fair to, give hopes of, hold out hopes,
    build up hopes, raise expectations, excite expectations, give hope

    The Original Roget's Thesaurus of English Words and Phrases (Americanized
    Version) is licensed from Longman Group UK Limited. Copyright © 1994 by
    Longman Group UK Limited. All rights reserved.

    preclude (verb)

    exclude: exclude, preclude, make impossible

    The Original Roget's Thesaurus of English Words and Phrases (Americanized
    Version) is licensed from Longman Group UK Limited. Copyright © 1994 by
    Longman Group UK Limited. All rights reserved.

    Quoted message said:


    Quoted message said:
    Quoted message said:


    >
    > High sensitivity C-reactive protein hs.CRP and myeloperoxidase, or


    MPO

    Quoted message said:

    > are
    > very promising markers for active inflammation and vulnerability for
    > heart
    > attack and stroke. I use hs.CRP to gauge progression of therapy in


    the

    Quoted message said:

    > short run (every few months) and CIMT for the long haul (annually).
    > Unfortunately, MPO is still investigational.
    >

    What is unfortunate about investigation?


    there are no standards, or bell shaped curve to position therapy.

    Without investigation there will be no data.

    I think we are in agreement here.

    Quoted message said:


    Quoted message said:
    Quoted message said:


    >
    > So yes, there are good markers for assesing plaque stability in my
    > opinion.
    >

    Neither CIMT nor hsCRP are good markers for assessing *coronary*


    plaque

    Quoted message said:

    stability, imho.


    'good' seems too subjective a word. can you be more specific?

    Your word choice. Something good for me in this context would have
    proven
    clinical utility.

    Perhaps I was not clear on this issue, let me explain...

    CIMT has proven clinical utility.

    hsCRP has proven clinical utility, although not as well validated as CIMT.

    MPO has possible clinical utility, although not as well validated as hsCRP.

    CIMT has not been proven capable of assesing stability of coronary plaque.
    Coronary angiography is not capable of assesing the stability of coronary
    plaque either. IVUS of the coronary arteries, using a radial catheter probe
    at lesser axial and lateral resolution than CIMT (lower frequency) is
    capable of assessing coronary plaque morphology and as you know is evolving
    into a good tool to guide angioplasty and stent placement. CIMT can asses
    carotid plaque morphology if performed with high resolution external 10Mhz
    linear array probes or better, although you will find conflicting reports
    in the literature as to the reliability of predicting hard clinical events
    with interpretation of carotid plaque morphology.

    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  15. Patrick Blanchard said:

    <snip>however, you have not addressed your reference point for 'significant
    coronary atherosclerotic disease'.

    Disease is clinically significant when there are signs and symptoms associated
    with it. Otherwise, it may still be important but not clinically significant.

    Quoted message said:

    <snip>

    Perhaps I was not clear on this issue, let me explain...

    CIMT has proven clinical utility.

    Not for assessing coronary plaque stability.

    Quoted message said:


    hsCRP has proven clinical utility, although not as well validated as CIMT.

    Not for assessing coronary plaque stability.

    Quoted message said:


    MPO has possible clinical utility, although not as well validated as hsCRP.

    From the recent NEJM article from Cleveland Clinic, it now has proven utility
    in assessing stability of coronary plaque(s) that are causing chest pain in the
    acute ER setting.

    Quoted message said:


    CIMT has not been proven capable of assesing stability of coronary plaque.

    Glad you agree.

    Quoted message said:

    Coronary angiography is not capable of assesing the stability of coronary
    plaque either.

    Correct.

    Quoted message said:

    IVUS of the coronary arteries, using a radial catheter probe
    at lesser axial and lateral resolution than CIMT (lower frequency) is
    capable of assessing coronary plaque morphology and as you know is evolving
    into a good tool to guide angioplasty and stent placement.

    And IVUS information of plaque lipid content does assess coronary plaque
    stability.

    Quoted message said:

    CIMT can asses
    carotid plaque morphology if performed with high resolution external 10Mhz
    linear array probes or better, although you will find conflicting reports
    in the literature as to the reliability of predicting hard clinical events
    with interpretation of carotid plaque morphology.

    Imho, you are looking at the wrong part of the body with CIMT.

    --
    Dr. Andrew B. Chung, MD/PhD
    Board-Certified Cardiologist
    http://www.heartmdphd.com/

  16. Dr. Andrew B. Chung said:


    Imho, you are looking at the wrong part of the body with CIMT.

    If the biochemical process is similar everywhere and there is
    mechanistic correlation between states likely to cause carotid disease
    as coronary disease, it should be a good proxy for increased risk
    probability. Not actual disease of course.

  17. Dr Chaos said:
    Dr. Andrew B. Chung said:


    Imho, you are looking at the wrong part of the body with CIMT.

    If the biochemical process is similar everywhere and there is
    mechanistic correlation between states likely to cause carotid disease
    as coronary disease, it should be a good proxy for increased risk
    probability.

    Ime, the CIMT information contributes very little additively to the CAD
    risk assessment ascertainable from a good history, physical exam, EKG, and
    basic blood work including serum glucose and a lipid profile.

