Angiogenesis and CHD

Matti Narkia said:

Angiogenesis seems to have both beneficial and detrimental
effects in CHD: after coronary blockage it helps
neovascularization of the heart and development of
coronary collateral circulation; on the other hand
atherosclerotic plaque angiogenesis promotes the growth of
atheromas, and inhibition of angiogenesis inhibits
atherosclerosis and may have beneficial effects on plaque
stability [5,8,9,16,17]. Moreover, vascular endothelial
growth factor (VEGF) elevation correlates with the
evidence of myocardial ischemia and indicates an adverse
outcome [7].

Statins have dual effect on angiogenesis: low doses
promote angiogenesis, but high doses inhibit it [4,12].

It seems to be a considerable challenge to use
angiogenesis promoters and/or inhibitors in CHD in optimal
way and correctly timed.

That is why medicine remains an art.

Servant to the humblest person in the universe,

Andrew

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Thanks for this post Matti, I am intrigued by your
persepective and hope to post later in this thread...

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Mon, 17 May 2004 17:21:10 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung, MD/PhD"

Quoted message said:

Matti Narkia said:

Angiogenesis seems to have both beneficial and
detrimental effects in CHD: after coronary blockage it
helps neovascularization of the heart and development of
coronary collateral circulation; on the other hand
atherosclerotic plaque angiogenesis promotes the growth
of atheromas, and inhibition of angiogenesis inhibits
atherosclerosis and may have beneficial effects on plaque
stability [5,8,9,16,17]. Moreover, vascular endothelial
growth factor (VEGF) elevation correlates with the
evidence of myocardial ischemia and indicates an adverse
outcome [7].

Statins have dual effect on angiogenesis: low doses
promote angiogenesis, but high doses inhibit it [4,12].

It seems to be a considerable challenge to use
angiogenesis promoters and/or inhibitors in CHD in
optimal way and correctly timed.

That is why medicine remains an art.

Hmmm... So how do/would you do it? What is/would be your
regimen in applying angiogenesis promotion and/or inhibition
in CHD and on what evidence it
is/would be based?

--
Matti Narkia

Matti Narkia said:

Mon, 17 May 2004 17:21:10 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung,

MD/PhD said:

Matti Narkia said:

Angiogenesis seems to have both beneficial and
detrimental effects in CHD: after coronary blockage it
helps neovascularization of the heart and development
of coronary collateral circulation; on the other hand
atherosclerotic plaque angiogenesis promotes the growth
of atheromas, and inhibition of angiogenesis inhibits
atherosclerosis and may have beneficial effects on
plaque stability [5,8,9,16,17]. Moreover, vascular
endothelial growth factor (VEGF) elevation correlates
with the evidence of myocardial ischemia and indicates
an adverse outcome [7].

Statins have dual effect on angiogenesis: low doses
promote angiogenesis, but high doses inhibit it [4,12].

It seems to be a considerable challenge to use
angiogenesis promoters and/or inhibitors in CHD in
optimal way and correctly timed.

That is why medicine remains an art.

Hmmm... So how do/would you do it?

By knowing the patient's history, examining him/her, and
reviewing all diagnostic testing data, thereby sensing the
relative balance of occlusive and angiogenic processes and
other contributing factors.

Quoted message said:

What is/would be your regimen in applying angiogenesis
promotion and/or inhibition in CHD and on what evidence it
is/would be based?

No regimen or formula. Each person is uniquely different in
much the same way each piece of art is unique and attempts
to regiment art into "painting by numbers" destroys the art.
Just as there are those who are blessed with God's gift for
being artistic, there are those who have God's gift for
healing and there are those who don't.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
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Tue, 18 May 2004 14:03:26 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung, MD/PhD"

Quoted message said:

Matti Narkia said:

Mon, 17 May 2004 17:21:10 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung,

MD/PhD said:

Matti Narkia wrote:

