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.
We read with great interest the article by Politi et al. (1) on
revascularisation of patients presenting with ST-elevation myocardial
infarction (STEMI) in the context of multivessel coronary disease, and its
accompanying Editorial. Whilst the data are interesting and hypothesis-
generating, they fall short of demanding any change in current practice
owing to a potential flaw in the study design and in the findings as
pre...
We read with great interest the article by Politi et al. (1) on
revascularisation of patients presenting with ST-elevation myocardial
infarction (STEMI) in the context of multivessel coronary disease, and its
accompanying Editorial. Whilst the data are interesting and hypothesis-
generating, they fall short of demanding any change in current practice
owing to a potential flaw in the study design and in the findings as
presented that makes it difficult to fully agree with the authors'
conclusions.
Firstly, no explanation is given for the MACE detriment seen in the
culprit-only revascularisation (COR) group; we would agree with previous
comments regarding the reasons for repeat rehospitalisation and repeat
revascularisation, that both require further clarification to understand
their importance. However, it is the high inhospital mortality rate in the
COR group compared with the staged revascularisation (SR) group that is
most perplexing: both groups would have been expected to have a similar
inhospital course given the same initial PCI strategy, with the SR group
perhaps being expected to perform better than COR at medium- or long-term
follow-up. This, along with the imbalance in patient numbers between
groups, perhaps suggests that the results are presented by treatment
received rather than by intention-to-treat (ie. patient randomised to SR
dies in hospital after initial PCI and is counted in COR group), thereby
introducing a bias that may render the results uninterpretable.
Secondly, and perhaps more importantly, the study by Qarawani et al.
(2) used to inform the power calculation to determine the sample size for
this study is not only a nonrandomised study with a huge imbalance in the
numbers within its 2 arms, but crucially is also an outlier in terms of
the difference in MACE rates between COR and CR during primary
angioplasty: inhospital MACE rates were 52% and 16.7% respectively,
compared with far more modest differences of 0 vs. 3.8% observed in the
study by Di Mario et al. (3) and 6.3 vs. 7.4% in the study by Ijsselmuiden
et al. (4). In this latter study, a randomised comparison with a similar
number of patients in the COR and CR arms as that of Politi et al. (1),
MACE rates at 1 year were still not significantly different between the
two arms (32.4 vs. 26.9%) in stark contrast to the findings described
here. Granted, these studies were performed when primary angioplasty
techniques were not as advanced as today in terms of device and
pharmacological developments, but even so it is difficult to justify the
retrospective application of a power calculation from a study that is more
contemporary (Qarawani et al. (2) published their findings in 2008, the
year after patient recruitment for the study of Politi et al (1) had
finished) simply to provide the statistical power to generate a
significant p value.
For the moment, we believe that in primary angioplasty for STEMI in
the absence of cardiogenic shock, there is not enough evidence to support
a change from the strategy of culprit-only revascularisation with a staged
approach to non-culprit lesions. Clearly we agree with the authors that
further research, likely in the form of a large multicentre randomised
trial, is needed to determine the optimal therapy for these patients.
References
1. A randomised trial of target-vessel versus multi-vessel
revascularisation in ST-elevation myocardial infarction: major adverse
cardiac events during long-term follow-up. Politi L, Sgura F, Rossi R et
al. Heart 2010; 96: 662-667.
2. Culprit only versus complete coronary revascularization during
primary PCI. Qarawani D, Nahir M, Abboud M et al. Int J Cardiol 2008; 123:
288-292.
3. Single vs. multivessel treatment during primary angioplasty:
results of the multicentre randomised HEpacoat for culprit or multivessel
stenting for Acute Myocardial Infarction (HELP-AMI) study. Di Mario C,
Mara S, Flavio A et al. Int J Cardiovasc Intervent 2004; 6: 128-133.
4. Complete versus culprit vessel percutaneous coronary intervention
in multivessel disease: A randomized comparison. Ijsselmuiden AJJ,
Ezechiels JP, Westendorp ICD et al. Am Heart J 2004; 148: 467-474.
The publication of not one but two reviews of catheter ablation for
atrial fibrillation (AF) in this week's edition of Heart is very
welcome.(1,2) The English and Welsh guidance from the National Institute
for Clinical and Public Health Excellence (NICE) was published in 2006,(3)
but a great deal of new comparative effectiveness evidence has been
published recently. However there is a significant gap...
