We thank Drs Kirchhof, Crijns and van Gelder for their interest in
our paper (1) referring pill-in-the-pocket treatment of recent-onset
atrial fibrillation (AF). The study was interrupted on the recommendation
of the data-and safety-monitoring committee because the results suggested
that the intravenous administration of flecainide or propafenone does not
predict the occurrence of adverse effects after a loading oral dos...
We thank Drs Kirchhof, Crijns and van Gelder for their interest in
our paper (1) referring pill-in-the-pocket treatment of recent-onset
atrial fibrillation (AF). The study was interrupted on the recommendation
of the data-and safety-monitoring committee because the results suggested
that the intravenous administration of flecainide or propafenone does not
predict the occurrence of adverse effects after a loading oral dose of
these drugs. A 5% incidence of major side effects during the first out-of-
hospital treatment was regarded as high, considering that such patients
have haemodynamically well-tolerated episodes of AF. All the patients
showing major side effects during the first loading oral dose were
receiving treatment with propafenone. No patient receiving flecainide had
major adverse effects; however, only 20 patients were on treatment with
this drug. This patient population is too small to draw conclusions
whether tolerance to intravenous administration of flecainide may predict
the safety of the pill-in-the-pocket treatment. We wrote (1) that "further
data on larger population samples should be collected in order to assess
the predictive ability of an intravenous testing with flecainide". We
agree with Dr Kirchhof et al that the bradyarrhythmias observed after a
loading oral dose of propafenone may be an expression of a latent sick
sinus syndrome. The 4 patients showing major adverse effects during the
first out-of-hospital treatment were ? 70 years old and this suggests that
the pill-in-the-pocket treatment could not be indicated in the elderly
because in this age group latent sick sinus syndrome may be more frequent.
However, because of the premature interruption of the study, the patient
population is too small to draw any conclusion. We carried out the present
study because the pill-in-the-pocket approach is underused since the
guidelines (2 ) recommend an in-hospital loading oral dose of flecainide
or propafenone as a screening for the out-of-hospital self-administration,
but the doctors of the Emergency rooms prefer intravenous administration,
which has a more rapid action than the time-consuming oral administration.
In the real world, the recording of 24-hours ECG before intravenous
administration of the drug is not feasible; moreover, we believe that a
prolonged ECG recording during AF is not useful to identify patients with
latent sick sinus syndrome. Only 7 patients were treated with
betablockers and none took verapamil or diltiazem. None of the 4 patients
showing major adverse effects during the first out-of-hospital treatment
took beta-blockers. We did not report the use of ACE-inhibitors and
angiotensin receptor blockers because in the first pill-in-the-pocket
study (3) there was not any correlation between the assumption of these
drugs and major side effects.
In our opinion, the present knowledge suggests that patient's tolerance to
intravenous administration of propafenone does not seem to predict adverse
effects during out-of-hospital self administration of this drug. At
present, the predictive ability of an intravenous testing with flecainide
represents an unsolved issue.
Paolo Alboni, Giovanni L. Botto, Giuseppe Boriani, Giovanni Russo,
Federico Pacchioni, Matteo Iori, Giovanni Pasanisi, Marina Mancini,
Barbara Maricanti, Alessandro Capucci
REFERENCES
1) Alboni P,Botto GL, Boriani G, et al. Intravenous administration of
flecainide or propafenone in patients with recent-onset atrial
fibrillation does not predict adverse effects during "pill-in-the-pocket"
treatment. Heart 2010; 96: 546-9.
2) Fuster V, Ryd?n LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for
the management of patients with atrial fibrillation. A report of the
American College of Cardiology/American Heart Association Task Force on
practice guidelines and the European Society of Cardiology for practice
guidelines (writing committee to revise the 2001 guidelines for the
management of patients with atrial fibrillation). Eur Heart J 2006; 27:
1979-2030.
3) Alboni P, Botto GL, Baldi N, et al. Outpatient treatment of recent-
onset atrial fibrillation with the "pill-in-the-pocket" approach. N Engl J
Med 2004; 351:2384-91.