    Quoted message said:

    Not actual disease of course.

    Of course.

    --
    Dr. Andrew B. Chung, MD/PhD
    Board-Certified Cardiologist
    http://www.heartmdphd.com/

  18. MD/PhD said:
    Patrick Blanchard said:

    <snip>however, you have not addressed your reference point for
    'significant
    coronary atherosclerotic disease'.

    Disease is clinically significant when there are signs and symptoms
    associated
    with it. Otherwise, it may still be important but not clinically
    significant.

    The decades-long, slow progression of atherosclerosis, clinically silent,
    without signs or symptoms is a very very significant and serious clinical
    problem.

    Cleve Clin J Med. 2003 May;70(5):431-4, 437-8, 440. Aggressive treatment of
    atherosclerosis: the time is now.

    Fonarow GC.

    Ahmanson-UCLA Cardiomyopathy Center, Cardiology Fellowship Training
    Program, UCLA Preventative Cardiology Program, Division of Cardiology, UCLA
    Division of Cardiology 90095, USA. [email hidden]

    In patients with known cardiovascular disease and those at high risk for
    it, physicians must begin to treat atherosclerosis earlier, with
    combination therapy of statins, aspirin, angiotensin-converting enzyme
    inhibitors, and beta-blockers.

    [censored] TJ, Nam BH, D'Agostino RB, Wolf PA, Lloyd-Jones DM, MacRae CA, Wilson
    PW, Polak JF, O'Donnell CJ.

    http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12874190&dopt=Abstract

    Carotid intima-media thickness is associated with premature parental
    coronary heart disease: the Framingham Heart Study.
    Circulation. 2003 Aug 5;108(5):572-6. Epub 2003 Jul 21. PMID: 12874190
    [PubMed - indexed for MEDLINE]

    Quoted message said:


    Quoted message said:

    <snip>

    Perhaps I was not clear on this issue, let me explain...

    CIMT has proven clinical utility.

    Not for assessing coronary plaque stability.

    I disagree with your blanket statement. You know we are discussing
    statistically significant issues.

    J Am Coll Cardiol. 2003 Sep 17;42(6):1026-32. Related Articles, Links
    Clinical implications of carotid artery remodeling in acute coronary
    syndrome: ultrasonographic assessment of positive remodeling.

    Kato M, Dote K, Habara S, Takemoto H, Goto K, Nakaoka K.

    Department of Cardiology, Hiroshima City Asa Hospital, Hiroshima, Japan.
    [email hidden]

    OBJECTIVES: We investigated the relationship between ultrasonographic
    features of the carotid artery and the angiographic features of coronary
    plaques in acute coronary syndrome (ACS). BACKGROUND: The carotid intima-
    media thickness (IMT) may be a marker of advanced coronary artery disease.
    METHODS: Consecutive ACS patients (N = 125) underwent B-mode
    ultrasonography within one week of the acute coronary event. Using a 7.5-
    MHz linear array transducer, the common carotid IMT, interadventitial
    diameter, and luminal diameter were examined. Carotid plaques were also
    assessed. Then patients were divided into two groups based on the number of
    complex plaques identified by coronary angiography. RESULTS: The carotid
    IMT of 75 patients with multiple complex coronary plaques was significantly
    larger than that of 50 patients with solitary plaques (p < 0.0003). The
    prevalence of soft and hard carotid plaques was higher in the group with
    multiple coronary plaques than in those with single plaques (28% vs. 12%, p
    < 0.04 and 13% vs. 0%, p < 0.008, respectively). Additionally, the carotid
    interadventitial diameter was larger in the patients with multiple plaques
    than in those with single plaques (7.93 +/-0.97 mm vs. 7.48 +/-0.88 mm, p <
    0.01), and a significant correlation was observed between the carotid IMT
    and interadventitial diameter (R = 0.54, p < 0.0001). CONCLUSIONS: In ACS,
    multiple complex coronary plaques are associated with positive carotid
    remodeling, suggesting that plaque vulnerability may be a systemic
    phenomenon.

    Quoted message said:


    Quoted message said:


    hsCRP has proven clinical utility, although not as well validated as
    CIMT.

    Not for assessing coronary plaque stability.

    Quoted message said:


    MPO has possible clinical utility, although not as well validated as
    hsCRP.

    From the recent NEJM article from Cleveland Clinic, it now has proven
    utility
    in assessing stability of coronary plaque(s) that are causing chest pain
    in the
    acute ER setting.

    Quoted message said:


    CIMT has not been proven capable of assesing stability of coronary
    plaque.

    Glad you agree.

    not the way you are debating it.

    Quoted message said:


    Quoted message said:

    Coronary angiography is not capable of assesing the stability of
    coronary
    plaque either.

    Correct.

    Quoted message said:

    IVUS of the coronary arteries, using a radial catheter probe
    at lesser axial and lateral resolution than CIMT (lower frequency) is
    capable of assessing coronary plaque morphology and as you know is
    evolving
    into a good tool to guide angioplasty and stent placement.