The publication of not one but two reviews of catheter ablation for
atrial fibrillation (AF) in this week's edition of Heart is very
welcome.(1,2) The English and Welsh guidance from the National Institute
for Clinical and Public Health Excellence (NICE) was published in 2006,(3)
but a great deal of new comparative effectiveness evidence has been
published recently. However there is a significant gap in both reviews:
they fail to mention the costs of alternative treatments, or even the
risks of hospital readmission for recurrent AF.
A cost-effectiveness analysis published in 2003(4) showed that
initiating treatment with pharmacologic cardioversion (CV) cost less per
successful CV than initiating treatment with electrivcal CV in all
patients (US$1,240 versus US$1,917 p=0.002). Little information was
available about longer term costs at that time, and so the results might
look quite different now.
References
(1)Hunter RJ, Schilling RJ. Long-term outcome after catheter ablation
for atrial fibrillation: safety, efficacy and impact on prognosis. Heart
2010;96:1259-1263.
(2)Kirchhof P, Eckardt L. Atrial fibrillation: Ablation of atrial
fibrillation: for whom and how? Heart 2010;96:1325-1330.
(3) National Collaborating Centre for Chronic Conditions. Atrial
fibrillation: national clinical guideline for management in primary and
secondary care. NICE 2006. Available from:
http://guidance.nice.org.uk/CG36/Guidance/pdf/English
4) de Paola AA, Figueiredo E, Sesso R et al. Effectiveness and costs
of chemical versus electrical cardioversion of atrial fibrillation.
International Journal of Cardiology. 2003;88:157-3.
Ullah and Stewart present a case of pacemaker-mediated tachycardia
(PMT) and described it as a "malfunction of dual chamber pacing". However,
I would contend that the pacemaker is functioning appropriately, ie: it is
sensing atrial activity in the atrium and pacing (capturing) the
ventricle. The problem in PMT is the retrograde atrial activation beyond
the PVARP as described and appropriate programming of the PVARP based o...
Ullah and Stewart present a case of pacemaker-mediated tachycardia
(PMT) and described it as a "malfunction of dual chamber pacing". However,
I would contend that the pacemaker is functioning appropriately, ie: it is
sensing atrial activity in the atrium and pacing (capturing) the
ventricle. The problem in PMT is the retrograde atrial activation beyond
the PVARP as described and appropriate programming of the PVARP based on
the VA conduction time (and/or the use of PVARP extension post-PVC) will
minimise this problem. It should also be noted that the PVARP is a
refractory period and not a "blanking period" as erroneously described in
the report. The differentiation of blanking and refractory periods is
fundamental to the understanding of pacemaker programming, function and
diagnostics.
Sir,
As a "jobbing cardiologist", I am grateful for the NICE guidance on the
investigation of stable chest pain. I am grateful for the emphasis on
clinical assessment, and I am grateful for the shift away from exercise
testing. I am astonished, however, that the guideline does not say one
word about the utility of a therapeutic trial in cases of uncertainty, and
nor does the editorial by Fox & McLean. Every cardiol...
Sir,
As a "jobbing cardiologist", I am grateful for the NICE guidance on the
investigation of stable chest pain. I am grateful for the emphasis on
clinical assessment, and I am grateful for the shift away from exercise
testing. I am astonished, however, that the guideline does not say one
word about the utility of a therapeutic trial in cases of uncertainty, and
nor does the editorial by Fox & McLean. Every cardiologist knows that
chest pain which responds to nitrate is much more likely to be cardiac and
if it doesn't it is much less likely to be cardiac. Every cardiologist
knows that chest pain which responds to a beta-blocker is much more likely
to be cardiac and if it doesn't it is much less likely to be cardiac.
However many non-invasive and/or invasive investigations we perform there
will always be cases of clinical uncertainty that can't be protocolised
out of existence and will require some clinical common sense. Something
that appears to be distinctly lacking from the NICE guidance.