In their Viewpoint article, Warner et al hypothesized that the
administration of aspirin to patients who are treated with potent
antagonists of the platelet P2Y12 receptors might increase cardiovascular
risk.1 The authors' hypothesis is based on the observation that P2Y12
antagonists inhibit the platelet production of thromboxane A2 (TxA2)
(which would render the use of aspirin superfluous), and on the
consideration tha...
In their Viewpoint article, Warner et al hypothesized that the
administration of aspirin to patients who are treated with potent
antagonists of the platelet P2Y12 receptors might increase cardiovascular
risk.1 The authors' hypothesis is based on the observation that P2Y12
antagonists inhibit the platelet production of thromboxane A2 (TxA2)
(which would render the use of aspirin superfluous), and on the
consideration that aspirin may cause adverse effects. It is my opinion
that there is no evidence yet to suggest that aspirin is superfluous or
even detrimental when administered in combination with P2Y12 antagonists.
In fact, the inhibition of TxA2 production by P2Y12 antagonists in
monotherapy is incomplete and may be insufficient to inhibit the TxA2-
dependent component of thrombus formation. The clinical relevance of
effective TxA2 inhibition is demonstrated by the extremely good efficacy
of aspirin in patients with acute coronary syndromes (ACS),2 which, in my
opinion, was underestimated by Warner et al.1 I think that the real
question is not whether or not aspirin should be associated with P2Y12
antagonists, but, rather, what is the best dose of aspirin to be used in
association. We recently showed that inhibition of the platelet P2Y12
receptor potentiates the anti-platelet effect of prostacyclin and
hypothesized that this effect may substantially contribute to the
antithrombotic efficacy of P2Y12 antagonists.3 Since aspirin, at high
doses, inhibits the endothelial production of prostacyclin, it can be
hypothesized that, the higher the dose of aspirin used in combination with
P2Y12 antagonists, the lower will be the prostacyclin-dependent
antithrombotic activity of P2Y12 antagonists.3 The results of the PLATO
trial, which showed that high-dose aspirin tended to be less effective
than low-dose aspirin in ACS patients treated with the potent P2Y12
antagonist ticagrelor,1 are compatible with our hypothesis and with the
suggestion by Warner et al that high-dose aspirin may be more detrimental
when associated with potent P2Y12 antagonists.1 However, the results of
the CURRENT OASIS-7 trial, which showed that high dose-aspirin was more
effective than low-dose aspirin in combination with high-dose clopidogrel
(but not with standard dose clopidogrel) oppose it.4 Therefore, the issue
of the best dose of aspirin to be associated to P2Y12 antagonists can only
be settled by the results of properly designed experimental studies.
REFERENCES
1. Warner TD, Armstrong PCJ, Curzen NP, Mitchell JA. Dual
antiplatelet therapy in cardiovascular disease: does aspirin increase
clinical risk in the presence of potent P2Y12 receptor antagonists? Heart
2010;96:1693-1694.
2. ISIS-2 (Second International Study of Infarct Survival) Collaborative
Group. Randomised trial of intravenous streptokinase, oral aspirin, both,
or neither among 17,187 cases of suspected acute myocardial infarction:
ISIS-2. Lancet.1988;2:349-60.
3. Cattaneo M, Lecchi A. Inhibition of the platelet P2Y12 receptor for
adenosine diphosphate potentiates the antiplatelet effect of prostacyclin.
J Thromb Haemost. 2007;5:577-82.
4. CURRENT-OASIS 7 Investigators, Mehta SR, Bassand JP, Chrolavicius S,
Diaz R, Eikelboom JW, Fox KA, Granger CB, Jolly S, Joyner CD, Rupprecht
HJ, Widimsky P, Afzal R, Pogue J, Yusuf S. Dose comparisons of clopidogrel
and aspirin in acute coronary syndromes. N Engl J Med. 2010;363:930-42.
In their recent editorial in this Journal Theodoraki and Bouloux [1]
question the cut-off values employed in our article on the association
between circulating androgens and mortality risk in heart failure (HF).[2]
While we (according to our local Central Hospital Laboratory) defined
androgen deficiency by total testosterone values <180 ng/dl for
patients >50 years and 260 ng/dl for younger patients, and by free
te...
