We thank Dr Kelion for his helpful comments regarding our recent
review on stress echocardiography in Heart [1]. We entirely agree with Dr
Kelion that both British Society of Echocardiography and British Nuclear
Cardiac Society need to raise awareness of the utility of functional tests
for the assessment of coronary artery disease and not squabble about which
technique is superior. Given the fact tha...
We thank Dr Kelion for his helpful comments regarding our recent
review on stress echocardiography in Heart [1]. We entirely agree with Dr
Kelion that both British Society of Echocardiography and British Nuclear
Cardiac Society need to raise awareness of the utility of functional tests
for the assessment of coronary artery disease and not squabble about which
technique is superior. Given the fact that both stress echocardiography
and SPECT imaging have similar diagnostic accuracy, either technique may
be used to perform functional testing.
The decision to proceed to
echocardiography or SPECT will depend on local availability and local
expertise. When both techniques are accessible with equal availability of
expertise, the choice of test will largely depend on the shorter waiting
time of the tests. It is time the National Institute of Excellence (NICE)
incorporated stress echocardiography alongside SPECT for the assessment of
CAD, not least, because the current guidelines by American College of
Cardiology (ACC) and American Heart Association recommend use of either
imaging technique for the assessment of CAD.
Yours sincerely,
R Senior
M Monaghan
H Becher
J Mayet
P Nihoyannopoulos
References
1. Senior R, Monaghan M, Becher H, Mayet J, Nihoyannopoulos P. Stress
echocardiography for the diagnosis and risk stratification of patients
with supected or known coronary artery disease: a critical appraisal.
Heart 2005; 91: 427-436.
While the role of internal defibrillator, as a life-saving
device, is established in Brugada syndrome, drugs like betablockers may precipitate a Brugada phenotype and are ineffective in this syndrome, therefore not recommended [1].
Reference
1. Charles Anzelevitch, Pedro Brugada, Martin Borggreffe. Brugada
syndrome. Report of the second consensus
conference. Circulation. 200...
While the role of internal defibrillator, as a life-saving
device, is established in Brugada syndrome, drugs like betablockers may precipitate a Brugada phenotype and are ineffective in this syndrome, therefore not recommended [1].
Reference
1. Charles Anzelevitch, Pedro Brugada, Martin Borggreffe. Brugada
syndrome. Report of the second consensus
conference. Circulation. 2005;111:000-000.
It is well known the relationship between coronary anomalies and
other congenital cardiac abnormalities [1-2]. Indeed, association between
atrial septal defect and coronary anomalies has been previously described
and in this situation compression of the anomalous coronary artery can
occur when septal defects is percutaneously closed [3-4]. We suggest that a transesophageal ecocardiogram should be don...
It is well known the relationship between coronary anomalies and
other congenital cardiac abnormalities [1-2]. Indeed, association between
atrial septal defect and coronary anomalies has been previously described
and in this situation compression of the anomalous coronary artery can
occur when septal defects is percutaneously closed [3-4]. We suggest that a transesophageal ecocardiogram should be done when
percutaneous closure is planned in patients with an atrial septal defect.
It would be useful to identify the ostium and initial course of both
coronary arteries, and will help to avoid possible additional procedure
complications.
References
1. Topaz O, DeMarchena EJ, Perin E et al. Anomalous coronary arteries:
angiographic findings in 80 patients. Int J Cardiol 1992;34:129-38.
2. Barriales-Villa R, Morís C, López-Muñiz A et al. Anomalías congénitas de
las arterias coronarias del adulto descritas en 31 años de estudios
coronariográficos en el Principado de Asturias: principales
características angiográficas y clínicas. Rev Esp Cardiol 2001;54:269-281.
3. Maki F, Ohtsuka T, Suzuki M et al. Myocardial ischemia induced by
anomalous aortic origin of the right coronary artery in a patient with
atrial septal defect. Jpn Heart J 2001;42:371-6.
4. Casolo G, Gensini GF, Santoro G et al. Anomalous origin of the
circumflex artery and patent foramen ovale: a rare cause of myocardial
ischaemia after percutaneous closure of the defect. Heart 2003;89:e23.
