Keith
Thu, Aug-10-06, 17:15
Published by Medical News Today at
http://www.medicalnewstoday.com/medicalnews.php?newsid=49244
Keith
New Explanation For The Cause Of Atherosclerosis: The Acidity
Theory Main Category: Cardiovascular / Cardiology News Article
Date: 10 Aug 2006 - 0:00am (PDT)
Recent findings were reported by a team of scientists at the
University
of California, San Diego, linking mechanical forces with
structural and
biochemical changes in blood vessel cells that could explain
why atherosclerotic lesions form preferentially at branches of
coronary arteries. The study from Roland Kaunas and colleagues
was published online in Cellular Signalling on February 28,
2006 and will appear in the journal's October 2006 issue.
Carlos Monteiro, an independent researcher and president of
Infarct Combat Project, wondering about the precursor (s) of
the mechanical forces over the coronary flow, generating
atherosclerostic lesions, researched through medical
literature and came to the following findings:
-- Lowered pH increase perfusion pressure and enhance
contractility of coronary arteries (von Ardenne M and
Reitnauer PG, 1989; Horai Y et al,
2005).
-- Lactate, lowered pH and lactic acid induce endocardial
damage (Carter G and Gavin JB, 1989)
-- Blood does not flow symmetrically, as scientists originally
believed. Instead, it flows in two opposing corkscrews
surrounded by a third corkscrew-like flow. This combination
creates an asymmetrical, spiraling flow that is encouraged by
the natural curves and bends of human arteries (Spiraling
Through the Arteries, Karniadakis G, 1998)
-- Changes in flow patterns can produce potentially
deleterious effects
on vascular biology. Lowered shear stress and oscillatory
shear stress are essential conditions in atherosclerotic
lesion size and vulnerability (Cunningham KS and Gotlieb AI,
2005; Cheng et al,
2006)
Acidity Theory of Atherosclerosis
Based in the findings above-mentioned, and taking into account
that pH sympathetic dominance migrates towards acidity, Carlos
Monteiro formulated a new hypothesis to explain the cause of
atherosclerosis in a revolutionary, straightforward and simple
idea. The sequence of events in Acidity Theory of
Atherosclerosis:
I. Sympathetic dominance by continuous stress plus
II. Deficiency in production of endogenous digitalis-like
compounds with alterations in Na(+), K(+)-ATPase activity
results in
III. Lowered pH (acidity) that leads to the generation of
mechanical forces in blood flow which may cause
atherosclerosis.
Many cardiovascular disease processes, including myocardial
ischemia, congestive heart failure, unstable angina pectoris,
acute myocardial infarction, heart broken syndrome and
arrhythmias, are precipitated or worsened by perturbations in
the autonomic nervous system, with sympathetic activation and
release of acidic pH - stress hormones.
Carlos Monteiro intends to publish an article about the
Acidity Theory of Atherosclerosis, in a scientific journal in
the near future.
Conflicts of interest: -- Infarct Combat Project supports the
"Myogenic Theory of Myocardial Infarction" -- Carlos Monteiro
is an unofficial member of The International Network
of Cholesterol Skeptics (THINCS - www.thincs.org)
Infarct Combat Project is an international non-profit
organization that
provides information, research and education to fight heart
disease. ICP website is http://www.infarctcombat.org
References:
1. Beyond Lipids: Understanding the Mechanics of
Atherosclerosis. UCSD News, July 12, 2006, at
http://tinyurl.com/llmdx
2. Regulation of stretch-induced JNK activation by stress
fiber orientation, Kaunas R et al, Cellular Signalling,
2006 (Epub ahead the print) at http://tinyurl.com/na6pt
3. Increase of perfusion pressure at constant perfusion rate
caused by low pH values, von Ardenne M, Reitnauer PG,
Biomed Biochim Acta, 1989;48(4):317-23 at
http://tinyurl.com/jfomd
4. Changes in pH increase perfusion pressure of coronary
arteries in the rat, Yasushi Horai et al, J Pharmacol Sci
97; 400: 407, 2005 (Full paper) at
http://www.jstage.jst.go.jp/article/jphs/97/3/400/_pdf
5. George Karniadakis, "Spiraling Through the Arteries", NCSA
News, 1998 at http://tinyurl.com/h26aq
6. Atherosclerotic lesion size and vulnerability are
determined by patterns of fluid shear stress. Cheng C et
al, Circulation 2006,
7:2744-2753 at http://circ.ahajournals.org/cgi/content/abstra-
ct/113/23/2744
8. The role of shear stress in the pathogenesis of
atherosclerosis (Mini review), Cunningham KS and Gotlieb
AI, Laboratory Investigation
(9) 85, 9-23, http://www.nature.com/labinvest/journal/v85/n1/-
full/3700215a.html
10. Endocardial damage induced by lactate, lowered pH and
lactic acid in
non-ischemic beating hearts, Carter G, Gavin JB, Pathology
1989 Apr;21(2):125-30 at http://tinyurl.com/ewq3z
11. Wilhelm Schoner - Endogenous cardiac glycosides, a new
class of steroid hormones, Eur J Biochem. 268, 2440-2448,
2002 at
http://www.ejbiochem.org/cgi/content/full/269/10/2440
12. Understanding the sodium potassium pump and its relevance
to disease. Rose AM and Valdes RJ, Cin. Chem. 1994; 40/9:
1674-1685 http://www.clinchem.org/cgi/reprint/40/9/1674
13. Acid-Evoked Currents in Cardiac Sensory Neurons - A
possible mediator of myocardial ischemic sensation, Benson
CJ et al, Circulation
Research, 1999;84:921-928 (Full paper) at
http://circres.ahajournals.org/cgi/content/full/84/8/921
14. Apical ballooning syndrome or takotsubo cardiomyopathy: a
systematic review, Monica Gianni et al. European Heart
Journal, V27,N13: 1523-1529 http://tinyurl.com/gam6r
15. Reversible left ventricular dysfunction "takotsubo"
cardiomyopathy related to catecholamine cardiotoxicity,
Akashi YJ et al, J. Electrocardiol 2002; 35:351-356 at
http://tinyurl.com/rdlma
16. Transient left ventricular apical ballooning after cocaine
use; is catecholamine cardiotoxicity the pathologic link?
