Pell considers the provision of AEDs in public places an
inappropriate use of health service funding because at present there is a
lack of evidence both of clinical effectiveness and cost effectiveness to
support this strategy.[1]
The basis for this assertion centres on the lack
of clinical trials of the use of AEDs in this situation, or a lack of
comparative or baseline data in published descript...
Pell considers the provision of AEDs in public places an
inappropriate use of health service funding because at present there is a
lack of evidence both of clinical effectiveness and cost effectiveness to
support this strategy.[1]
The basis for this assertion centres on the lack
of clinical trials of the use of AEDs in this situation, or a lack of
comparative or baseline data in published descriptive series of their use
on which to judge their effectiveness. Only one small one study of the
many published (from airports in Chicago) is quoted to support her
argument.[2]
Pell incorrectly quotes this study from O’Hare airport stating that
successful defibrillation occurred in 10 out of 18 subjects with cardiac
arrest due to VF, a success rate of 56%. In fact the paper states that 11
of the 18 (61%) were successfully resuscitated and discharged from
hospital, although one subject died several weeks afterwards from other
causes. She dismisses the stark comparison with a community study of
resuscitation by emergency services in the same area that reported a
successful resuscitation rate of 2.9%. While not strictly comparable
(because of differences in populations and presenting rhythm), it is
typical of the results seen with conventional responses from the emergency
medical services who have to travel to reach the casualty. She does not
comment on the very poor outcome in the patients reported from O’Hare in
whom defibrillation was delayed.
Pell did not quote the much larger study from Casinos in Las Vegas
where overall, 56 of 105 (53%) patients in VF survived after
defibrillation by security guards.[3] In those defibrillated within 3
minutes of collapse the survival rate was 74%. The paramedics in the
conventional EMS response in the area arrived at these patients a mean of
9.8 minutes after collapse, and sufficient data from epidemiological
studies exists to be able to predict that the likely survival at this time
would be around 5%.[4]
In the UK AEDs have been installed by the department of health (DH)
in busy public places where ambulance data showed there to be an
appreciable risk of cardiac arrest.[5,6] The BHF have also equipped a
variety of sites frequented by the public, and experience shows that
overall 20% of all patients with cardiac arrest at these places survive to
leave hospital, and in those with VF as the presenting rhythm the figure
is 24%.[7] In nearly all cases defibrillation is performed within 5
minutes of collapse. The success of ambulance crews who arrive much later
is much poorer; a large recent audit of ambulance service resuscitation
attempts showed a survival rate of 2% for non-crew witnessed arrests.[8]
While there is no debate that strict comparison of the two treatment
strategies is possible from this evidence; there is no doubt which
achieves the better results in the population that it serves. The evidence
for the clinical effectiveness of ‘on site’ defibrillators is very strong
and totally in accord with what is known about the consequences of
delaying defibrillation. Survival from cardiac arrest at major stations,
airports and gymnasiums has now become commonplace since AEDs were
installed, whereas in the past it was rare. There is enough evidence to
justify the policy of installing AEDs at appropriate sites and to ensure
that no controlled trial could ever be ethical.
The evidence to support strategies that minimise the delay between
collapse and defibrillation is overwhelming, and the siting of AEDs in
public places is one very effective strategy to achieve this. Pell
criticises the strategy because it is unlikely to make an appreciable
impact on mortality in population terms as only the minority of arrests
occur in public places. No one disputes this - it has been known for many
years that around 70% of arrests occur at home. But many other widely
employed and sometimes costly interventions like PCI, CABG or implantation
of ICDs also have little impact on the mortality of populations. But all
of these interventions make an enormous impact on the life and health of
individual patients; and many health care resources are rightly directed
towards the wellbeing of individuals.
The evidence shows that the deployment of AEDs in busy public places
and used by trained responders working at the site is an effective
strategy for treating a specific group of patients with out of hospital
cardiac arrest. It is a justifiable strategy to deal with a predictable
event at a site where there is a duty of care to the clients and customers
present.