I have never seen a satisfactory hypothesis to account for the
occurrence and distribution of atheromatous deposits in arteries but not
veins. One possibility is a Venturi effect, induced by anatomical,
physiological and pathological changes in the geometry in arteries but
not in veins, accounts for the differences. Might such a effect account
for the increased vulnerability of a remodelled vessel...
I have never seen a satisfactory hypothesis to account for the
occurrence and distribution of atheromatous deposits in arteries but not
veins. One possibility is a Venturi effect, induced by anatomical,
physiological and pathological changes in the geometry in arteries but
not in veins, accounts for the differences. Might such a effect account
for the increased vulnerability of a remodelled vessel and the "shoulder"
of a plaque addressed in this study [1].
A differential pressure exists when a flowing fluid passes through a
constricted region or changes direction due to a turn or elbow in a pipe.
The inference is that it also does so in an artery especially at
atherosclotic stenoses and anatomical bifurcations. The relationship
between flow rate and pressure difference in these locations might be
determined by the Bernoulli equation. The low pressure at the point of
highest velocity in these locations may create the possibility for blood
carrying oxygen and carbon dioxide, to partially vaporize; it might
remain partially vaporized after these regions in the arterial wall
(called flashing when applied to flow meters) or it might return to its
liquid state as the pressure increases after the lowest pressure point
(called cavitation again when applied to flow meters) [2].
An atheroscleotic plaque creates in effect a venturi tube. The change
in cross-sectional area in a venturi tube causes a pressure change between
the convergent section and the throat, and the flow rate can be determined
from this pressure drop. Vortices may also be formed by athrosclrotic
plaques. Within these regions of low pressure hypobaric hypoxia and
hypocarbia might exist. Consider the local metabolic implications.
Hypobaric hypoxia might induce a localized lipid shift to accommodate
the accompanying loss in efficiency of ATP resynthesis by oxidative
phosporylation. Any hypocarbia induced might also increase the local rate
of lipid uptake and consumption by increasing the efficiency of oxidative
phosporylation by mass action. If the anaerobic threshold is approached,
intuitively an unlikely event in an artery, oxidative phosporylation will
be inhibited and anaerobic glycolysis stimulated precipitating a fall in
intimal pH but not necessarily free radical release because of the
accompanying hypobaric hypoxia.
In these circumstances free radicals might be responsible for
increasing metabolic rate to accommodate the decrease in efficiency of ATP
resynthesis, by increasing temperature. If so this hypothetical
compensatory mechanism might be compromised and a decline in energy charge
large enough to cause functional impairments induced. If larger apoptosis
and even necrosis with its accompanying inflammatory changes might occur
within the intima and/or media.
One of the functional impairments that might hypothetically be
induced, short of apoptosis or necrosis and inflammation, at bifurations
and in stenotic plaques is the ability of HDL to remove cholesterol from
vessel walls and carry it to the liver where it is can be removed from
blood. In other words a venturi effect might create the metabolic
circumstances in which cholestrol deposition and plaque formation and
growth ate promoted with the passage of time. They might also create
circumstances in which the likelihood of plaque rupture is also increased.
These circumstances should not exist in veins.
References
1. Ramarathnam Krishna Kumar and Komarakshi R. Balakrishnan
Influence of lumen shape and vessel geometry on plaque stresses: possible
role in the increased vulnerability of a remodelled vessel and the
"shoulder" of a plaque
Heart 2005; 0: hrt.2004.049072v1
The recent review of stress echocardiography in Heart is a good
overview of a technique which has clearly come of age [1]. However it
really is time that the echo community stopped being so defensive about
the alternative technique of myocardial perfusion scintigraphy (MPS).
In November 2003 the National Institute for Clinical Excellence
(NICE) published the positive results of its Technolo...
The recent review of stress echocardiography in Heart is a good
overview of a technique which has clearly come of age [1]. However it
really is time that the echo community stopped being so defensive about
the alternative technique of myocardial perfusion scintigraphy (MPS).
