To the Editor: I read with great interest the article by Hobbs et al. [1] I commend the authors for their original review of the diagnosis of heart failure in primary care.
Heart failure as defined by current guidelines published by professional societies in North America[2] and Europe[3] is a syndrome in which patients must have both typical signs and symptoms of heart failure and objective evidence of structural or functional a...
To the Editor: I read with great interest the article by Hobbs et al. [1] I commend the authors for their original review of the diagnosis of heart failure in primary care.
Heart failure as defined by current guidelines published by professional societies in North America[2] and Europe[3] is a syndrome in which patients must have both typical signs and symptoms of heart failure and objective evidence of structural or functional abnormality.
I agree with the conclusion that this clinical syndrome may be difficult for a primary care physician to diagnose accurately particularly if the symptoms develop slowly and are not as severe as to warrant immediate hospitalization. I also agree with the key point that early diagnosis can favorably alter prognosis and mortality.
However, I would like to emphasize that heart failure is also a disease spectrum with four stages as highlighted in the current AHA classification.[2]
Stage A - Patients at risk asymptomatic without structural or functional abnormality.
Stage B - Patients with structural abnormality but without signs or symptoms.
Stage C - Patient with structural abnormality with current or prior signs or symptoms.
Stage D - Patients with refractory heart failure requiring specialized interventions.
This staging system recognizes that Heart Failure has established risk factors and structural prerequisites; that the development of Heart Failure has asymptomatic and symptomatic phases; and that specific treatments targeted at each stage can reduce the morbidity and mortality of Heart Failure.[2]
Therefore, if priority is given to diagnosing the initial stages of Heart Failure, the complexity of the diagnosis will be lessened to some extent. Improving cardiovascular health and quality of life through the prevention, detection, and treatment of risk factors; and reducing hospitalizations of older adults with heart failure as the principal diagnosis are essential objectives of Healthy People 2020.[4] Do you then agree that diagnosing the first two stages or in other words asymptomatic heart failure should be the priority of the primary care physician?
References
1 Hobbs FD, Doust J, Mant J, et al. Heart failure: Diagnosis of heart failure in primary care. Heart. 2010 Nov;96(21):1773-7.
2 Hunt SA et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005 Sep 20;46(6):e1-82.
3 Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail. 2008 Oct;10(10):933-89.
4 Healthy People 2020. Accessed on www.healthypeople.gov/hp2020/Objectives/TopicArea.aspx?id=28&TopicArea=Heart Disease and Stroke on October 25, 2010.
I read with interest the paper by Gotzmann and colleagues [1]
demonstrating some very important differences after TAVI, particularly
improvements in exercise tolerance and quality of life. I did have some
reservations however on the statistical methodology that the group
employed. The study involved a cohort of 44 patients, assessed before and
after TAVI, so clearly paired statistical tests are appropriate. However,
the...
I read with interest the paper by Gotzmann and colleagues [1]
demonstrating some very important differences after TAVI, particularly
improvements in exercise tolerance and quality of life. I did have some
reservations however on the statistical methodology that the group
employed. The study involved a cohort of 44 patients, assessed before and
after TAVI, so clearly paired statistical tests are appropriate. However,
the group chose to use the unpaired Student's t, Mann-Whitney U and Chi-
squared tests, instead of the correct (and more powerful) paired Student's
t, Wilcoxon and McNemar tests. Use of these tests would very probably have
considerably increased the significance of observed differences.
On the other hand, the paper contains at least sixteen independent
comparative tests, and no allowance has been made for multiple comparison.
Using the crudest method of correction (the Bonferroni correction), they
should have considered tests to be significant not at p<0.05, but at
p<0.003, which would render some of the apparent significant
differences to be not significant (such as LVEF and BNP).
I would recommend that the authors re-examine their stats before
making the conclusions about BNP stated in the paper; it may turn out that
(using the Wilcoxon test) BNP is in fact significantly reduced after TAVI
in this group of patients.
Having read the appeal for a 'new dawn in imaging training' I suspect
that Rajani et al have not read the current UK cardiology training
curriculum (www.jrcptb.org.uk/specialties/ST3-
SpR/Documents/2010%20Cardiology%20Curriculum.pdf) and appreciated the
flexibility and options open to trainees and their trainers It is
factually incorrect to state that UK trainees 'only appear to be able to
obtain "in-program" experience i...