Pell argues that the use of AEDs by ‘first responders’ – police, fire
personnel or lay persons dispatched by ambulance control centres – might
be a more appropriate use of resources but offers little concrete evidence
to support this assertion. Such evidence offered is largely based on
theoretical models derived exclusively from Scottish data. Audit of the
use of AEDs supplied by the BHF for use by such first responders suggests
only limited clinical effectiveness at present. This is because the time
between collapse and defibrillation, although quicker than a conventional
ambulance response could achieve under the conditions, varied between 8
and 13 minutes (estimated medians) with 13 survivors out of 296
resuscitation attempts (4.4%). Moreover, half these survivors arrested
after the arrival of the responder who had been identified as vulnerable
by the emergency call taker.
The relative cost effectiveness of the two strategies will only be
apparent from further audit. ‘On site’ defibrillators require more
machines which are used infrequently but with a greater chance of success,
whereas first responder AEDs are used more frequently, so the cost per
life saved might be comparable. The two strategies are complimentary and
serve different populations. Little robust data about cost effectiveness
for either strategy is currently available, but the costs per life saved
with ‘on site’ defibrillators appear relatively modest - estimated at
$7000 at Chicago, and £20 000 in the DH scheme.
References
(1) Pell JP. The debate on public place defibrillators: charged but
shockingly ill informed. Heart 2003;89:1375-1376
(2) Caffrey S, Willoughby PJ, Pepe PE et al. Public use of automated
external defibrillators. N Engl J Med 2002;347:1242–7
(3) Valenzuela TD, Roe D, Nichol G et al. Outcomes of rapid
defibrillation by security officers after cardiac arrest in casinos. N
Engl J Med 2000;343:1206–9
(4) De Maio VJ, Steill IG, Wells GA et al. Optimal defibrillation
response intervals for maximum out of hospital cardiac arrest survival
rates. Ann Emerg Med.2003;42:242-250
(5) Department of Health. Saving lives: our healthier nation. London:
HMSO, 1999.
(6) Davies CS, Colquhoun M, Graham S, et al. Public Access
Defibrillation; the establishment of a national scheme for England.
Resuscitation 2002;52:13-21.
(7) Resuscitation Council UK and British Heart Foundation data
(8) Cave L, Evans L. On behalf of the South East Ambulance Clinical
Audit Group (SEACAG). A joint audit of out-of-hospital cardiac arrest
using the core Utstein style. http://www.seacag.org/downloads/finalreport.pdf
Accessed 15.12.03
Campbell et al. describe a study of ischaemic heart disease (IHD) and
HFE gene mutations in a population where there is a high prevalence of
both. They find no association between IHD and HFE genotype.
In discussing these results they conclude that this is the largest
study to date of the prevalence of the HFE gene mutations in a randomly
selected mainland UK or Irish population. We a...
Campbell et al. describe a study of ischaemic heart disease (IHD) and
HFE gene mutations in a population where there is a high prevalence of
both. They find no association between IHD and HFE genotype.
In discussing these results they conclude that this is the largest
study to date of the prevalence of the HFE gene mutations in a randomly
selected mainland UK or Irish population. We are surprised that they have
not commented on a much larger study of 10,500 blood donors from S Wales.[1] Here, the C282Y allele frequency is lower (8.3%) and that for H63D is
slightly higher (15.3%). The size of the study means that the 95%
confidence intervals are smaller, being 7.7 - 8.8% for C282Y and 14.6 -
16.0% for H63D. The authors may rightly consider that blood donors are
not a randomly selected population. Nonetheless they provide a
representative sample of relatively young, healthy adults and a sound
basis for assessing allele frequencies in a UK population. We have
studied HFE mutations in men with angina and conclude that HFE mutations
are not a risk factor for angina.[2]
References
(1) Jackson HA, Carter K, Darke C, Guttridge MG, Ravine D, Hutton RD et al. HFE mutations, iron deficiency and overload in 10 500 blood donors.
British Journal of Haematology 2001;114:474-84.
(2) Feeney GP, Ashfield-Watt,PAL. Burr, ML, Dunstan,FDJ, McDowell, IFW ,
Worwood, M. Heterozygosity for the haemochromatosis mutation HFE C282Y is
not a risk factor for angina. Heart, accepted for publication.