In November 2003 the National Institute for Clinical Excellence
(NICE) published the positive results of its Technology Appraisal 73,
entitled “Myocardial perfusion scintigraphy for the diagnosis and
management of angina and myocardial infarction” [2]. The value of
myocardial perfusion scintigraphy (MPS) as a mature diagnostic and
prognostic investigation was recognised, and it was estimated that an
approximately four-fold increase in MPS activity in the UK might be
appropriate. The Appraisal has aroused much controversy, particularly from
proponents of stress echocardiography, who feel that NICE should have
considered the full range of non-invasive tests available for patients with
known or suspected coronary disease. This grievance has spilled over into
the review cited above, and the authors have erred in making ill-informed
negative comments about MPS.
The stock objections to MPS raised by the authors are that “its
widespread use is limited by cost, radiation, and relative lack of
availability” [1]. It is time that these myths were dispelled, beginning
with the cost argument. A small-field-of-view dedicated cardiac gamma
camera now costs the same as a decent echo machine, and both require one
member of staff for scanning and a similar sized room. The facilities
required for stress in terms of space, hardware, and staff (usually two in
the room) are independent of the imaging modality being used. The cost of
consumables is roughly the same for both imaging modalities, and is
dominated by the price of the radiopharmaceutical (MPS) or echo contrast
agent (stress echo). One important advantage of MPS is that, compared with
other modalities, the imaging side of MPS is fixed and automated so that
the requirement for “hands-on” consultant time (an expensive resource in
the NHS) is limited to reporting. Ultimately, any difference in the cost
per patient between modalities is largely a function of patient
throughput, which can be extremely efficient using MPS with a dedicated
cardiac gamma camera (more than 2000 patients per year).
The radiation argument is specious. The effective dose equivalent
from a MPS study performed using a modern technetium-99m-based tracer is
10mSv, which is similar to that from a coronary angiogram or CT scan [3].
In a healthy 40 year old male, after a 10 year latency period, this
confers an increased risk of developing cancer of 1 in 3000, compared with
a background lifetime risk of 1 in 6. Radiation exposure is (rightly in
our opinion) not a consideration when deciding, for example, whether a
patient should have an abdominal CT scan instead of an abdominal
ultrasound, or prior to coronary angiography, and so the focus on nuclear
medicine procedures in this regard is difficult to understand.
The argument that MPS in inherently more difficult to set up and
therefore less available than other imaging modalities is demonstrably
false internationally. In a recent European survey of 3779 patients
presenting to a cardiologist with angina, a stress-based imaging test was
performed in 18% of cases [4]. This test was MPS in 95% of patients in
northern Europe (including the UK), 91% in the Mediterranean, 84% in
western Europe, and 66% in central Europe: clearly our European colleagues
are unaware that MPS is more difficult to set up than its alternatives.
The only real difficulty, particularly in the UK, is the tight regulatory
framework which governs nuclear medicine procedures. However, the majority
of reasonably sized district general hospitals already have a nuclear
medicine department, and so the framework is almost always already in
place.
The real reason that MPS has been slow to be adopted in the UK is
“political”. MPS, in contrast to other cardiac imaging techniques, is
usually performed by radiologists and nuclear physicians rather than
cardiologists. This makes alternative cardiologist-led techniques such as
stress echocardiography more attractive when a functional imaging test is
required. The answer to this is not to disparage MPS itself, but to
motivate cardiologists to become more involved. This has occurred in the
USA, where more than 20,000 MPS studies per million population per year
are currently performed (compared with 5000 across Europe and just over
1000 in the UK).
In reality, The UK is so far behind the rest of the developed World
in terms of noninvasive imaging for coronary disease that squabbles
between the proponents of the various imaging modalities are an unhelpful
distraction. The clinical information provided by all of the stress-based
imaging tests, when performed by appropriately skilled staff, is more-or-less equivalent. It matters little how many of the 4000 patients pmp per
year identified by NICE undergo stress echocardiography rather than MPS:
if the wider cardiology community accepts that functional imaging is a
valuable exercise, there will be more than enough work for all of us.