Fox & Mclean suggest that application of the NICE guideline would
lead to a 20% increase in invasive angiography and a 42% increase in non-
invasive imaging from the rapid-access chest pain clinic. These are
absolute rather than relative increases. This is a bizarre way of
expressing the data, if not a disingenous one. The relative increase in
invasive angiography is 83% and the relative increase in non-invasive
imaging is 717% ! These are very different headline figures and give a
much truer idea of the mountain we have to climb !
The recent editorial of Fox and Mclean concludes ââ¬à The NICE guidance on chest pain provides a series of important advances over the current status of investigation and triage of chest pain and should be welcomed by the profession 1. One of the key recommendations of the recently published National Institute for Health and Clinical excellence (NICE) guidelines for the early management of unstable...
The recent editorial of Fox and Mclean concludes â₁“The NICE guidance on chest pain provides a series of important advances over the current status of investigation and triage of chest pain and should be welcomed by the profession 1. One of the key recommendations of the recently published National Institute for Health and Clinical excellence (NICE) guidelines for the early management of unstable angina and non-ST-segment-elevation myocardial infarction is the formal assessment of individual risk of future adverse cardiovascular events using the Global Registry of Acute Coronary Events (GRACE) risk stratification score 2. GRACE is a simple risk model that is able to predict the level of risk for individual patients for both in hospital and 6-month risk of mortality and mortality or MI and is based upon outcome data derived from a large, multinational, prospective observational study of patients with an ACS (N=43 810).
Under the current guidelines, using the GRACE risk score, patients found to be at lowest risk, defined as 6-month mortality, 1.5%, would not require clopidogrel and would be managed conservatively. Similarly, patients found to be at low risk, defined as 6-month mortality of 1.5-3%, are to be treated with clopidogrel but also managed conservatively with the value of non-invasive testing questioned. In the absence of recurrent ischaemia, coronary angiography and revascularization are recommended only if predicted 6 month mortality exceeds 3%.
The NICE algorithm is based on analysis of the benefits of clopidogrel and an invasive versus conservative strategy in relation to mortality risk. However, the algorithm does not take into account risk of MI which in young patients may be considerable despite a very low risk of mortality. We propose that this is a major flaw in the guidelines for the following reasons. The trial evidence for the value of clopidogrel in ACS comes predominantly from the CURE trial, in which the main component of cardiovascular risk reduction was the significant reduction in MI with a relative risk reduction of 23% 3. Similarly, in a recent meta-analysis of 5 RCTs involving 7818 patients the main component of benefit for an invasive compared to a conservative strategy was the significant reduction in MI rather than mortality, with a relative risk reduction of 27% 4. The NICE algorithm therefore does not recommend treatments shown to significantly reduce risk of MI, to young patients at high risk of MI. For example, using the GRACE risk calculator, a 40 to 50 year old male without co-morbidities admitted with cardiac chest pain, a normal ECG and raised troponin with a heart rate of 70-89, a systolic blood pressure of at least 120mmHg, normal renal function (creatinine 71-105 ï�ÂÂmol/l) and no evidence of heart failure, the predicted 6 month mortality risk is 1% (lowest risk). The NICE algorithm for this patient does not recommend either clopidogrel (despite a very low bleeding risk) or invasive approach or mandate non-invasive testing despite a 6-month risk of nonfatal MI of 12%. If that patient also has ECG changes his predicted 6-month mortality risk is 2% (low risk) and so he would receive clopidogrel but be managed conservatively despite a predicted 6-month risk of nonfatal MI of 19%. Furthermore, as hypertension is protective in terms of mortality, if this patient was 39 years old with an admission BP of at least 160 mmHg and was admitted with a cardiac arrest in addition to ECG changes and a raised Troponin his predicted 6 month mortality is 3% (low risk) and so he would still be managed conservatively despite a predicted 6-month risk of nonfatal MI of 31 %.
Young patients therefore, with a low predicted mortality but a substantial risk of MI are not well served by the NICE guidelines that do not recommend clopidogrel in some or an invasive approach in most of these patients despite good evidence that these interventions would substantially reduce the risk of MI. Furthermore the NICE guidelines are directly opposed to the European Society of Cardiology 5 and American College of Cardiology / American Heart Association guidelines 6 in these patients which recommend an invasive strategy in patients with either elevated cardiac biomarkers or new ECG changes. Our proposal therefore, is not that the GRACE risk score is not useful in predicting risk but that it's predicted risk of both mortality and nonfatal MI should be used to make treatment decisions. Although written as a guideline for treatment, many units may choose to adopt the NICE algorithm as their hospital ACS protocol perhaps without direct physician or cardiologist involvement in individual patients. This makes it especially important that all patient groups are well served by this guidance.