Having read the appeal for a 'new dawn in imaging training' I suspect
that Rajani et al have not read the current UK cardiology training
curriculum (www.jrcptb.org.uk/specialties/ST3-
SpR/Documents/2010%20Cardiology%20Curriculum.pdf) and appreciated the
flexibility and options open to trainees and their trainers It is
factually incorrect to state that UK trainees 'only appear to be able to
obtain "in-program" experience in one imaging modality' and I think this
has lead to the mistaken belief that 'the structure of cardiac imaging
training' is somehow disadvantaged compared to other areas of cardiology
practice.
The curriculum was written by the cardiology specialist advisory
committee (SAC) with advice from trainees and the specialist imaging
societies British Nuclear Cardiology Society, British Society of
Echocardiography, British Society for Cardiac Magnetic Resonance and the
British Society of Cardiac Imaging. The importance of 'imaging' in
contemporary clinical practice is reflected in the requirements for all
cardiologists in training to achieve basic competence in all areas of
cardiovascular imaging nuclear, echo, CMR and CT.
For those wanting to develop more advanced knowledge, skills and
experience there is the requirement to undertake further training in their
last two years to achieve further competences building on their core
competences - defined in the curricular advanced modules. All advisors to
the SAC curriculum writing committee were adamant that the acquisition of
advanced skills and experience should be to expert level and should not be
spread too thinly across clinical areas - no room for dabbling. UK
trainees need to be true experts in an increasingly international arena.
This will additionally help to maintain the UK as a world leader in
cardiac imaging research.
Inevitably training to expert level requires considerable time and
commitment and given the constraints of the two years available for
advanced modules in a five year cardiology training programme and the
constraints of EWTD, trainees can not be expected to achieve this level of
competence in all areas. Hence, imaging trainees and their trainers focus
on two of the four modalities e.g. echo + CMR or nuclear + CT etc.
Alternatively, trainees can combine imaging with other advanced skills
e.g. heart failure training + CMR or device therapy + echo etc. It may be
that imaging trainers wish to ensure that their trainees, whilst
concentrating on one or two modalities to advanced level, are exposed to
broad-based training to fully appreciate the strengths and weakness of
different modalities. However, despite the sometimes unbridled enthusiasm
of trainees it has to be recognized that there is not enough time to train
to advanced level in everything.
It is therefore encouraging to see that the job market reflects this.
Rajani et al note that in recent job advertisements for cardiologists with
an interest in imaging 90% had listed as desirable experience in cardiac
CT or cardiac MRI (not both). It would therefore appear that the current
training curriculum is appropriate to satisfy these demands.
The opportunities for trainees do not end there however; those
trainees who wish to add to their portfolio of skills and experience can
undertake out-of-programme experience, OOPE. Although this extends
training and delays their CCT date (and hence entry of others to the
deanery based training programme) trainees who are supported by their
trainers are rarely prevented from obtaining SAC and GMC approval for OOPE
and most deaneries are happy to accommodate their wishes. These optional
extra training years are undoubtedly expensive and difficult to organize
so the BCS/ACC fellowships are a welcome addition to the options open to
UK trainees.
A key challenge which remains is to encourage trainees to opt for
advanced training in imaging. The BJCA trainee survey in 2008 showed that
only 18.5% of cardiology trainees plan a career with a major interest in
cardiac imaging. This is still well short of the BCS projected workforce
need of around 40% of the consultant workforce
(www.bcs.com/documents/guidelines/BCS%20Cardiac%20Workforce%202005%20final%20draft%20June%202005.pdf).
The recent pronouncements from NICE may produce a shift in career
preferences but this has not been evident in the past e.g. following the
publication of the NICE MPS guidelines in 2003. The BCS and the Cardiology
SAC are continuing to work with the specialist societies to provide not
only regional and national training days but also guides to educational
resources available for trainers and trainees which will make it easier
for trainees to see how they can best acquire the necessary knowledge,
skills and attitudes for their chosen career path.
I believe the current curriculum provides the necessary flexibility
for trainees to achieve advanced competences in cardiac imaging and that
it will produce the leaders and role models of tomorrow who will advance
the practice of this particular area of cardiology and inspire future
generations of cardiologists. Rajani et al can be reassured that the
specialist imaging societies will continue to have a major influence in
the design and implementation of cardiology training. The scope of
cardiology training will not be a static arena and the curriculum will
have to continue to evolve to meet the demands of trainees, trainers and
more importantly the general public and our patients.
