We read with interest the Image in Cardiology by Brown &
Agarwal documenting the phenomenon of T wave memory in a patient with
Ebstein's anomaly who presented with tachycardia[1]. We would be interested
to know whether any further investigation for her dysrhythmia was
performed. The ECGs presented strongly suggest that she may have an
atriofascicular bypass tract - an unusual variant of pree...
We read with interest the Image in Cardiology by Brown &
Agarwal documenting the phenomenon of T wave memory in a patient with
Ebstein's anomaly who presented with tachycardia[1]. We would be interested
to know whether any further investigation for her dysrhythmia was
performed. The ECGs presented strongly suggest that she may have an
atriofascicular bypass tract - an unusual variant of preexcitation which
is more prevalent in patients with Ebstein's anomaly.
The following are classic ECG features of an antidromic tachycardia
due to an atriofascicular bypass tract: the QRS is relatively narrow
(<150 ms), the axis is leftward (between 0 and -75 degrees), there is
an R wave in lead I and an rS pattern in lead V1, and the precordial
transition is beyond lead V4.[2] In sinus rhythm, patients classically
have an rS pattern in lead III.[3] The ECGs presented by Brown &
Aggarwal have all the hallmarks of this condition. These accessory
pathways have decremental properties (hence minimal evidence of
preexcitation on the ECG in sinus rhythm) and tend to originate at the lateral tricuspid
annulus, inserting into distal fascicles of the right bundle branch. They
are important to recognise since they are very amenable to curative
catheter ablation - certainly, in congenital heart disease where the
dysrhythmia is poorly tolerated this should be considered.
The T wave memory may be a consequence of the period of abnormal
ventricular activation during her tachycardia. It is common to see such T
wave changes after ablation of conventional accessory pathways in the
Wolff Parkinson White syndrome, and it has also been described after
ablation of atriofascicular pathways.[4]
References:
[1] Brown AJ & Aggarwal A. Cardiac memory in Ebstein anomaly.
Heart 2010;96:2046-2047
[2] Sternick EB, Cruz FE, Timmermans C, Sosa EA, et al.
Electrocardiogram during tachycardia in patients with anterograde
conduction over a Mahaim fiber: old criteria revisited. Heart Rhythm 2004
10;1:406-413.
[3] Sternick EB, Timmermans C, Sosa E, et al. The electrocardiogram
during sinus rhythm and tachycardia in patients with Mahaim fibers: the
importance of an "rS" pattern in lead III. J Am Coll Cardiol 2004
10/19;44(8):1626-1635.
[4] Josephson, ME. Clinical Cardiac Electrophysiology: Techniques and
Interpretations, 4th edition. Philadelphia, PA: Lippincott Williams &
Wilkins 2008: 773.
We read with great interest the article published by Mathew G.D.
Bates in your journal [1]. We congratulate the authors for the original
management of this case. In similar cases of large thrombus, we have
administered intrathrombus eptifibatide through the 3F Twin Pass catheter
(Vascular Solutions, Minnesota 55369 USA), and then performed thrombus
aspiration. Finally, conventional stenting was performed. Postprocedural,...
We read with great interest the article published by Mathew G.D.
Bates in your journal [1]. We congratulate the authors for the original
management of this case. In similar cases of large thrombus, we have
administered intrathrombus eptifibatide through the 3F Twin Pass catheter
(Vascular Solutions, Minnesota 55369 USA), and then performed thrombus
aspiration. Finally, conventional stenting was performed. Postprocedural,
a grade 3 Blush and complete ST segment resolution occurred.
The technical issue is sometimes very important and consists in
gently rotating the Export catheter, manoeuvre that detaches the old
thrombus. The other possibility, is changing the guiding catheter and
using a 7F Export catheter.
The use of a distal filter protection system, with excellent results in
this case (probably old thrombus), could be dangerous in the presence of
fresh platelet thrombus, due to the platelet aggregates embolisation
and/or squeezing them, causing no-reflow.[2,3]
1. Matthew G D Bates, Iain G Matthews, Jim A Hall. Large thrombus
burden in acute myocardial infarction: successful use of distal protection
device following failure of thrombus aspiration. Heart 2010
Sept;96(17):1371
2. Paul A Gurbel, Udaya S Tantry. Delivery of Glycoprotein IIb/IIIa
Inhibitor Therapy for Percutaneous Coronary Intervention: Why Not Take the
Intracoronary Highway? Circulation 2010 Feb; 121: 739- 741
3. Sebastiaan C.A.M. Bekkers, Saami K. Yazdani, Renu Virmani, Johannes
Waltenberger. Microvascular Obstruction: Underlying Pathophysiology and
Clinical Diagnosis. J Am Coll Cardiol. 2010; 55: 1649-1660
Heras and her colleagues make a good point.[1] Perhaps those planning systematic reviews should be required by journal editors to register their protocol on a central database, as we currently do for Cochrane reviews? Authors should also perhaps be required to state what they consider their review adds (e.g. that previous reviews were methodologically flawed, reported inadequate information on search strate...