Drs Sabharwal and Lahiri are to be congratulated on their review. And
their pictures, particularly the one chosen for the cover illustration,
are exquisite. The labelling of this image, however, illustrates a
fundamental problem with the way that nuclear cardiologists currently
describe the heart, as we pointed out in our recent Editorial published in Heart.[1]
Drs Sabharwal and Lahiri are to be congratulated on their review. And
their pictures, particularly the one chosen for the cover illustration,
are exquisite. The labelling of this image, however, illustrates a
fundamental problem with the way that nuclear cardiologists currently
describe the heart, as we pointed out in our recent Editorial published in Heart.[1]
The image that is described as "Anterior" by Sabharwal and Lahiri, in
reality, shows the superior aspect of the ventricular mass. We are well
aware that the designation shown by your authors is the one chosen by the
joint European - North American radiological working group, but that does
not alter the fact that it is anatomically incorrect. It is the septal
surface of the left ventricle that is anterior when the heart is viewed in
attitudinally correct orientation. The surface labelled as being
"anterior" should be correctly re-labelled as being "superior".
Reference
(1) Cook AC, Anderson RH. Attitudinally correct nomenclature. Heart
2002;87:503-506).
I read with great interest the editorial by JE Sanderson,[1] which
focuses on the current controversy about the term of "diastolic heart
failure".[2-5]
There is now evidence that in patients with symptoms and
signs of heart failure without overt evidence of impaired left ventricular
systolic function, delayed relaxation and/or abnormal stiffness are almost
constant regardless of the severity of s...
I read with great interest the editorial by JE Sanderson,[1] which
focuses on the current controversy about the term of "diastolic heart
failure".[2-5]
There is now evidence that in patients with symptoms and
signs of heart failure without overt evidence of impaired left ventricular
systolic function, delayed relaxation and/or abnormal stiffness are almost
constant regardless of the severity of symptoms.[6,7] Accordingly, the term
of "diastolic heart failure" has been simplistically proposed in this
setting by some authors.[6] However, besides the controversy that the term
of "diastolic heart failure" should be recognized or not as synonymous
with "heart failure with preserved systolic function", it appears on
interest to point out two major clinical features encountered in this
clinical syndrome in daily practice.
First, isolated symptoms such as
asthenia and breathless, that are well known to be non-specific for heart
failure, frequently result in the misdiagnosis of "diastolic heart
failure" when isolated diastolic abnormalities are found at Doppler
echocardiography.[8] Accordingly, the Brain Natriuretic Peptide assay may be
very helpful for an accurate diagnosis of heart failure when signs of
pulmonary congestion at the auscultation and on Xray, which respond
favourably to loop diuretics, are not present.
Second, the key-assumption
that signs and symptoms of heart failure with preserved systolic function
relate mainly to severe diastolic dysfunction, as it is generally observed
in hypertrophic and restrictive cardiomyopathies, is henceforth questioned
in the elderly.[7]
In this setting, associated factors, such as silent
myocardial ischemia, high systolic blood pressure, arrhythmia,
hypoalbuminemia and volume overload related to high sodium intake and
renal failure, are usually the straightforward events which precipitate
the critical decrease in the oncotic – hydrostatic pulmonary pressure
gradient and, therefore, lead to the transient exacerbation of heart
failure. Thus, these aggravating factors must be checked and treated
systematically.
(2) Banerjee P, Banerjee T, Khand A, et al. Diastolic heart failure :
neglected or misdiagnosed ? J Am Coll Cardiol 2002; 39: 138-41.
(3) Cohen Solal A. Diastolic heart failure : myth or reality ? Eur J
Heart Fail 2002; 4: 395-400.
(4) Burkhoff D, Maurer MS, Packer M. Heart failure with a normal
ejection fraction : is it really a disorder of diastolic function ?
Circulation 2003; 107: 656-8.
(5) Zile MR. Heart failure with preserved ejection fraction : is this
diastolic heart failure ? J Am Coll Cardiol 2003; 41: 1519-22.
(6) Zile MR, Gaasch WH, Carroll JD, et al. Heart failure with a normal
ejection fraction. Is measurement of diastolic function necessary to make
the diagnosis of heart failure? Circulation 2001; 104: 779-82.