References
1. Fox KAA, McLean S. Nice guidance on the investigation of chest pain. Heart 2010; 96: 903-906 (Editorials)
2. Unstable angina and NSTEMI: the early management of unstable angina and non-ST-segment-elevation myocardial infarction; Clinical guidelines CG94: March 2010; 1-360. http://www.nice.org.uk/guidance/CG94.
3. Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK; Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345(7):494-502.
4. Hoenig MR, Aroney CN, Scott IA. Early invasive versus conservative strategies for unstable angina and non-ST elevation myocardial infarction in the stent era. Cochrane Database Syst Rev. 2010;3:CD004815.
5. Bassand JP, Hamm CW, Ardissino D et al. Task Force for Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of European Society of Cardiology. Guidelines for the diagnosis and treatment of non-ST-elevation acute coronary syndromes, Eur Heart J 2007; 28: 1598-1660.
6. Anderson JL, Adams CD, Antman EM et al. ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial infarction) Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol. 2007; 50(7):e1-157.
Author Contributions
Dr Mamas Mamas and Dr Doug Fraser contributed equally to the article and text.
Conflicts of Interest
All authors declare that the answer to the questions on your competing interest form are all No and therefore have nothing to declare
The avoidance of redundant publication is the core of the editorial
task; therefore editors have established clear policies posted in their
instructions for authors. The term Redundant publication has always been
used for research reported by the same author and sent to two or more
different journals. We report here a different situation that also results
in unplanned redundant publication....
The avoidance of redundant publication is the core of the editorial
task; therefore editors have established clear policies posted in their
instructions for authors. The term Redundant publication has always been
used for research reported by the same author and sent to two or more
different journals. We report here a different situation that also results
in unplanned redundant publication.
We bring to your attention the following facts relating to the meta-
analysis published in Heart in 2009 by Zhang et al[1]. We have found out
that 4 very similar meta-analyses on the same subject were published last
year in different journals within a 6 month period, by different
investigators working at different institutions. The enclosed table
contains the relevant details of the 4 publications. Several comments are
pertinent on this issue. Neither the editors nor the authors could have
been aware of the redundancy because they were written simultaneously and
accepted on the same week of July (this information is not available for
the EuroIntervention article). Likewise, the same worrying considerations
apply to this surprising situation in that there has been a waste of
reviewers' and readers' time and published pages. It is worth noting that
both a general cardiology journal such as Heart[1] and sub speciality
ones, such as Journal of Invasive Cardiology,[2] Circulation
Cardiovascular Intervention[3] and EuroIntervention[4] have found the
article appealing. In 3 cases the publications were original articles,
while the last one was an expert review; remarkably, only one journal has
impact factor. This unfortunate coincidence could be further deleterious
for all these journals, as they will be competing for citations on the
very same topic. Although this letter focuses on the editorial aspects of
this coincidence, it is also interesting to consider that, even though the
main conclusions of the 4 articles are identical, the results of the meta-
analyses are slightly different due probably to the methods used. We have
also analyzed a possible trigger for this sudden interest in this topic,
but could not find any reasonable explanation.
References:
1.- Zhang F, Dong L, Ge J. Simple versus complex stenting strategy for
coronary artery bifurcation lesions in the drug-eluting stent era: a meta-
analysis of randomised trials. Heart. 2009;95:1676-81. Epub 2009 Jul 29.
2.- Hakeem A, Khan FM, Bhatti S, et al. Provisional vs complex stenting
strategy for coronary bifurcation lesions: Meta-analysis of randomized
trials. J Invasive Cardiol 2009;21:589-95
3.- Katritsis DG, Siontis GCM, Ioannidis JPA. Double versus single
stenting for coronary bifurcation lesions. A Meta-analysis. Cir Cardiovasc
Intervent. 2009;2:409-15
4.- Brar SJ, Gray WA, Dangas G, et al. Bifurcation stenting with drug-
eluting stents: a systematic review and meta-analysis of randomised
trials. Eurointervention 2009;5:475-84
note: the following information is formatted as a table and not
supported by your submission system. The information is paramount for the
understanding of this letter and too long to include in the text.