References
[1] Senior R, Monaghan M, Becher H, Mayet J, Nihoyannopoulos P.
Stress echocardiography for the diagnosis and risk stratification of
patients with supected or known coronary artery disease: a critical
appraisal. Heart 2005; 91: 427-436.
[3] Picano E. Informed consent and communication of risk from
radiological and nuclear medicine examinations: how to escape from a
communication inferno. BMJ 329: 849-51.
[4] Daly CA, Clemens F, Lopez Sendon JL, Tavazzi L, Boersma E,
Danchin N, et al. The clinical characteristics and investigations planned
in patients with stable angina presenting to cardiologists in Europe: from
the Euro Heart Survey of Stable Angina. Eur Heart J 2005 (E-published
ahead of print).
At the outset let me thank Dr. Zhi Young Li for his observations and
the following is my reply:
Li: Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it.
At the outset let me thank Dr. Zhi Young Li for his observations and
the following is my reply:
Li: Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it.
Reply: I understand that Dr. Li may want us to use singular
elements? We do not consider that such special elements are required. In
this case there is no crack tip and is a simple bimaterial interface. We
are not studying the effect of sharp bimaterial interface, as the sharp
edge is more mathematical than physical. There is no crack tip singularity
and the bimaterial is assumed to be perfectly bonded. All results are for
far field stresses as seen from the figure itself. We have used a hybrid
element which takes care of incompressibility. Also, we have done a mesh
sensitivity study and the results presented are for the optimized mesh.
Li: Secondly, in figure 4a and figure 4b, the results showed maximal
stress actually in the opposite side of the plaque, which is in grey. This
is not in the shoulder region which is in red. This is due to the very
thin fibrous in that region.
Reply: Yes, the observation is true and we agree. But our interest is
only to find the maximum stress in proximal regions to the lipid since the
rupture of the cap is the main interest.
Li: Thirdly, figure 4c doesn’t prove anything, and it possibly is
wrong. Thin fibrous cap does result in high stress concentration in the
thin fibrous region. The result shows the stress only increases in the
other parts of the fibrous cap but not in the shoulders, which seems
incorrect.
Reply: It may be noted that the graph is plotted from 0 deg. to 90
deg. which is the major axis of the elliptical lumen. What is reported is
for the variation of lipid thickness at the minor axis. The stresses do
increase with lipid thickness as seen from the figure in this region. As
one moves to the shoulder the lipd increase in terms of thickness is low.
In other words, the increase in lipid increases the stresses only locally
and is one of the major emphasis of the paper. This is clearly brought out
in 6c and 6d.
Li: Fourthly, in figure 5a, maximal stress decreases when degree of
stenosis increases. This is due to the lumen is decreased with large
stenosis, and this results in less loading (pressure) applied on the lumen
wall. This certainly decreases the maximal stress on the fibrous cap. The
same lumen areas should be chosen when comparing the stenosis effect.
Reply: What Dr. Li states is the essence of Laplace law
which we have quoted. Engineers konw this for pressure vessels where
stress is directly proportional to radius of curvature for a given
internal pressure. We have not varied the area as the idea is to compare
stresses for the same pressure. Also in a given artery one cannot choose
the same area and vary the stenosis!
Li: Finally, the finite element method needs to be refined for this
model. The FEM actually affected the results (including figure 7), and
resulted incorrect conclusion.
Reply: As we have stated before what we have reported is for the
optimized mesh. Also the mesh density is retained for all the study and
hence will not enter into the major conclusions. The increase in stress
for the same pressure is again due to Law of Laplace as stated before and
in the text.
We agree that the lack of drug specificity indicates that other
factors, such as those relating to underlying depression, may explain the
associations we have found with myocardial infarction. If amelioration of
depression reduces the risk of myocardial infarction, then, yes,
antidepressants may reduce the risk of later MI. Our data indicate that
people with remaining time on antidepressants for a l...