(7) Arques S, Ambrosi P, Gelisse R, et al. Hypoalbuminemia in elderly
patients with acute diastolic heart failure. J Am Coll Cardiol 2003; 42:
712-6.
(8) Caruana L, Petrie M, Davie A, et al. Do patients with suspected
heart failure and normal systolic function suffer from `diastolic heart
failure' or from misdiagnosis? A prospective descriptive study. Br Med J
2000; 321: 215–9.
We read with interest the article by Nielsen et al.[1] One of the
interesting findings of that study is the rather low rates of ACE
inhibitor use (16% and 8% respectively for hospitalized and community
dwelling heart failure patients, and 1.7% for patients with heart disease
but no heart failure). The fact that the study was done conducted between
1993 and 1996 partly explains these low rates. H...
We read with interest the article by Nielsen et al.[1] One of the
interesting findings of that study is the rather low rates of ACE
inhibitor use (16% and 8% respectively for hospitalized and community
dwelling heart failure patients, and 1.7% for patients with heart disease
but no heart failure). The fact that the study was done conducted between
1993 and 1996 partly explains these low rates. However, survival benefit
of ACE inhibitors in heart failure patients with left ventricular systolic
dysfunction was well known by the early 1990’s.[2] In addition, the lack of
distinction between systolic and diastolic heart failure also likely have
diluted the rate of ACE inhibitor use. Assuming that about half of the
hospitalized and 20% of the community dwelling heart failure patients have
systolic heart failure, and all ACE inhibitors were used in these patients
(which was likely not the case), not all eligible heart failure patients
were receiving this life saving drug.
Presence of systolic dysfunction and lack of use of ACE inhibitors
are independently associated with increased mortality in heart failure
patients.[3] Once a clinical diagnosis of heart failure is made, the single
most important evaluation is the left ventricular systolic function
evaluation, preferably by an echocardiogram.[4] The authors’ conclusion that
echocardiography should be restricted to heart failure patients with
significant risk of death is in contradiction to the recommendation by
heart failure guidelines.[4,5] Once the diagnosis of systolic heart failure
is established, ACE inhibitors should be prescribed to all such patients
unless an absolute contraindication such as past history of allergy or
angioedema exists. Most general practitioners should also be able to
initiate a beta blocker. General practitioners unfamiliar or uncomfortable
with use of beta blockers in systolic heart failure should refer patients
to cardiologists. Systolic heart failure patients with angina or sudden
worsening of symptoms who are eligible and willing candidates for
revascularization should also be referred for cardiac catheterization and
coronary angiography.
Reference
(1) Wendelboe Nielsen O, Hilden J, McDonagh T, Fischer Hansen J.
Survival differences between heart failure in general practices and in
hospitals. Heart 2003; 89:1298-1302.
(2) Williams J, Bristow M, Fowler M, et al. Guidelines for the Evaluation
and Management of Heart Failure: Report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation 1995; 92:2764-84.
(3) Ahmed A, Roseman JM, Duxbury AS, Allman RM, DeLong JF. Correlates and
outcomes of preserved left ventricular systolic function among older
adults hospitalized with heart failure. Am Heart J 2002; 144:365-72.
(4) Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the
evaluation and management of chronic heart failure in the adult: executive
summary. A report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee to revise the
1995 Guidelines for the Evaluation and Management of Heart Failure). J Am
Coll Cardiol 2001; 38:2101-13.
(5) Remme WJ, Swedberg K. Guidelines for the diagnosis and treatment of
chronic heart failure. Eur Heart J 2001; 22:1527-60.
We sincerely appreciate the comments by Tetsuya Sato et al.
concerning our report of transient apical ballooning associated with
apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated,
using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients
have extensive myocardial stunning as the result of sympathetic
denervation. Reduction of MIBG accumulation, suggestive...