Arora S et al. Mayo Clin Proc. 2006; 81:820-832
http://www.mayoclinicproceedings.com/pdf/8106/8106cr2.pdf
17. Neurohumoral features of myocardial stunning due to sudden
emotional stress, Wittstein IS et al. New Engl J Med 2005
Feb 10, V352:
539-548
18. Sympathetic neural hyperactivity and its normalization
following unstable angina and acute myocardial infarction,
Graham LN, Smith PA et
al. Clin Sci (Lond) 2004 Jun;106(6):605-11
19. Plasma catecholamine concentrations in myocardial
infarction and angina pectoris, Gazes PC, Richardson JA et
al. Circulation 1959;19:657-661
20. A possible role of noradrenaline in the development of
myocardial infarction, Waldenstrom AP et al. Am Heart J.
1978;95:43-51
21. Plasma catecholamine in acute myocardial infarction Nadeau
RA, de Champlain J, Am Heart J. 1979;98:548-554
22. Increased cardiac sympathetic nervous activity in patients
with unstable coronary heart disease, McCance AJ, Thompson
PA, Forfar JC. Eur Heart J 1993 Jun;14(6):751-7
23. Sympathetic neural hyperactivity and its normalization
following unstable angina and acute myocardial infarction,
Graham LN, Smith PA et
al. Clin Sci (Lond) 2004 Jun;106(6):605-11
http://www.medicalnewstoday.com/medicalnews.php?newsid=49244
Keith
New Explanation For The Cause Of Atherosclerosis: The Acidity
Theory Main Category: Cardiovascular / Cardiology News Article
Date: 10 Aug 2006 - 0:00am (PDT)
Recent findings were reported by a team of scientists at the
University
of California, San Diego, linking mechanical forces with
structural and
biochemical changes in blood vessel cells that could explain
why atherosclerotic lesions form preferentially at branches of
coronary arteries. The study from Roland Kaunas and colleagues
was published online in Cellular Signalling on February 28,
2006 and will appear in the journal's October 2006 issue.
Carlos Monteiro, an independent researcher and president of
Infarct Combat Project, wondering about the precursor (s) of
the mechanical forces over the coronary flow, generating
atherosclerostic lesions, researched through medical
literature and came to the following findings:
-- Lowered pH increase perfusion pressure and enhance
contractility of coronary arteries (von Ardenne M and
Reitnauer PG, 1989; Horai Y et al,
2005).
-- Lactate, lowered pH and lactic acid induce endocardial
damage (Carter G and Gavin JB, 1989)
-- Blood does not flow symmetrically, as scientists originally
believed. Instead, it flows in two opposing corkscrews
surrounded by a third corkscrew-like flow. This combination
creates an asymmetrical, spiraling flow that is encouraged by
the natural curves and bends of human arteries (Spiraling
Through the Arteries, Karniadakis G, 1998)
-- Changes in flow patterns can produce potentially
deleterious effects
on vascular biology. Lowered shear stress and oscillatory
shear stress are essential conditions in atherosclerotic
lesion size and vulnerability (Cunningham KS and Gotlieb AI,
2005; Cheng et al,
2006)
Acidity Theory of Atherosclerosis
Based in the findings above-mentioned, and taking into account
that pH sympathetic dominance migrates towards acidity, Carlos
Monteiro formulated a new hypothesis to explain the cause of
atherosclerosis in a revolutionary, straightforward and simple
idea. The sequence of events in Acidity Theory of
Atherosclerosis:
I. Sympathetic dominance by continuous stress plus
II. Deficiency in production of endogenous digitalis-like
compounds with alterations in Na(+), K(+)-ATPase activity
results in
III. Lowered pH (acidity) that leads to the generation of
mechanical forces in blood flow which may cause
atherosclerosis.