In their recent editorial in this Journal Theodoraki and Bouloux [1]
question the cut-off values employed in our article on the association
between circulating androgens and mortality risk in heart failure (HF).[2]
While we (according to our local Central Hospital Laboratory) defined
androgen deficiency by total testosterone values <180 ng/dl for
patients >50 years and 260 ng/dl for younger patients, and by free
testosterone values <9 ng/dl, Theodoraki and Bouloux - referencing
Wang et al. [3] - suggest a more liberal and age-independent cut-off value
for total testosterone (<230 ng/dl), but a more restrictive cut-off
level for free testosterone (<6.5 ng/dl). If these alternative cut-off
levels were applied to our data, prevalence of androgen deficiency defined
by total testosterone would hardly be affected (15 instead of 9%), while
it would be markedly reduced if defined by free testosterone (from 79 to
51%). Since we performed all survival analyses using continuous rather
than categorized variables, however, these considerations do not affect
the main finding of our study, namely the lacking association between
androgen levels and mortality risk after adjustment for important
confounders. We agree, however, that reaching a consensus on both
standardized testosterone measurement and definition of (possibly age-
dependent) cut-off values is mandatory in order to establish direct
comparability between studies.
Current guidelines advocate testosterone replacement only in
"symptomatic" patients with repeatedly "low" testosterone levels.[4] HF,
like any chronic illness, profoundly affects sex steroid metabolism, and
better understanding of underlying pathologies is warranted to disentangle
the cause-effect relations in this situation. Theodoraki and Bouloux build
their line of arguments on two small trials on testosterone therapy in
patients with HF, which were considered positive as they improved
patients' symptoms. However, the authors omit to comment on the liberal
inclusion criteria not demanding established testosterone deficiency (in
both studies prevalence of androgen deficiency <30%), and on the very
high drop-out rate in one study. We would conclude that liberal
testosterone therapy in patients with HF is presently not justified since
conclusive evidence of benefit is lacking, pathophysiology is ill
understood, and important safety concerns are unresolved.[4, 5]
1 Theodoraki A, Bouloux PM. Low sex hormones in heart failure.
Heart;96:496-7.
2 Guder G, Frantz S, Bauersachs J, et al. Low circulating androgens
and mortality risk in heart failure. Heart;96:504-9.
3 Wang C, Nieschlag E, Swerdloff R, et al. ISA, ISSAM, EAU, EAA and
ASA recommendations: investigation, treatment and monitoring of late-onset
hypogonadism in males. Int J Impot Res 2009;21:1-8.
4 Bhasin S CG, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS,
Montori VM. Testosterone Therapy in Men with Androgen Deficiency
Syndromes: An Endocrine Society Clinical Practice Guideline. J Clin
Endocrinol Metab 2010;Jun;95(6)::2536-59.
5 Basaria S, Coviello AD, Travison TG, et al. Adverse events
associated with testosterone administration. N Engl J Med;363:109-22.
To the editor: With great interest we have read the paper on
hypertrophic cardiomyopathy by ten Berg et al.1 As the paper has an
educational aim, we would like to address some minor misconceptions that
could have major implications.
Genotyping in HCM to establish a molecular diagnosis in HCM patients
can indeed probably not be used to guide prognosis or therapy. However, it
has been proven to be a more cost-effe...
To the editor: With great interest we have read the paper on
hypertrophic cardiomyopathy by ten Berg et al.1 As the paper has an
educational aim, we would like to address some minor misconceptions that
could have major implications.
Genotyping in HCM to establish a molecular diagnosis in HCM patients
can indeed probably not be used to guide prognosis or therapy. However, it
has been proven to be a more cost-effective strategy than cardiac
screening to identify relatives at risk.2 This is mainly due to the
inability of ECG and echocardiography to exclude a future risk of HCM -
which is possible by genotyping-, because contrary to what the authors
state hypertrophy in relatives often develops after adolescence. Studies
in HCM mutation carriers have shown that disease penetrance increases with
age and a significant subset of carriers develops hypertrophy well into
adulthood.3 4 Unfortunately the misconception that hypertrophy does not
develop after adolescence is still around leading to inappropriate cardiac
care and sometimes even sudden cardiac death, because relatives are
incorrectly discharged from cardiac follow-up.