We sincerely appreciate the comments by Tetsuya Sato et al.
concerning our report of transient apical ballooning associated with
apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated,
using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients
have extensive myocardial stunning as the result of sympathetic
denervation. Reduction of MIBG accumulation, suggestive of sympathetic
denervation, normalized over time accompanied by the disappearance of
deeply negative T waves. A similar case, has recently been documented in
another patient with this syndrome.[3] Of interest, reduced myocardial
MIBG uptake has also been observed in patients with pheochromocytoma [4]
that also may exhibit left ventricular wall motion abnormalities and
striking electrocardiographic features. Likewise, Kurisu et al.[5] assessed myocardial perfusion and fatty acid metabolism (idodine-123-beta-
methyl-p-iodophenyl penta-decanoid acid), in a series of patients with
this condition. They demonstrated that the extent of fatty acid metabolism
derangement was greater than expected according to the size of the
myocardial perfusion defect, and that this abnormal metabolism gradually
improved over the time, suggesting again the presence of stunned
myocardium.
By definition, however, myocardial stunning consist of prolonged
“post-ischemia” ventricular dysfunction. A problem with the apical
ballooning syndrome is that the ultimate cause for ischemia -if any-,
remains elusive. Normal epicardial coronary arteries are required for the
diagnosis of this entity, that also includes extensive and reversible wall
motion abnormalities not necessarily following the distribution of a main
epicardic vessel. Enzyme release is typically disproportionate to the
striking "Tako-Tsubo" like left ventricular morphology described in
Japanese and, more recently in Western patients.[6-8] Our patient had a
clear-cut intense emotional stress (major family discussion) as the
potential trigger. Another condition that may be associated with deeply
negative T waves, even of acute onset, is hypertrophic cardiomyopathy.[9-11] In some of these patients ischemia and/or metabolic abnormalities at
the left ventricular apex have also been proposed. Of interest, dynamic
intraventricular gradients may also occur in patients with apical
ballooning, and sympathetic activation leading to basal hypercontractility
may be implicated in its genesis.[12,13] In fact, treatment with
adrenergic blockers has been suggested.[12]
Therefore the role of sympathetic denervation/activation in this
challenging novel syndrome remains yet to be fully established. The "unique" finding in our patient, however, was the associated huge left
ventricular thrombus that, to the best of our knowledge, has not been
previously described in this entity.
References
(1) Barrera Ramirez C, Jiménez Mazuecos J, Alfonso F. Apical thrombus
associated with left ventricular apical ballooning. Heart 2003;89:927.
(2) Sato T, Tani Y, Fujieda H, Murao S, Sato H. Extensive myocardial
stunning showing transient regression of prolonged T wave inversion and
prolonged sympathetic denervation. Internal Med 2001;40:312-319.
(3) Kawabata M, Suzuki K, Terai T, et al. Tako-Tsubo cardiomyopathy
associated with syndrome malign reversible left ventricular dysfunction.
Circ J 2003; 67:721-724.
(4) Suga K, Tsukamoto K, Nishigauchi K et al. Iodine-123-MIBG imaging in
pheochromocytoma with cardiomyopathy and pulmonary edema. J Nucl Med
1996;37:1361-4.
(5) Kurisu S, Inoue I, Kawagoe T et al. Myocardial perfusion and fatty
acid metabolism in patients with Tako-Tsubo-Like left ventricular
dysfunction. J Am Coll Cardiol 2003;41:743-8
(6) Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular
apical ballooning without coronary artery stenosis: a novel heart syndrome
mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-8.
(7) Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular
dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking
acute myocardial infarction. Am Heart J 2002;143:448-455.
(8) Desmet WJR, Adriaenssens BFM, Dens JAY. Apical ballooning of the left
ventricle first series in white patients. Heart 2003;89:1027-1031.
(9) Alfonso F, Nihoyannopoulos P, Stewart J, Dickie S, Lemery M, McKenna
WJ. Clinical significance of giant T waves in hypertrophic cardiomyopathy.
J Am Coll Cardiol 1990;15:965-971.
(10) Alfonso F, Balaguer J, Grande A, Palomo J, Macaya C, Zarco P. Sudden
appearance of "giant" negative T waves in patients with hypertrophic
cardimyopathy. Am Heart J 1992;123:1392-1394.