    And IVUS information of plaque lipid content does assess coronary plaque
    stability.

    when you state this, you are actually supporting CIMT as a method for
    assesing coronary plaque stability because, as you know, atherosclerosis is
    a global process. However, neither CIMT nor Intravascular ultrasound (IVUS)
    has been proven to asses coronary plaque stability.

    Quoted message said:


    Quoted message said:

    CIMT can asses
    carotid plaque morphology if performed with high resolution external
    10Mhz
    linear array probes or better, although you will find conflicting
    reports
    in the literature as to the reliability of predicting hard clinical
    events
    with interpretation of carotid plaque morphology.

    Imho, you are looking at the wrong part of the body with CIMT.

    You cannot interpret CIMT as you have been trained to interpret coronary
    angiography. They look at the atherosclerotic process in completely
    different criteria.
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  19. MD/PhD said:
    Dr Chaos said:
    Dr. Andrew B. Chung said:


    Imho, you are looking at the wrong part of the body with CIMT.

    If the biochemical process is similar everywhere and there is
    mechanistic correlation between states likely to cause carotid disease
    as coronary disease, it should be a good proxy for increased risk
    probability.

    Ime, the CIMT information contributes very little additively to the CAD
    risk assessment ascertainable from a good history, physical exam, EKG,
    and
    basic blood work including serum glucose and a lipid profile.

    Quoted message said:

    Not actual disease of course.

    Of course.

    --
    Dr. Andrew B. Chung, MD/PhD
    Board-Certified Cardiologist
    http://www.heartmdphd.com/

    you are wrong on both counts. here are 2 of hundreds of articles you will
    find at www.pubmed.gov on carotid intima and global atherosclerosis, and
    its use to identify atherosclerotic burden in people wanting to avoid heart
    attack and stroke, among other vascular problems. Yes, it is complex, and
    cannot be simplified to 5 words in one sentence.

    Sramek A, Bosch JG, Reiber JH, Van Oostayen JA, Rosendaal FR.

    Ultrasound assessment of atherosclerotic vessel wall changes:
    reproducibility of intima-media thickness measurements in carotid and
    femoral arteries.
    Invest Radiol. 2000 Dec;35(12):699-706.

    CONCLUSIONS: Ultrasonography is a reliable and accurate technique to
    determine intima-media thickness in superficial arteries. In studies in
    which the intima-media thickness determination is used as a marker for
    generalized and coronary atherosclerosis, the common carotid artery should
    always be included, whereas the benefit of inclusion of other arteries
    depends on age and the expected extent of atherosclerosis in the
    individuals studied.

    Atherosclerosis. 2003 Sep;170(1):181-5.
    Impaired insulin sensitivity is an independent predictor of common
    carotid intima-media thickness in a population sample of elderly men.

    Wohlin M, Sundstrom J, Arnlov J, Andren B, Zethelius B, Lind L.

    Department of Public Health and Caring Sciences, Uppsala University,
    Uppsala, Sweden. [email hidden]

    Most previous studies of associations between insulin sensitivity and
    common carotid artery (CCA) atherosclerosis have been conducted in small
    samples, have not used direct measurement of insulin sensitivity, and have
    yielded inconclusive results. We investigated associations of CCA intima-
    media thickness (IMT) and diameter (CCA-D) measured by B-mode ultrasound
    and insulin sensitivity measured by the euglycemic hyperinsulinemic clamp
    test together with risk factors of the insulin resistance syndrome in a
    community-based sample of 493 elderly men. The clamp glucose disposal rate
    was an independent predictor of CCA-IMT in multivariate models adjusting
    for blood pressure, smoking, serum cholesterol, and body mass index (1%
    decrease in CCA-IMT for a 1 unit increase in glucose disposal rate,
    P=0.009). Glucose disposal rate was significantly related to CCA-D in
    univariate (r=-0.11, P=0.02) but not in multivariate models. In conclusion,
    this study is the first to establish impaired insulin sensitivity, measured
    by the euglycemic hyperinsulinemic clamp test, as an independent predictor
    of CCA-IMT in a population-based sample of elderly men.

    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

  20. Dr Chaos said:
    Dr. Andrew B. Chung said:


    Imho, you are looking at the wrong part of the body with CIMT.

    If the biochemical process is similar everywhere and there is
    mechanistic correlation between states likely to cause carotid disease
    as coronary disease, it should be a good proxy for increased risk
    probability. Not actual disease of course.

    Firstly, CIMT measures the actual disease process of atherosclerosis, and
    has been so very well validated by hundreds of studies.
    Go to www.pubmed.gov and search for carotid intima atherosclerosis to get
    started.

    And yes, it is similar everywhere with the exception that the arterial beds
    in the "arterioles" and the "capillaries" and the "veins" are not
    influenced in the same way as "arteries". Here is an example of the
    vascular system:

    Heart>arteries (aorta, arms, legs, brain, heart, kidneys,
    etc...>arterioles>capillaries>veins>heart

    I also addressed this issue even futher in Dr. Chung's response to your
    question.

    You are on the right course of thought!

    --
    ~~~
    Patrick Blanchard, M.D., A.B.F.P.
    Board Certified in Family Practice

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