The incomplete and age dependent disease penetrance together with the
clinical heterogeneity of the disease also explain why many HCM patients
do not know of any affected relatives. The latter is therefore probably
not due to sporadic mutation and more complex patterns of inheritance as
the authors suggest. With today's knowledge the main causal genetic defect
arises seldom de novo and is usually inherited in an autosomal dominant
way. Individuals without the disease-causing mutation therefore do not
have an increased risk of developing HCM and carriers do. Clinical
heterogeneity and disease penetrance, however, are likely to be influenced
by genetic modifiers, which still need to be identified. Hopefully, future
genetic research in HCM will enable us to better predict the phenotype and
prognosis in the individual HCM patient or carrier of a disease-causing
mutation.
References
1. ten Berg J, Steggerda RC, Siebelink HM. Myocardial disease: the
patient with hypertrophic cardiomyopathy. Heart 2010;96:1764-72.
2. Wordsworth S, Leal J, Blair E, et al. DNA testing for hypertrophic
cardiomyopathy: a cost-effectiveness model. Eur Heart J 2010;31:926-35.
3. Niimura H, Bachinski LL Sangwatanaroj S, et al. Mutations in the
gene for cardiac myosin binding protein C and late-onset familial
hypertrophic cardiomyopathy. N Engl J Med 1998;338:1248-57.
4. Christiaans I, Birnie E, van Langen IM, et al. The yield of risk
stratification for sudden cardiac death in hypertrophic cardiomyopathy
Myosin-Binding Protein C gene mutation carriers: focus on predictive
screening. Eur Heart J 2010;31:842-8.
It was with interest that we read the featured correspondence from
Rajani et al (ref). We entirely agree with their assertion that there is
a growing need for multi-modality cardiac imagers and acknowledge their
concerns about the lack of structured "in-programme" training
opportunities, such as cardiac imaging fellowships, to support this
requireme...
It was with interest that we read the featured correspondence from
Rajani et al (ref). We entirely agree with their assertion that there is
a growing need for multi-modality cardiac imagers and acknowledge their
concerns about the lack of structured "in-programme" training
opportunities, such as cardiac imaging fellowships, to support this
requirement.
As an initial step, The British Society of Cardiovascular Imaging (BSCI)
has recently followed the lead of the British Society of Cardiovascular
Magnetic Resonance (BSCMR) in producing detailed competency frameworks for
cardiac CT, incorporating competency based assessment tools such as Mini
CEX, DOPS and CbD to support the evolving cardiac imaging curricula
produced by the respective Royal Colleges. This, in conjunction with
other training frameworks, will hopefully allow a structure for more
formalised imaging training in the UK.
As is noted by Rajani et al some deaneries have started delivering
dedicated training in cardiovascular imaging and indeed the BSCI is now
running twice yearly core training days in cardiovascular CT, open to all
trainees and consultants alike as part of the overall cardiac imaging
training run with the Royal Society of Medicine. These conferences are
delivered essentially at cost to recognise and to provide for the growing
requirement for dedicated multi-modality imaging training for radiologists
and cardiologists alike.
As a next step, the BSCI, in conjunction with London STC in cardiology and
head of radiology training in London, have set up six formal, structured,
in-programme fellowships in cardiac CT that are to be launched imminently.
This model has previously been developed and successfully delivered for
CMR colleagues in London and it provides aspirant trainees the opportunity
to gain on-site experience at established centres of excellence. This
hands-on training is supported by a monthly lecture series to cover the
didactic training and knowledge components of the advanced curriculum. At
the core of this endeavour is to provide high quality training in cardiac
imaging within the current constraints of the curriculum, to equip
trainees with the skills required to be able to lead and direct cardiac
imaging services in the future. It is our hope that this model may be
able to be reproduced across other regions and also across the wider remit
of cardiac imaging modalities.