> Angiogenesis seems to have both beneficial and
> detrimental effects in CHD: after coronary blockage it
> helps neovascularization of the heart and development
> of coronary collateral circulation; on the other hand
> atherosclerotic plaque angiogenesis promotes the
> growth of atheromas, and inhibition of angiogenesis
> inhibits atherosclerosis and may have beneficial
> effects on plaque stability [5,8,9,16,17]. Moreover,
> vascular endothelial growth factor (VEGF) elevation
> correlates with the evidence of myocardial ischemia
> and indicates an adverse outcome [7].
>
> Statins have dual effect on angiogenesis: low doses
> promote angiogenesis, but high doses inhibit it
> [4,12].
>
> It seems to be a considerable challenge to use
> angiogenesis promoters and/or inhibitors in CHD in
> optimal way and correctly timed.

That is why medicine remains an art.

Hmmm... So how do/would you do it?

By knowing the patient's history, examining him/her, and
reviewing all diagnostic testing data, thereby sensing the
relative balance of occlusive and angiogenic processes and
other contributing factors.

Under what circumstances would you use angiogenesis
inhibitors? What angiogenesis inhibitors would you use?

Quoted message said:

Quoted message said:

What is/would be your regimen in applying angiogenesis
promotion and/or inhibition in CHD and on what
evidence it
is/would be based?

No regimen or formula. Each person is uniquely different in
much the same way each piece of art is unique and attempts
to regiment art into "painting by numbers" destroys the
art. Just as there are those who are blessed with God's
gift for being artistic, there are those who have God's
gift for healing and there are those who don't.

Hmmm.. How come I get this nagging feeling that you don't
have clue how and when to use angiogenesis inhibitors and
what inhibitors to use, but I'd be glad if you prove that
feeling unsubstantiated showing that you actually know
something about the subject (above God's gift for healing
and truth discernment).

--
Matti Narkia

Matti Narkia said:

Tue, 18 May 2004 14:03:26 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung,

MD/PhD said:

Matti Narkia said:

Mon, 17 May 2004 17:21:10 -0400 in article
<[email hidden]> "Dr. Andrew B.
Chung, MD/PhD" <[email hidden]> wrote:

>Matti Narkia wrote:
>
>> Angiogenesis seems to have both beneficial and
>> detrimental effects in CHD: after coronary blockage
>> it helps neovascularization of the heart and
>> development of coronary collateral circulation; on
>> the other hand atherosclerotic plaque angiogenesis
>> promotes the growth of atheromas, and inhibition of
>> angiogenesis inhibits atherosclerosis and may have
>> beneficial effects on plaque stability
>> [5,8,9,16,17]. Moreover, vascular endothelial growth
>> factor (VEGF) elevation correlates with the evidence
>> of myocardial ischemia and indicates an adverse
>> outcome [7].
>>
>> Statins have dual effect on angiogenesis: low doses
>> promote angiogenesis, but high doses inhibit it
>> [4,12].
>>
>> It seems to be a considerable challenge to use
>> angiogenesis promoters and/or inhibitors in CHD in
>> optimal way and correctly timed.
>
>That is why medicine remains an art.
>
Hmmm... So how do/would you do it?

By knowing the patient's history, examining him/her, and
reviewing all diagnostic testing data, thereby sensing
the relative balance of occlusive and angiogenic
processes and other contributing factors.

Under what circumstances would you use angiogenesis
inhibitors?

Neoplasm, keloid formation, in-stent restenosis, age-related
macular degeneration would be a few examples.

Quoted message said:

What angiogenesis inhibitors would you use?

Many cytotoxic chemotherapy drugs are angiogenesis
inhibitors. Brachytherapy and rapamycin are other
angiogenesis inhibitors that I may elect to use.

Quoted message said:

Quoted message said:

Quoted message said:

What is/would be your regimen in applying angiogenesis
promotion and/or inhibition in CHD and on what
evidence it
is/would be based?

No regimen or formula. Each person is uniquely different
in much the same way each piece of art is unique and
attempts to regiment art into "painting by numbers"
destroys the art. Just as there are those who are
blessed with God's gift for being artistic, there are
those who have God's gift for healing and there are
those who don't.