It is quite incredible how far the notion of a population-wide
benefit accruing from salt reduction has gone in view of the contradictory
clinical evidence. In the first instance we know that the population
response to salt reduction is rather limited (2-6 mm Hg) and
heterogeneous, with 30% experiencing a small drop in BP, about 20%
experiencing an increase in BP and the residual 50% o the population
undergoing no impac...
It is quite incredible how far the notion of a population-wide
benefit accruing from salt reduction has gone in view of the contradictory
clinical evidence. In the first instance we know that the population
response to salt reduction is rather limited (2-6 mm Hg) and
heterogeneous, with 30% experiencing a small drop in BP, about 20%
experiencing an increase in BP and the residual 50% o the population
undergoing no impact at all (1) .
Indeed, the most recent evidence seems to indicate that so-called
salt sensitivity on either side of the response is due to a genetically-
based imbalance of aldosterone production. Those with abnormally high
production of aldosterone show a slight reduction in BP with decreased
salt intake (2) while abnormally low aldosterone levels may be responsible
for the demonstrated increase in BP with reduced salt intakes (3). In
both cases, since abnormal aldosterone levels carry a range of risks aside
from hypertension, the strategy should be to manage aldosterone, not salt.
In the second instance, the Geoffrey Rose reduced-salt approach to
slightly reduce blood pressure across the entire population in hopes of
achieving meaningful reductions in the incidence of cardiovascular disease
(CVD) will only possibly work in the absence of negative consequences.
Using this approach, a population-wide reduction in salt intake will
inevitably result in a population-wide increase in renin-angiotensin-
aldosterone system (RAAS) activity - also considered to be a risk factor
for CVD, thus shifting the curve towards a higher risk. Without
incorporating the normal increase in RAAS activity expected with salt
reduction, the concept behind the approach is fundamentally flawed
This year (2010) has shown a number of models projecting savings in
lives and treasure based upon the flawed speculation in Rose's population
approach. No new clinical evidence has been presented - only an
extrapolation of old controversial evidence - the equivalent of lipstick
on a pig. This latest paper falls into this genre of using assumptions
that are based upon a highly biased view of the available evidence. There
have been more meta-reviews questioning the benefits of population-wide
sodium reduction (4)(5)(6), than supporting it (7).
More recently, Harvard researchers Adam Bernstein and Walter Willett
(8) found that the amount of sodium consumed by Americans over the past
four decades has remained unchanged, while the rates of hypertension have
increased significantly. This data reveals a total disconnect between
rising rates of hypertension/obesity and salt consumption. Yet, the
purported connection between rising hypertension and salt consumption was
the myth behind the recommended figures we all use.
Because an adequate dietary recommended intake for sodium "could not
be established because of inadequate data from dose-response studies" (9),
the figure was subjectively and arbitrarily set at 1,500 mg/day. Somehow
this figure morphed into an international standard as if it was based upon
real evidence - but it wasn't. The same for the upper limit of 2,300 mg
Na/day, precisely 100 mmoles - as if we were all cast in Avogadro's image.
The idea of mandatory sodium reduction referred to in the paper by
Cobiac et al, in view of so much contradictory evidence seem to throw
caution to the wind. Surely, before mandatory measures are considered
that will limit the intakes of a nutrient to a level lower than previously
experienced in recorded human history and considerably less than that of
any other modern society in the world, some pause should be taken to carry
out a full dispassionate review of all the available evidence. As an
employee of the salt industry, I would certainly recuse myself from such a
review and would hope that all other committed activists and advocates on
all sides of the issue do likewise, so that it can proceed in a fully
objective manner. Consumers deserve no less.
________
(1) Miller, J.Z., Weinberger, M.H., Daugherty, S.A., et al.
"Heterogeneity of blood pressure responses to dietary sodium restriction
in normotensive adults," J Chronic Dis, 40, 245-250, (1987).
(2) Kammerer, C.M. et al, "Linkage of Plasma Aldosterone
Concentration to Chromosome 5 in Families of African Ancestry," American
Heart Association High Blood Pressure Research - 2010 Scientific Sessions,
Washington, DC, Oct., 14, (2010).
(3) Makhanova, N., Sequeira-Lopez, M.L.S., Gomez, R.A, Hyung-Suk Kim,
and Smithies. O., "Disturbed Homeostasis in Sodium-Restricted Mice
Heterozygous and Homozygous for Aldosterone Synthase Gene Disruption,"
Hypertension, 48, 1151-1159, (2006).