There are however significant hurdles to be overcome. Firstly cardiac
imagers must seek to both work and train collaboratively. They must start
engaging with each other, regardless of chosen specialty, from the outset
and bring their differing skills and approaches to each other to enhance
the service delivered by all. Secondly, there is a clear requirement for
these individual training opportunities to be brought together as true
multi-modality imaging fellowships. Thirdly, if the four main cardiac
imaging societies (BNCS, BSCI, BSCMR and BSE) could sign up to a formal
concordat ensuring joint advertising of training opportunities, running
joint or concurrent meetings and providing a forum to develop advanced
subspecialty "in programme" fellowships, open to all cardiac imagers at
affordable costs, this would be a major step towards making cardiac
imaging training more robust and comprehensive. Very few cardiac imagers
practice in isolation from other cardiac imaging modalities and a broad
understanding of complementary techniques is fundamental to high quality
care. The formation of the British Cardiac Society Imaging Council has
been an important initial step and would seem the obvious vehicle to
facilitate these goals.
Achieving the vision set by Rajani et al will require significant
cooperation by cardiac imagers in the broadest sense. There will no doubt
be significant challenges along the way but by achieving this goal we will
be a stronger community both nationally and internationally but most
importantly locally for our patients.
Acknowledgements:
Dr Ed Nicol is a London cardiology SpR and trainee representative on the
BSCI Executive and Education Committees
Dr Stephen Harden is a consultant cardiac radiologist in Southampton,
chairs the BSCI Education Sub-committee and is a regional training lead in
Radiology
Dr Roger W Bury is a consultant cardiac radiologist in Blackpool and the
President of the BSCI.
It is with great interest to read a recent article of " Evidence of
the role of short-term exposure to ozone on ischaemic cerebral and cardiac
events: the Dijon Vascular Project (DIVA)" by Henrotin et al.1 They
detailed addressed the analysis procedure and considerations and presented
findings on the relationship of air pollution and ischaemic cerebral and
cardiac events in a large population-based setting. However, a few...
It is with great interest to read a recent article of " Evidence of
the role of short-term exposure to ozone on ischaemic cerebral and cardiac
events: the Dijon Vascular Project (DIVA)" by Henrotin et al.1 They
detailed addressed the analysis procedure and considerations and presented
findings on the relationship of air pollution and ischaemic cerebral and
cardiac events in a large population-based setting. However, a few
methodological considerations need to be further discussed.
The human body is affected by the thermal environment, which is not
only air temperature and rain. A potential environment risk factor is, in
fact, influenced by many different climatic factors such as air
temperature, air humidity, vapor pressure, wind speed, cloud cover,
radiation flux, etc. Thus, meteorological conditions adjusted in the model
may not be appropriate from an epidemiological point of view since the
assumption was based on a significant association between climactic
variables and ischaemic cerebral and cardiac events. Yet, this was not
clearly addressed in the article in firstly evaluating if the association
existed.2 If there is no association, is it still appropriate to "adjust"
meteorological conditions for air pollution assessment? In addition, when
considering meteorological variables, wind speed, cloud cover, radiation
flux, etc also have certain influences on human beings besides air
temperature and humidity. Is it appropriate to ignore in the assessment?
Finally, sex difference examination is recommended since females may be
more sensitive to the environmental change than males.
Given that conflicting results exist worldwide, a suggestion is to
have a physically equivalent temperature (PET) by combining all the
relevant climatic variables to be adjusted when assessing the relationship
of air pollution and cardiovascular disease.3, 4 This may give a more
precise indication close to human experience in exposing to the weather.
No doubt, future studies are needed to firstly confirm the association of
PET and cardiovascular events and then with the effect of air pollution
before clinical practice can be made.
There is more and more evidence that the mechanical properties of the
aorta, and arterio-ventricular coupling, are of great clinical importance
in cardiovascular diseases. Therefore, we have read the manuscript of
Vitarelli et. all with great interest [1].
Whereas, given the recent evolution of ultrasound equipment and processing
tools, the idea to assess the aorta using velocity and deformation
information is interesting,...