(11) Alfonso F, Frenaux P, McKenna WJ. Clinical sustained monomor-phic
ventricular tachycardia in hypertrophic cardiomyopathy: Association with
left ventricular apical aneurysm. Br Heart J 1989;61:178-181.
(12) Villareal RP, Achari A, Wilansky S, et al. Anteroapical stunning and
left ventricular outflow obstruction. Mayo Clin Proc 2001;76:79-83.
(13) Penas-LLado M,Barriales R, Goicolea J. Transient left ventricular
apical ballooning and outflow tract obstruction. J Am Coll Cardiol
2003;42:1143.
Like all medals, also flecainide has two faces. One is that of a fast
and efficient antiarrhythmic drug, the other one being that of a drug with
a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of
ventricular fibrillation in a neonate suffering from supraventricular
tachycardia (SVT), likely due to the pro...
Like all medals, also flecainide has two faces. One is that of a fast
and efficient antiarrhythmic drug, the other one being that of a drug with
a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of
ventricular fibrillation in a neonate suffering from supraventricular
tachycardia (SVT), likely due to the proarrhytmic effect of flecainide.
However, in their presentation several issues might be misleading or
neglected.
First of all, it is unclear what kind of rhythm disturbance the
neonate suffered from and if a specific pharmacological therapy had been
used during pregnancy, since an urgent caesarean section was necessary for
child delivery. Then, if the arrhythmia was not tolerated, it is unclear
why they chased an oral administration protocol of flecainide over an
intravenous one or why external electric cardioversion was not preferred
over drug therapy. The authors describe that after flecainide
administration, heart rate decreased from 240 beats/min to 170 beats/min
and then QRS complex duration increased. This behaviour is rather typical
of flecainide effect, relying on its own pharmacodynamics. Flecainide acts
blocking Na+ channels in myocardial cells membrane, thus prolonging the
duration of the action potential, possibly prolonging QRS duration. Thus,
the broad complex tachycardia seen after flecainide may well be the same
SVT with an aberrant conduction. Indeed, heart rate was the same for both
arrhythmias (170 beats/min). Flecainide administration in children has
been reported to be associated to a significant risk for arrhythmias and
fatal events,[3] as amiodarone.[4] Potential advantages of flecainide
over amiodarone are a faster effect, due to its high early uptake from the
heart, a shortest elimination (half-life of about 6 hours), and as
reported by Dr Ackland,[2] the plasmatic dosability, which may help to
avoid toxicity.
In a recently published paper [5] we reported our very
good results with the use of intravenous flecainide for the treatment of
postoperative junctional ectopic tachycardia in neonates, which is often a
lifethreatening arrhythmia. About 35 children followed-up at our centre
(with an age range at administration from 2 days to 13 years) currently
receive daily flecainide for their arrhythmias and only one adverse event
occurred in a 5-years-old girl who presented with a sinus rhythm at 65
beats/min and a QRS duration of about 200 milliseconds. Parent’s interview
revealed an over-administration of the drug. Blood sample revealed a
plasmatic drug concentration of 720 mcg/l at about 12 hours after the last
administration. Owing a flecainide elimination half life of 6 hours, we
presumed peak plasmatic values exceeding 1000 mcg/l (which is the upper
limit to avoid toxicity). Further caution should be taken with flecainide
administration in critically ill infants, since drug metabolism may be
impaired, thus accumulating in the blood. Therefore, in the setting of
resistant SVT, we endorse the use of intravenous flecainide at the loading
dose of 0.5-2 mg/kg with continuous infusion of 0.4 mg/Kg/h when the
arrhythmia is tolerated, using a smaller bolus (0.5-1 mg/kg) when the
clinical condition suggests an impaired metabolism, like in low cardiac
output patients. Immediate external electric cardioversion represents the
treatment of choice when collapse is pending. In conclusion, we do not
think that the case report by Ackland [2] should discourage the use of
flecainide in neonates with SVT, but it rather draws the attention to the
fact that all care providers should be aware of drug toxicity and of
possible proarrhythmic effects related to the administration of this
powerful drug.
References
(1) The Cardiac Arrhythmia Suppression Trial (CAST) Investigators:
Preliminary report: effect of encainide and flecainide on mortality in a
randomized trial of arrhythmia suppression after myocardial infarction. N
Engl J Med 1989;321:406-412.