(4) Hooper L, Bartlett C, Davey SG, Ebrahim S. Advice to reduce
dietary salt for prevention of cardiovascular disease. Cochrane Database
Syst Rev. 2004;(1):CD003656.
(5) Institute for Quality and Efficiency in Health Care. Executive
summary of report A05- 21B, Benefit assessment of non-drug treatment
strategies in patients with essential hypertension: reduction in salt
intake (Nutzenbewertung nichtmedikament?ser Behandlungsstrategien bei
Patienten mit essenzieller Hypertonie: Kochsalzreduktion). Cologne,
Germany, June 18, 2009. Executive summary in English can be accessed at:
http://www.iqwig.de/download/A05-21B_Executive_Summary_Nondrug_
treatment_strategies_for_hypertension-reduction_in_salt_intake.pdf
(6) Jurgens G, Graudal NA. Effects of low sodium diet versus high
sodium diet on blood pressure, renin, aldosterone, catecholamines,
cholesterols, and triglycerides. Cochrane Database Syst Rev.
2004;(1):CD004022
(7) He FJ, MacGregor GA. Effect of longer-term modest salt reduction
on blood pressure. Cochrane Database of Systematic Reviews 2004, Issue 1.
Art. No.: CD004937.
(8) Bernstein, AM and Willett, WC, Trends in 24-h urinary sodium
excretion in the United States, 1957-2003: a systematic review. Am J Clin
Nutr doi: 10.3945/ajcn.2010.29367.
(9) Institute of Medicine, "Dietary Reference Intakes for Water,
Potassium, Sodium, Chloride, and Sulfate," (National Academy Press,
Washington, DC, 2005).
I read with interest Blessberger and Binder's article on the clinical
applications of two dimensional speckle tracking following their excellent
previous article detailing the technique's basic principles[1, 2]. The two
articles carry significant detail but fall down in one major regard.
Whilst the authors state that the reproducibility of speckle tracking is
greater than tissue Doppler imaging (TDI), at...
I read with interest Blessberger and Binder's article on the clinical
applications of two dimensional speckle tracking following their excellent
previous article detailing the technique's basic principles[1, 2]. The two
articles carry significant detail but fall down in one major regard.
Whilst the authors state that the reproducibility of speckle tracking is
greater than tissue Doppler imaging (TDI), at no point during either
article do they elaborate on this important point.
Nearly ten years ago the main stream cardiology community took on board on
the advice of the specialists in echocardiography to adopt the use of TDI
in patient selection for cardiac resynchronisation therapy. Enthusiasm for
this technique has waned following the publication of the randomised
PROSPECT trial[3] such that it has been removed from current international
guidelines. One of the salient features of that trial was the poor core
lab reproducibility. To this day there have been no large studies properly
investigating the reproducibility of TDI that include the analysis of
image acquisition and result repeatability across 'real world' centres.
Whilst speckle tracking remains an interesting research tool, it too
should remain as such until large 'real world' studies demonstrate that
the technique can be robustly translated from highly specialised research
teams to busy mainstream departments where the technique occupies only a
fraction of the workload. The lack of any detail on reproducibility or
feasibility is a major omission in the author's two articles and future
investigators need to concentrate on this vital area prior to suggesting
that speckle tracking can be adopted for routine clinical use.
1. Blessberger, H. and T. Binder, Two dimensional speckle tracking
echocardiography: clinical applications. Heart, 2010. 96(24): p. 2032-
2040.
2. Blessberger, H. and T. Binder, Non-invasive imaging: Two dimensional
speckle tracking echocardiography: basic principles. Heart, 2010. 96(9):
p. 716-22.
3. Chung, E.S., A.R. Leon, L. Tavazzi, J.P. Sun, P. Nihoyannopoulos, J.
Merlino, W.T. Abraham, S. Ghio, C. Leclercq, J.J. Bax, C.M. Yu, J.
Gorcsan, 3rd, M. St John Sutton, J. De Sutter, and J. Murillo, Results of
the Predictors of Response to CRT (PROSPECT) trial. Circulation, 2008.
117(20): p. 2608-16.
We would like to congratulate the authors for the paper about gender
differences in aortic valve replacement (AVR) in severe aortic stenosis
(SAS)(1). Traditionally there have been mortality perioperatory
differences depending of the gender (2), and these differences have been
included in operatory risk calculators.
In this work, the authors do not find differences in mortality between men
and women. Our attention on the...