There is more and more evidence that the mechanical properties of the
aorta, and arterio-ventricular coupling, are of great clinical importance
in cardiovascular diseases. Therefore, we have read the manuscript of
Vitarelli et. all with great interest [1].
Whereas, given the recent evolution of ultrasound equipment and processing
tools, the idea to assess the aorta using velocity and deformation
information is interesting, the way it is used by the authors is very
confusing.
They measure the velocity of one point on the aortic wall and suggest this
is related to stiffness of the wall. However, the velocity describes the
motion of the wall within the thorax rather than only the extension of the
wall due to the internal pressure (the intrinsic deformation, determined
by the pressure within and the stiffness of the vessel). As opposed to the
carotid artery, that is not showing substantial overall motion, to measure
aortic distension, the difference in motion of proximal and distal wall
has to be assessed, as described in e.g. [2]. This can easily be seen on
the m-mode (fig. 1A [1]), where the whole aorta is moving substantially
during the cardiac cycle and the velocity thus mainly describes this
motion. Additionally, from aortic pressure curves, there is no evidence of
the biphasic diastolic decrease of the aortic diameter, with a large
atrial phase, as shown in fig 1B. Whereas this motion might be an
interesting parameter to assess in pathological cases in clinical
practice, it does not directly describe the properties of the aorta. It is
much more related to the motion of the aorta by the LV and therefore
rather represents LV systolic and diastolic function.
Distensibility was calculated as D=2(As-Ad)/[Ad(Ps-Pd)]. Most authors
would not use the multiplication by 2. There also seems a problem with the
units since they report a normal average D=79 Pa-1 while published values
are in the order of 37x10-3 kPa-1 [3].
A more important problem is the assessment of radial strain (aortic wall
thinning), which is calculated from the temporal integration of strain
rate, and strain rate is assessed based on spatial differences in
velocities. To calculate this, a region of interest and a calculation
length has to be chosen. The authors used a 3mm strain length and a ROI of
2-4 mm. Looking at the implementation of the strain analysis in the
system, the experience learns that this corresponds to a range of >5 mm
used for the quantification [4]. Considering that the wall of the aorta is
not 5 mm and a scan plane close to the valve is used, it is clear that
(aliased) velocities of the blood in the RV outflow and aortic lumen are
included. Therefore, the calculated strain is not the radial deformation
(or thinning) of the aortic wall. This is clearly seen from the strain
curve in fig 1C, where it is difficult to explain why the aortic wall
would thin substantially during atrial contraction and not start thinning
fast and gradually from aortic valve closure as would be expected when
analysing pressure traces in the aorta (keeping in mind that aortic strain
is directly related to pressure so it should have a profile similar to
local aortic pressure). Additionally, the measured strain values are not
realistic. To show this, we simulated the radial strain (wall thinning) in
a tube resembling the aorta and assuming the wall is incompressible
(conservation of volume). We used a wide range of realistic parameters:
end-diastolic diameter ranging from 20-40 mm; wall thickness of 2-4 mm;
distensibility between 4x10-3 and 9x10-3 mmHg-1 for normal individuals and
between 1x10-3 and 3x10-3 mmHg-1 for hypertensives [3]; and a pressure
gradient of 45 mmHg (normals) and 70 mmHg (hypertensives) (the extreme
values from [1]). Additionally, a longitudinal strain of 1% was assumed to
account for the lengthening of the aorta during systole. Fig. 1 shows the
resulting ranges for the radial strain. In extreme conditions (certainly
not the average patient), the strain can range from 6-15 % in normals and
3-9 % in hypertensives. This is clearly substantially less than the in [1]
reported average values of 23.1 and 8.8%.
Fig 1: Left: the range of radial strain values as a function of end-
diastolic (ED) radius and wall thickness for a large distensibility range
in normals (blue) and hypertensives (red). Middle: radial strain as a
function of ED radius for a wall thickness of 2.5 mm; Right: radial strain
as a function of wall thickness for an ED radius of 12 mm
A thorough analysis of what is measured using these techniques would
be appropriate before reporting clinical results.