Hmmm.. How come I get this nagging feeling that you don't
have clue how and when to use angiogenesis inhibitors and
what inhibitors to use, but I'd be glad if you prove that
feeling unsubstantiated showing that you actually know
something about the subject (above God's gift for healing
and truth discernment).

My explanation would be that you lack experience beyond
PubMed searches.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

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Tue, 18 May 2004 16:57:59 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung, MD/PhD"

Quoted message said:

Matti Narkia said:

Tue, 18 May 2004 14:03:26 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung,

MD/PhD said:

Matti Narkia wrote:

> Mon, 17 May 2004 17:21:10 -0400 in article
> <[email hidden]> "Dr. Andrew B.
> Chung, MD/PhD" <[email hidden]> wrote:
>
> >Matti Narkia wrote:
> >
> >> Angiogenesis seems to have both beneficial and
> >> detrimental effects in CHD: after coronary blockage
> >> it helps neovascularization of the heart and
> >> development of coronary collateral circulation; on
> >> the other hand atherosclerotic plaque angiogenesis
> >> promotes the growth of atheromas, and inhibition of
> >> angiogenesis inhibits atherosclerosis and may have
> >> beneficial effects on plaque stability
> >> [5,8,9,16,17]. Moreover, vascular endothelial
> >> growth factor (VEGF) elevation correlates with the
> >> evidence of myocardial ischemia and indicates an
> >> adverse outcome [7].
> >>
> >> Statins have dual effect on angiogenesis: low doses
> >> promote angiogenesis, but high doses inhibit it
> >> [4,12].
> >>
> >> It seems to be a considerable challenge to use
> >> angiogenesis promoters and/or inhibitors in CHD in
> >> optimal way and correctly timed.
> >
> >That is why medicine remains an art.
> >
> Hmmm... So how do/would you do it?

By knowing the patient's history, examining him/her, and
reviewing all diagnostic testing data, thereby sensing
the relative balance of occlusive and angiogenic
processes and other contributing factors.

Under what circumstances would you use angiogenesis
inhibitors?

Neoplasm, keloid formation, in-stent restenosis, age-
related macular degeneration would be a few examples.

This thread is about angiogenesis and CHD, so please limit
your messages to CHD. So in CHD you would use angiogenesis
inhibitors for in-stent restenosis. What's the current
evidence supporting this choice? What angiogenesis
inhibitor(s) would you use in this case? Rapamycin?

Any other CHD circumstances where you would use angiogenesis
inhibitors?

Quoted message said:

Quoted message said:

What angiogenesis inhibitors would you use?

Many cytotoxic chemotherapy drugs are angiogenesis
inhibitors.

Such as?

Quoted message said:

Brachytherapy and rapamycin are other angiogenesis
inhibitors that I may elect to use.

Brachytherapy is interstitial radiotherapy. Although it
suppresses growth by killing cells, it can hardly be called
an angiogenesis inhibitor in the usual meaning of the word.
Rapamycin (sirolimus) instead is indeed an angiogenesis
inhibitor and an immunosuppressant.

Is the current choice of angiogenesis inhibitors in CHD
limited to rapamycin and some unspecified cytotoxic agents?

--
Matti Narkia

Matti Narkia said:

Tue, 18 May 2004 16:57:59 -0400 in article
<[email hidden]> "Dr. Andrew B. Chung,

MD/PhD said:

Matti Narkia said:

Tue, 18 May 2004 14:03:26 -0400 in article
<[email hidden]> "Dr. Andrew B.
Chung, MD/PhD" <[email hidden]> wrote:

>Matti Narkia wrote:
>
>> Mon, 17 May 2004 17:21:10 -0400 in article
>> <[email hidden]> "Dr. Andrew B.
>> Chung, MD/PhD" <[email hidden]> wrote:
>>
>> >Matti Narkia wrote:
>> >
>> >> Angiogenesis seems to have both beneficial and
>> >> detrimental effects in CHD: after coronary
>> >> blockage it helps neovascularization of the heart
>> >> and development of coronary collateral
>> >> circulation; on the other hand atherosclerotic
>> >> plaque angiogenesis promotes the growth of
>> >> atheromas, and inhibition of angiogenesis
>> >> inhibits atherosclerosis and may have beneficial
>> >> effects on plaque stability [5,8,9,16,17].
>> >> Moreover, vascular endothelial growth factor
>> >> (VEGF) elevation correlates with the evidence of
>> >> myocardial ischemia and indicates an adverse
>> >> outcome [7].
>> >>
>> >> Statins have dual effect on angiogenesis: low
>> >> doses promote angiogenesis, but high doses
>> >> inhibit it [4,12].
>> >>
>> >> It seems to be a considerable challenge to use
>> >> angiogenesis promoters and/or inhibitors in CHD
>> >> in optimal way and correctly timed.
>> >
>> >That is why medicine remains an art.
>> >
>> Hmmm... So how do/would you do it?
>
>By knowing the patient's history, examining him/her,
>and reviewing all diagnostic testing data, thereby
>sensing the relative balance of occlusive and
>angiogenic processes and other contributing factors.
>
Under what circumstances would you use angiogenesis
inhibitors?

Neoplasm, keloid formation, in-stent restenosis, age-
related macular degeneration would be a few examples.

This thread is about angiogenesis and CHD, so please limit
your messages to CHD. So in CHD you would use angiogenesis
inhibitors for in-stent restenosis. What's the current
evidence supporting this choice? What angiogenesis
inhibitor(s) would you use in this case? Rapamycin?

Any other CHD circumstances where you would use
angiogenesis inhibitors?

Quoted message said:

Quoted message said:

What angiogenesis inhibitors would you use?

Many cytotoxic chemotherapy drugs are angiogenesis
inhibitors.

Such as?

Quoted message said:

Brachytherapy and rapamycin are other angiogenesis
inhibitors that I may elect to use.

Brachytherapy is interstitial radiotherapy. Although it
suppresses growth by killing cells, it can hardly be
called an angiogenesis inhibitor in the usual meaning of
the word. Rapamycin (sirolimus) instead is indeed an
angiogenesis inhibitor and an immunosuppressant.

Is the current choice of angiogenesis inhibitors in
CHD limited to rapamycin and some unspecified
cytotoxic agents?

--
Matti Narkia

Gollum,

I would be more than happy to continue this discussion in
the HeartMDPhD.com chatroom:

heartmdphd.comchat.aspOpen ↗

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
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What is all this about?
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Matti Narkia said:

Angiogenesis seems to have both beneficial and detrimental
effects in CHD: after coronary blockage it helps
neovascularization of the heart and development of
coronary collateral circulation; on the other hand
atherosclerotic plaque angiogenesis promotes the growth of
atheromas, and inhibition of angiogenesis inhibits
atherosclerosis and may have beneficial effects on plaque
stability [5,8,9,16,17]. Moreover, vascular endothelial
growth factor (VEGF) elevation correlates with the
evidence of myocardial ischemia and indicates an adverse
outcome [7].

Interesting perspective on various effects of statins...

Have you come across any data on the use of low-dose
statin therapy vs. no statin therapy and mortality?
Complication rates of angioplasty with low-dose statin
therapy vs. no statin therapy? Inflammatory markers and
angioplasty outcomes?

I would like to comment that angiogenesis has not been
proven as a cause for plaque vulnerability. Promotion of
plaque vascularization may be an important therapeutic step
for long term management after a period of time during which
therapy has sufficiently stabilized vulnerable plaques.

However, following this transition process would be almost
impossible with today's clinical tools. It has been
suggested that with the CHAMP program at UCLA (incorporating
various treatment pathways) that within 6 weeks, vulnerable
plaques have stabilized and plaque reduction occurs over the
ensuing 12 months (and longer). Perhaps promoting
angiogenesis after 6 weeks of inhibition of angiogenesis may
provide for better outcomes, but of course it is only a
hypothesis.

Thanks Matti :: great post!

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