We agree that the lack of drug specificity indicates that other
factors, such as those relating to underlying depression, may explain the
associations we have found with myocardial infarction. If amelioration of
depression reduces the risk of myocardial infarction, then, yes,
antidepressants may reduce the risk of later MI. Our data indicate that
people with remaining time on antidepressants for a longer period than 28
days do have a lower point estimate risk of MI, however the confidence
intervals for these risk estimates crossed 1.
Why should lipid lowering drugs be associated with an increased risk
of developing peripheral neuropathies [1,2]? For the same reason that
rapid glycaemic control might be [3]? That would imply that fatty acids can
be used as a substrate for oxidative phosphorylation in the brain just as
it is peripherally and the current view is that it cannot. The brain can
use glucose and in some circumstances ket...
Why should lipid lowering drugs be associated with an increased risk
of developing peripheral neuropathies [1,2]? For the same reason that
rapid glycaemic control might be [3]? That would imply that fatty acids can
be used as a substrate for oxidative phosphorylation in the brain just as
it is peripherally and the current view is that it cannot. The brain can
use glucose and in some circumstances ketone bodies but it is claimed not
fatty acids.
What almost every in vitro biochemical experiment has done has been
to buffer pH and gas with 95% O2 and 5% CO2. [That is a highly abnormal
state]. What is more the liver has been excluded and hence the opportunity
for recycling anaerobic metabolites and maintaining ATP resynthesis by
anaerobic glycolysis. [The same applies to almost every in vitro
experiment that has been performed on the heart]. In any event the brain
[and even the heart] contains large amounts of lipid [4] a significant
portion of which must exist in mobile pools.
Might a lipid shift increase the efficiency of ATP resynthesis during
reductive stress in the brain just as it has been proposed to do
peripherally? Being highly diffusable ketone bodies might operate a
particularly effective shuttle analogous to that proposed in the lactate
shuttle hypothesis. If so might lipid lowering drugs compromise this in
patients exposed to some degree of reductive stress and who might have
become dependent upon this source of nutrient for efficient neurological
energy metabolism as proposed might be the case in diabetics?
References
1. Corrao G, Zambon A, Bertu L, Botteri E, Leoni O, Contiero P. Lipid
lowering drugs prescription and the risk of peripheral neuropathy: an
exploratory case-control study using automated databases.
J Epidemiol Community Health. 2004 Dec;58(12):1047-51.
2. G Corrao, A Zambon, L Bertù, E Botteri, O Leoni, and P Contiero
Lipid lowering drugs prescription and the risk of peripheral neuropathy:
an exploratory case-control study using automated databases
Heart 2005; 91: 560.
3. Grounds for abandoning "diabetes" as a diagnosis?
Richard G Fiddian-Green (9 March 2005) eLetter re: M K S Leow and J
Wyckoff
Under-recognised paradox of neuropathy from rapid glycaemic control
Postgrad Med J 2005; 81: 103-107.
4. Isabelle Carriéa,b, Michel Clémenta, Dominique de Javelb,
Henriette Francèsa, and Jean-Marie Bourrea Specific phospholipid fatty
acid composition of brain regions in mice: effects of n;–3 polyunsaturated
fatty acid deficiency and phospholipid supplementation Journal of Lipid
Research, Vol. 41, 465-472, March 2000.
The article using a FE model described the biomechanics of plaque
rupture, which is very interesting. However, there are a few points that I
disagree.
Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it....
The article using a FE model described the biomechanics of plaque
rupture, which is very interesting. However, there are a few points that I
disagree.
Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it.
Secondly, in figure 4a and figure 4b, the results showed maximal stress
actually in the opposite side of the plaque, which is in grey. This is not
in the shoulder region which is in red. This is due to the very thin
fibrous in that region.
Thirdly, figure 4c doesn’t prove anything, and it possibly is wrong. Thin
fibrous cap does result in high stress concentration in the thin fibrous
region. The result shows the stress only increases in the other parts of
the fibrous cap but not in the shoulders, which seems incorrect.