As reported by the authors, the measured values might correlate with
changes induced by hypertension, but they surely do not specifically
describe changes in the aortic wall. Dedicated analysis of aortic
properties should investigate measurements that directly reflect aortic
wall mechanics or blood hydrodynamics instead of statistical analysis of a
set of observations.
1. Vitarelli A, Giordano M, GermanÃÆ’ƒÃâ€Â ’ÃÆ’‚² G, Pergolini M,
Cicconetti P, Tomei F, Sancini A, Battaglia D, Dettori O, Capotosto L, De
Cicco V, De Maio M, Vitarelli M, Bruno P. Assessment of ascending aorta
wall stiffness in hypertensive patients by tissue Doppler imaging and
strain Doppler echocardiography. Heart, doi:10.1136/hrt.2010.198358, 2010.
2. Long A, Rouet L, Bissery A, Rossignol P, Mouradian D, Sapoval M.
Compliance of abdominal aortic aneurysms evaluated by tissue Doppler
imaging: Correlation with aneurysm size. Journal of Vascular Surgery,
42(1): 18-26, 2005.
3. Resnick LM, Militianu D, Cunnings AJ, Pipe JG, Evelhoch JL and Soulen
RL. Direct Magnetic Resonance Determination of Aortic Distensibility in
Essential Hypertension: Relation to Age, Abdominal Visceral Fat, and In
Situ Intracellular Free Magnesium. Hypertension. 1997;30:654-659
4. Bjastad T, Aase SA and Torp H. Velocity Sensitivity Mapping in Tissue
Doppler Images. Proceedings of the IEEE Ultrasonics Symposium, 4:1968-
1971, 2005.
To the Editor:
We thank Dr Rosenthal and Bell for their insightful editorial comments 1
relating to our study. 2 There is little doubt that until we have longer
follow-up on the incidence of potential adverse events following
coarctation stenting, some form of advanced imaging is required and this
is endorsed by ongoing large follow-up studies. 3 Although we agree that
with specific imaging techniques MRI may provide inf...
To the Editor:
We thank Dr Rosenthal and Bell for their insightful editorial comments 1
relating to our study. 2 There is little doubt that until we have longer
follow-up on the incidence of potential adverse events following
coarctation stenting, some form of advanced imaging is required and this
is endorsed by ongoing large follow-up studies. 3 Although we agree that
with specific imaging techniques MRI may provide information regarding
complications particularly in newer platinum stents, there are numerous
reports demonstrating almost complete loss of signal with stainless steel
stents when imaging with MRI. 4 Although the authors have demonstrated a
case where protrusion of the aortic wall is seen with MRI following a
stainless steel stent, smaller aneurysms have been missed (personal
communication Professor Andrew Taylor). In many countries including the
US, platinum stents are not available and stainless steel stents are
almost exclusively used. MRI as the authors point out is less available
than CT and this has implications for patient follow-up requiring patients
to travel to a specialised centre for imaging and this has had
implications on patient compliance in our region.
As the authors also point out MRI will not detect stent fractures, however
it is not true that it is only complications of these that require
intervention. It is our practice to re-stent in the setting of a
circumferential stent fracture and this may be missed with MRI. Also the
ability of MRI to demonstrate increased flow velocity distal to the stent
is very dependent on where the restenosis occurs within the stent and
where the velocity sample is acquired below the stent. CT offers excellent
in-stent imaging allowing pre-procedural planning of further intervention
and limiting unnecessary catheter procedures. It is beyond argument that
MRI offers more functional data on left ventricular dynamics however this
requires time and cost and is not usually indicated in the setting of
specific post-stent follow-up imaging.
We fully accept the radiation doses associated with CT and the authors are
correct to point out that this dose is cumulative, however the ultimate
goal of a screening tool should be to provide sensitive and specific data
to guide further management. MRI may provide this in selected cases but it
is questionable whether it will do so over the general population and over
the range of stents used in coarctation of the aorta and thus we continue
to advocate the use of CT with continued efforts to minimise radiation
doses.