Heras and her colleagues make a good point.[1] Perhaps those planning systematic reviews should be required by journal editors to register their protocol on a central database, as we currently do for Cochrane reviews? Authors should also perhaps be required to state what they consider their review adds (e.g. that previous reviews were methodologically flawed, reported inadequate information on search strategies, missed key studies; or identify new evidence)? I note that such an initiative has recently been described, funded jointly by the UK National Institute for Health Research and others. [2]
Conflict of interest: I co-authored a recent Cochrane SR on oxygen in MI
References
1. Magda Heras, P Avanzas, A Bayes-Genis, M Pan, L Perez de Isla, J Sanchis. Unplanned redundant publication. A consequence of too many cardiovascular journals? Heart 2010;96:1780 Published Online First: 23 August 2010 doi:10.1136/hrt.2010.205021
2. Alison Booth, M Clarke, D Ghersi, D Mower, M Petticrew, L Stewart. An international registry of systematic-review protocols. Lancet. Published online July 13, 2010 DOI: 10.1016/S0140-6736(10)60903-8
Dear Editor
With great interest we read the paper of Alboni et al. [1]. The investigators studied intravenous class Ic antiarrhythmic drug administration (propafenone and flecainide) as a predictor for adverse effects when used in a 'pill-in-the-pocket'Ãâ regimen (PITP).
Alboni and colleagues suggest that intravenous administration of flecainide or propafenone for pharmacological conversion of AF to sinus rhy...
Dear Editor
With great interest we read the paper of Alboni et al. [1]. The investigators studied intravenous class Ic antiarrhythmic drug administration (propafenone and flecainide) as a predictor for adverse effects when used in a 'pill-in-the-pocket'Ãâ regimen (PITP).
Alboni and colleagues suggest that intravenous administration of flecainide or propafenone for pharmacological conversion of AF to sinus rhythm cannot predict the occurrence of adverse effects when these agents are subsequently used in a PITP treatment modality. In fact, intravenous AAD administration was accompanied by a 6% incidence of serious adverse effects when the AAD was used as an oral compound, particularly with propafenone. The authors concluded that clinical intravenous drug testing should not be used as a safety indicator for PITP approach.
First, the pharmacologic and pharmacokinetic profile of flecainide differs from propafenone, particularly with respect to the intrinsic adrenergic receptor blocking actions[2,3]. As the authors mentioned in the discussion section, only propafenone caused serious side effects requiring hospital admission. In addition, in the majority of cases these side effects were related to brady-arrhythmic phenomena. In our opinion this is a very important observation with clinical implications. Second, the observed brady-arrhythmic side effects of propafenone only occurred in elderly, at least one SD above the mean study population age. In this age group latent sick sinus syndrome may be present and may become manifest by using drugs with intrinsic beta blocking properties (e.g. propafenone). Did the authors consider to further specify the study conclusion for octagonians, or use 24-hours Holter criteria prior to intravenous infusion to preselect subjects with increased risk for brady-arrhythmic complications? Third, could the simultaneous use of other cardiovascular agents like ARBs, ACE-inhibitors or beta-blocking agents have interfered with propafenone in causing brady-arrhythmic or hypotension related side effects?
To our opinion the take-home-message that intravenous drug testing in general should not be used to predict PITP adverse effects, is not demonstrated by the current data. Instead, the current data emphasize that further investigations are necessary to specify patient selection criteria for safe PITP use with propafenone in the treatment of paroxysmal AF.
C.J.H.J. Kirchhof
H.J.G.M. Crijns
I.C. van Gelder
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. Grant AO. Propafenone: an effective agent for the management of supraventricular arrhythmias. J Cardiovasc Electrophysiol. 1996;7:353-64.
3. Faber TS, Camm AJ. The differentiation of propafenone from other class Ic agents, focusing on the effect on ventricular response rate attributable to its beta-blocking action. Eur J Clin Pharmacol. 1996;51:199-208.
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.
To the Editor.
We read with interest the Image in Cardiology by Brown & Agarwal documenting the phenomenon of T wave memory in a patient with Ebstein's anomaly who presented with tachycardia[1]. We would be interested to know whether any further investigation for her dysrhythmia was performed. The ECGs presented strongly suggest that she may have an atriofascicular bypass tract - an unusual variant of pree...
We read with great interest the article published by Mathew G.D. Bates in your journal [1]. We congratulate the authors for the original management of this case. In similar cases of large thrombus, we have administered intrathrombus eptifibatide through the 3F Twin Pass catheter (Vascular Solutions, Minnesota 55369 USA), and then performed thrombus aspiration. Finally, conventional stenting was performed. Postprocedural,...
Dear Editor
Heras and her colleagues make a good point.[1] Perhaps those planning systematic reviews should be required by journal editors to register their protocol on a central database, as we currently do for Cochrane reviews? Authors should also perhaps be required to state what they consider their review adds (e.g. that previous reviews were methodologically flawed, reported inadequate information on search strate...
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...
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 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...
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...
Sir,
Cardiac imaging training in the United Kingdom
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 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...
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