Fourthly, in figure 5a, maximal stress decreases when degree of stenosis
increases. This is due to the lumen is decreased with large stenosis, and
this results in less loading (pressure) applied on the lumen wall. This
certainly decreases the maximal stress on the fibrous cap. The same lumen
areas should be chosen when comparing the stenosis effect.
Finally, the finite element method needs to be refined for this
model. The FEM actually affected the results (including figure 7), and
resulted incorrect conclusion.
The lack of difference between the size of the effects associated
with tricyclic and selective serotonin reuptake inhibitor antidepressants
points to some intrinsic characteristic of the underlying depressive
disorder which determined the increased risk of myocardial infarction.
Actually, these antidepressants may even have reduced the risk of
myocardial infarction later.
Dear Editor,
We thank Dr Kelion for his helpful comments regarding our recent review on stress echocardiography in Heart [1]. We entirely agree with Dr Kelion that both British Society of Echocardiography and British Nuclear Cardiac Society need to raise awareness of the utility of functional tests for the assessment of coronary artery disease and not squabble about which technique is superior. Given the fact tha...
Dear Editor,
While the role of internal defibrillator, as a life-saving device, is established in Brugada syndrome, drugs like betablockers may precipitate a Brugada phenotype and are ineffective in this syndrome, therefore not recommended [1].
Reference
1. Charles Anzelevitch, Pedro Brugada, Martin Borggreffe. Brugada syndrome. Report of the second consensus conference. Circulation. 200...
Dear Editor,
It is well known the relationship between coronary anomalies and other congenital cardiac abnormalities [1-2]. Indeed, association between atrial septal defect and coronary anomalies has been previously described and in this situation compression of the anomalous coronary artery can occur when septal defects is percutaneously closed [3-4]. We suggest that a transesophageal ecocardiogram should be don...
Dear Editor,
I have never seen a satisfactory hypothesis to account for the occurrence and distribution of atheromatous deposits in arteries but not veins. One possibility is a Venturi effect, induced by anatomical, physiological and pathological changes in the geometry in arteries but not in veins, accounts for the differences. Might such a effect account for the increased vulnerability of a remodelled vessel...
Dear Editor,
The recent review of stress echocardiography in Heart is a good overview of a technique which has clearly come of age [1]. However it really is time that the echo community stopped being so defensive about the alternative technique of myocardial perfusion scintigraphy (MPS).
In November 2003 the National Institute for Clinical Excellence (NICE) published the positive results of its Technolo...
Dear Editor,
At the outset let me thank Dr. Zhi Young Li for his observations and the following is my reply:
Li: Firstly, the geometries were used with two sharp angles in the shoulder regions, which will cause errors for FEA simulation. Special method needs to use in this regions for correct results, while the authors didn’t do anything with it.
Reply: I understand that Dr. Li may wa...
Dear Editor,
We agree that the lack of drug specificity indicates that other factors, such as those relating to underlying depression, may explain the associations we have found with myocardial infarction. If amelioration of depression reduces the risk of myocardial infarction, then, yes, antidepressants may reduce the risk of later MI. Our data indicate that people with remaining time on antidepressants for a l...
Dear Editor,
Why should lipid lowering drugs be associated with an increased risk of developing peripheral neuropathies [1,2]? For the same reason that rapid glycaemic control might be [3]? That would imply that fatty acids can be used as a substrate for oxidative phosphorylation in the brain just as it is peripherally and the current view is that it cannot. The brain can use glucose and in some circumstances ket...
Dear Editor,
The article using a FE model described the biomechanics of plaque rupture, which is very interesting. However, there are a few points that I disagree.
Firstly, the geometries were used with two sharp angles in the shoulder regions, which will cause errors for FEA simulation. Special method needs to use in this regions for correct results, while the authors didn’t do anything with it....
Dear Editor,
The lack of difference between the size of the effects associated with tricyclic and selective serotonin reuptake inhibitor antidepressants points to some intrinsic characteristic of the underlying depressive disorder which determined the increased risk of myocardial infarction. Actually, these antidepressants may even have reduced the risk of myocardial infarction later.
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