We would like to congratulate the authors for the paper about gender
differences in aortic valve replacement (AVR) in severe aortic stenosis
(SAS)(1). Traditionally there have been mortality perioperatory
differences depending of the gender (2), and these differences have been
included in operatory risk calculators.
In this work, the authors do not find differences in mortality between men
and women. Our attention on the one hand, the absence of more significant
prevalence of coronary artery disease in men, even though they have more
ventricular dysfunction (it would be interesting checking the antecedents
of cardiac infarct). On the other hand, although it has been described
that women have a higher EuroSCORE than men, the main factors contributing
to it are the age and the own female gender. So, if the gender is not
related to the mortality, we can suppose that women are not going to have
more mortality than men.
In a recent paper published by our group (3), initially, the gender
was a risk factor for AVR in SAS. However, when we adjusted by the body
surface (this variable was not related to mortality), the significance
disappeared. This change can be explained because there are several
factors specially associated with AVR in women. Some of these factors have
been well explained in the paper that the authors have presented (SAS more
evolved, women more symptomatic or more needed of aortic root enlargement)
but there are others that we also think interesting like the more left
ventricular hypertrophy as a response to the pressure overload (in this
article is paradoxical more prevalent in men) (4), which rises the morbi-
mortality risk. In an interesting editorial published by Pibarot P (5), he
showed the mismatch patient-prosthesis, the more ventricular hypertrophy
and the underestimated of symptoms in women as possible causes of the
mayor mortality in women in AVR.
We can conclude that female gender is not a risk factor for AVR in SAS,
but there are some specific factors that are more prevalent in them and
require specific attention and treatment.
References:
1- Klaar U, Scholten C,Heger M et al. Gender differences in clinical
presentation and surgical outcome of aortic stenosis. Heart 2010;96:539-
545
2- Edwards FH, Peterson ED, Coombs LP, DeLong ER, Jamieson WR, Shroyer
ALW, et al. Prediction of operative mortality after valve replacement
surgery. J Am Coll Cardiol. 2001;37:885-92.
3- Caballero-Borrego J, Gomez-Doblas JJ, Valencia-Serrano F et al.
Influence of sex on perioperative outcomes in patients undergoing valve
replacement for severe aortic stenosis. Rev Esp Cardiol. 2009 Jan;62(1):31
-8.
4- Carroll JD, Carroll EP, Feldman T et al. Sex-associated differences in
left ventricular function in aortic stenosis of the elderly. Circulation.
1992;86:1099-107.
5- Pibarot P. Aortic Valve Surgery: Unveiling the Mystery of a Woman's
Heart. Rev Esp Cardiol. 2009;62:7-9.
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.
I read with interest the paper by Gotzmann and colleagues [1] demonstrating some very important differences after TAVI, particularly improvements in exercise tolerance and quality of life. I did have some reservations however on the statistical methodology that the group employed. The study involved a cohort of 44 patients, assessed before and after TAVI, so clearly paired statistical tests are appropriate. However, the...
Having read the appeal for a 'new dawn in imaging training' I suspect that Rajani et al have not read the current UK cardiology training curriculum (www.jrcptb.org.uk/specialties/ST3- SpR/Documents/2010%20Cardiology%20Curriculum.pdf) and appreciated the flexibility and options open to trainees and their trainers It is factually incorrect to state that UK trainees 'only appear to be able to obtain "in-program" experience i...
It is quite incredible how far the notion of a population-wide benefit accruing from salt reduction has gone in view of the contradictory clinical evidence. In the first instance we know that the population response to salt reduction is rather limited (2-6 mm Hg) and heterogeneous, with 30% experiencing a small drop in BP, about 20% experiencing an increase in BP and the residual 50% o the population undergoing no impac...
Dear Sir,
I read with interest Blessberger and Binder's article on the clinical applications of two dimensional speckle tracking following their excellent previous article detailing the technique's basic principles[1, 2]. The two articles carry significant detail but fall down in one major regard. Whilst the authors state that the reproducibility of speckle tracking is greater than tissue Doppler imaging (TDI), at...
We would like to congratulate the authors for the paper about gender differences in aortic valve replacement (AVR) in severe aortic stenosis (SAS)(1). Traditionally there have been mortality perioperatory differences depending of the gender (2), and these differences have been included in operatory risk calculators. In this work, the authors do not find differences in mortality between men and women. Our attention on the...
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...
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