Brar
Article: Expert review
Journal: EuroIntervention
Submission date: N/A
Acceptance date: N/A
Publication date: Sep 2009
Method: Search several databases
no. studies: 6
no. patients: 1.641
Endpoint: Death, MI, TVR, stent thrombosis 1yr
OR death: 1,12 (0,42-3,02)
OR MI: 0,57 (0,37-0,87)
OR TVR: 0,91 (0,61-1,35)
OR Stent thrombosis: 0,56 (0,23-1,35)
Hakeem
Article: Original
Journal: J Invasive Cardiol
Submission date: 28.5.2009
Acceptance date: 20.7.2009
Publication date: 11.11.2009
Method: Search several databases
no. studies: 6
no. patients: 1.641
Endpoint: Clinical and angiographic **
OR death: 0,93 (0,37-2,33)
OR MI: 1,71 (1,02-2,88)
OR TVR: 1,1 (0,73-1,64)
OR Stent thrombosis: 1,6 (0,65-3,91)
Kastritis
Article: Original
Journal: Cir Cardiovas Intervent
Submission date: 24.3.2009
Acceptance date: 22.7.2009
Publication date: 3.11.2009
Method: Search several databases
no. studies: 6
no. patients: 1.642
Endpoint: Death, MI, TVR, stent thrombosis
OR death: 0,81
OR MI: 1,78
OR TVR: 1,09
OR Stent thrombosis: 1,85
Zhang
Article: Original
Journal: Heart
Submission date: N/A
Acceptance date: 21.7.2009
Publication date: 29.7.2009 (on-line)
Method: Search several databases
no. studies: 5*
no. patients: 1.553
Endpoint: Death, MI, TVR, stent thrombosis
OR death: 0,68 (0,21-2,25)
OR MI: 0,54 (0,37-0,78)
OR TVR: 0,93 (0,62-1,41)
OR Stent thrombosis: 0,50 (0,19-1,32)
N/A: not available
* excluded Sirius Bifurcation Study because the results of the paper
were not reported as 'intention to treat', but rather by treatment
received
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,...
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...
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....
The very best that...
We read with great interest the article by Politi et al. (1) on revascularisation of patients presenting with ST-elevation myocardial infarction (STEMI) in the context of multivessel coronary disease, and its accompanying Editorial. Whilst the data are interesting and hypothesis- generating, they fall short of demanding any change in current practice owing to a potential flaw in the study design and in the findings as pre...
Dear Editor
The publication of not one but two reviews of catheter ablation for atrial fibrillation (AF) in this week's edition of Heart is very welcome.(1,2) The English and Welsh guidance from the National Institute for Clinical and Public Health Excellence (NICE) was published in 2006,(3) but a great deal of new comparative effectiveness evidence has been published recently. However there is a significant gap...
Ullah and Stewart present a case of pacemaker-mediated tachycardia (PMT) and described it as a "malfunction of dual chamber pacing". However, I would contend that the pacemaker is functioning appropriately, ie: it is sensing atrial activity in the atrium and pacing (capturing) the ventricle. The problem in PMT is the retrograde atrial activation beyond the PVARP as described and appropriate programming of the PVARP based o...
Sir, As a "jobbing cardiologist", I am grateful for the NICE guidance on the investigation of stable chest pain. I am grateful for the emphasis on clinical assessment, and I am grateful for the shift away from exercise testing. I am astonished, however, that the guideline does not say one word about the utility of a therapeutic trial in cases of uncertainty, and nor does the editorial by Fox & McLean. Every cardiol...
The recent editorial of Fox and Mclean concludes ââ¬à The NICE guidance on chest pain provides a series of important advances over the current status of investigation and triage of chest pain and should be welcomed by the profession 1. One of the key recommendations of the recently published National Institute for Health and Clinical excellence (NICE) guidelines for the early management of unstable...
Dear editor,
The avoidance of redundant publication is the core of the editorial task; therefore editors have established clear policies posted in their instructions for authors. The term Redundant publication has always been used for research reported by the same author and sent to two or more different journals. We report here a different situation that also results in unplanned redundant publication....
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