References:
1. Rosenthal E, Bell A. Optimal imaging after coarctation stenting.
Heart 2010; 96:1169-71.
2. Chakrabarti S, Kenny D, Morgan G, et al. Balloon expandable stent
implantation for native and recurrent coarctation of the aorta :
prospective computed tomography assessment of stent integrity, aneurysm
formation and stenosis relief. Heart 2010; 96:1212-16.
3. Forbes TJ, Moore P, Pedra CA, et al. Intermediate follow-up
following intravascular stenting for treatment of coarctation of the
aorta. Catheter Cardiovasc Interv 2007;70:569-77.
4. Wang Y, Truong TN, Yen C, et al. Quantitative evaluation of
susceptibility and shielding effects of nitinol, platinum, and stainless
steel stents. Magn Reson Med 2003; 49:972-6.
Ullah and Stewart present a case of pacemaker-mediated tachycardia
(PMT). There are 2 specific issues that require clarification. Firstly,
the authors suggest that this was a pacemaker malfunction. I would contend
that the pacemaker was functioning appropriately as programmed (ie: it is
the programming of the pacemaker that resulted in the PMT). Hence,
programming changes can often prevent, detect and terminate PMT....
Ullah and Stewart present a case of pacemaker-mediated tachycardia
(PMT). There are 2 specific issues that require clarification. Firstly,
the authors suggest that this was a pacemaker malfunction. I would contend
that the pacemaker was functioning appropriately as programmed (ie: it is
the programming of the pacemaker that resulted in the PMT). Hence,
programming changes can often prevent, detect and terminate PMT.
Secondly, the authors applied the terms 'blanking period' to the post
-ventricular atrial refractory period (PVARP), which is misleading.
Blanking and refractory periods are functionally distinct and should not
be used interchangeably. The authors are correct in that lengthening the
PVARP can prevent PMT, but PVARP is neither a blanking period nor is
extending the blanking period the treatment for PMT.
Chew et al claim that their registry study six month survival benefits associated with clinical guideline recommendations in acute coronary syndromes 1ââ¬à suggests that invasive management resulting in revascularisation does provide a reduction in mortality, reinforcing clinical trial data that have relied upon composite ischaemic end points that have at times been inconsistent".
Chew et al claim that their registry study six month survival benefits associated with clinical guideline recommendations in acute coronary syndromes 1â₁“suggests that invasive management resulting in revascularisation does provide a reduction in mortality, reinforcing clinical trial data that have relied upon composite ischaemic end points that have at times been inconsistent".
The very best that retrospective analysis of registry data can achieve is a hypothesis. If we didnt already have numerous randomised trials in NSTEMI and in STEMI then the analysis might suggest it would be good idea to do one, but to suggest that a retrospective case control study has anything at all to contribute to the debate on the benefits of PCI in ACS above the randomised trials is statistical nonsense.
Furthermore their claim that it reinforces clinical trial data is incorrect. Clinical trial data in repeated studies and metaanalyses has shown no mortality benefit for routine early PCI in NSTEMI2,3. As far as STEMI is concerned the data does not appear to include timeliness of thrombolysis or PCI, and this is more important than which intervention is received.
Their study does raise the possibility that beta blockers are not helpful but we dont know why they were withheld so a randomised trial should be considered to answer this question. A registry study cannot.
References
1. D P Chew, F A Anderson, A Avezum, K A Eagle, G Fitzgerald, J M Gore, R Dedrick, D Brieger, for the GRACE Investigators. Six-month survival benefits associated with clinical guideline recommendations in acute coronary syndromes. Heart hrt.2009.184853 Published Online First: 7 June 2010 doi:10.1136/hrt.2009.184853
2. ODonoghue M, Boden WE, Braunwald E, et al. Early invasive vs
conservative treatment strategies in women and men with unstable
angina and non-ST-segment elevation myocardial infarction: a metaanalysis.
JAMA 2008; 300: 71-80.
3. Peters RJ, Mehta S, Yusuf S. Acute coronary syndromes without ST
segment elevation. BMJ 2007; 334: 1265-1269.
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Sir,
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The very best that...
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