Many cardiovascular disease processes, including myocardial
ischemia, congestive heart failure, unstable angina pectoris,
acute myocardial infarction, heart broken syndrome and
arrhythmias, are precipitated or worsened by perturbations in
the autonomic nervous system, with sympathetic activation and
release of acidic pH - stress hormones.
Carlos Monteiro intends to publish an article about the
Acidity Theory of Atherosclerosis, in a scientific journal in
the near future.
Conflicts of interest: -- Infarct Combat Project supports the
"Myogenic Theory of Myocardial Infarction" -- Carlos Monteiro
is an unofficial member of The International Network
of Cholesterol Skeptics (THINCS - www.thincs.org)
Infarct Combat Project is an international non-profit
organization that
provides information, research and education to fight heart
disease. ICP website is http://www.infarctcombat.org
References:
1. Beyond Lipids: Understanding the Mechanics of
Atherosclerosis. UCSD News, July 12, 2006, at
http://tinyurl.com/llmdx
2. Regulation of stretch-induced JNK activation by stress
fiber orientation, Kaunas R et al, Cellular Signalling,
2006 (Epub ahead the print) at http://tinyurl.com/na6pt
3. Increase of perfusion pressure at constant perfusion rate
caused by low pH values, von Ardenne M, Reitnauer PG,
Biomed Biochim Acta, 1989;48(4):317-23 at
http://tinyurl.com/jfomd
4. Changes in pH increase perfusion pressure of coronary
arteries in the rat, Yasushi Horai et al, J Pharmacol Sci
97; 400: 407, 2005 (Full paper) at
http://www.jstage.jst.go.jp/article/jphs/97/3/400/_pdf
5. George Karniadakis, "Spiraling Through the Arteries", NCSA
News, 1998 at http://tinyurl.com/h26aq
6. Atherosclerotic lesion size and vulnerability are
determined by patterns of fluid shear stress. Cheng C et
al, Circulation 2006,
7:2744-2753 at http://circ.ahajournals.org/cgi/content/abstra-
ct/113/23/2744
8. The role of shear stress in the pathogenesis of
atherosclerosis (Mini review), Cunningham KS and Gotlieb
AI, Laboratory Investigation
(9) 85, 9-23, http://www.nature.com/labinvest/journal/v85/n1/-
full/3700215a.html
10. Endocardial damage induced by lactate, lowered pH and
lactic acid in
non-ischemic beating hearts, Carter G, Gavin JB, Pathology
1989 Apr;21(2):125-30 at http://tinyurl.com/ewq3z
11. Wilhelm Schoner - Endogenous cardiac glycosides, a new
class of steroid hormones, Eur J Biochem. 268, 2440-2448,
2002 at
http://www.ejbiochem.org/cgi/content/full/269/10/2440
12. Understanding the sodium potassium pump and its relevance
to disease. Rose AM and Valdes RJ, Cin. Chem. 1994; 40/9:
1674-1685 http://www.clinchem.org/cgi/reprint/40/9/1674
13. Acid-Evoked Currents in Cardiac Sensory Neurons - A
possible mediator of myocardial ischemic sensation, Benson
CJ et al, Circulation
Research, 1999;84:921-928 (Full paper) at
http://circres.ahajournals.org/cgi/content/full/84/8/921
14. Apical ballooning syndrome or takotsubo cardiomyopathy: a
systematic review, Monica Gianni et al. European Heart
Journal, V27,N13: 1523-1529 http://tinyurl.com/gam6r
15. Reversible left ventricular dysfunction "takotsubo"
cardiomyopathy related to catecholamine cardiotoxicity,
Akashi YJ et al, J. Electrocardiol 2002; 35:351-356 at
http://tinyurl.com/rdlma
16. Transient left ventricular apical ballooning after cocaine
use; is catecholamine cardiotoxicity the pathologic link?
Arora S et al. Mayo Clin Proc. 2006; 81:820-832
http://www.mayoclinicproceedings.com/pdf/8106/8106cr2.pdf
17. Neurohumoral features of myocardial stunning due to sudden
emotional stress, Wittstein IS et al. New Engl J Med 2005
Feb 10, V352:
539-548
18. Sympathetic neural hyperactivity and its normalization
following unstable angina and acute myocardial infarction,
Graham LN, Smith PA et
al. Clin Sci (Lond) 2004 Jun;106(6):605-11
19. Plasma catecholamine concentrations in myocardial
infarction and angina pectoris, Gazes PC, Richardson JA et
al. Circulation 1959;19:657-661
20. A possible role of noradrenaline in the development of
myocardial infarction, Waldenstrom AP et al. Am Heart J.
1978;95:43-51
21. Plasma catecholamine in acute myocardial infarction Nadeau
RA, de Champlain J, Am Heart J. 1979;98:548-554
22. Increased cardiac sympathetic nervous activity in patients
with unstable coronary heart disease, McCance AJ, Thompson
PA, Forfar JC. Eur Heart J 1993 Jun;14(6):751-7
23. Sympathetic neural hyperactivity and its normalization
following unstable angina and acute myocardial infarction,
Graham LN, Smith PA et
al. Clin Sci (Lond) 2004 Jun;106(6):605-11