(2) Ackland F, Singh R, Thayyil S. Flecainide induced ventricular
fibrillation in a neonate.Heart 2003;89:1261
(3) Fish FA, Gillette PC, Benson DW Jr. Proarrhythmia, cardiac arrest and
death in young patients receiving encainide and flecainide. The Pediatric
Electrophysiology Group. J Am Coll Cardiol 1991;18:356-365.
(4) Figa FH, Gow RM, Hamilton RM, Freedom RM. Clinical efficacy and safety
of intravenous Amiodarone in infants and children. Am J Cardiol
1994;74:573-577.
(5) Bronzetti G, Formigari R, Giardini A, et al. Intravenous Flecainide for
the Treatment of Junctional Ectopic Tachycardia after Surgery for
Congenital Heart Disease. Ann Thorac Surg 2003:76:148-151.
We greatly appreciate Dr Nobrega’s interest in our recent
publication on
the acute effects of pyridostigmine on post-exercise heart rate recovery
in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic
threshold, our more complete analysis of submaximal exercise
demonstrated no differences between the effects of pyridostigmine 30
mg and pl...
We greatly appreciate Dr Nobrega’s interest in our recent
publication on
the acute effects of pyridostigmine on post-exercise heart rate recovery
in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic
threshold, our more complete analysis of submaximal exercise
demonstrated no differences between the effects of pyridostigmine 30
mg and placebo on heart rate, oxygen consumption, or oxygen pulse at
work rates corresponding to 25-50% of maximal oxygen uptake.
Contrary findings during submaximal exercise or mental stress cited by
Dr Nobrega may be attributable to differences in the study populations,
confounding effects of background medications, or dose of
pyridostigmine.[2,3] Indeed, in two of the studies cited by Dr Nobrega, 30mg of pyridostigmine did not change heart rate during submaximal
exercise or mental stress in normal subjects.[4,5] We chose to
administer 30 mg of pyridostigmine to our heart failure subjects as
higher doses have been associated with mild cholinergic side effects in
normal subjects.[5,6]
A recent publication on the effects of pyridostigmine on heart rate
variability in chronic heart failure patients was not available at the
time
of our manuscript submission.[7] We agree that our study and the recent
publication by Dr Nobrega and colleagues together provide preliminary
evidence to suggest that cholinesterase inhibition with pyridostigmine
may be a promising new therapeutic modality in patients with chronic
heart failure.[1,7] Additional work is needed to determine the optimal
dose, formulation, and longer-term safety profile of cholinesterase
inhibition in chronic heart failure.
References
(1) Androne AS, Hryniewicz K, Goldsmith R, Arwady A, Katz SD.
Acetylcholinesterase inhibition with pyridostigmine improves heart rate
recovery after maximal exercise in patients with chronic heart failure.
Heart 2003;89(8):854-8.
(2) Kawada T, Sugimachi M, Shishido T, Miyano H, Sato T, Yoshimura R, et al. Simultaneous identification of static and dynamic vagosympathetic
interactions in regulating heart rate. Am J Physiol 1999;276(3 Pt
2):R782-9.
(3) Nakahara T, Kawada T, Sugimachi M, Miyano H, Sato T, Shishido T, et al. Cholinesterase affects dynamic transduction properties from vagal
stimulation to heart rate. Am J Physiol 1998;275(2 Pt 2):R541-7.
(4) Nobrega AC, Carvalho AC, Santos KB, Soares PP. Cholinergic
stimulation with pyridostigmine blunts the cardiac responses to mental
stress. Clin Auton Res 1999;9(1):11-6.
(5) Serra SM, Costa RV, Bastos BG, Santos KB, Ramalho SH, da Nobrega
AC. Exercise stress testing in healthy subjects during cholinergic
stimulation after a single dose of pyridostigmine. Arq Bras Cardiol
2001;76(4):279-84.
(6) Sant'anna ID, de Sousa EB, de Moraes AV, Loures DL, Mesquita ET, da
Nobrega AC. Cardiac function during mental stress: cholinergic
modulation with pyridostigmine in healthy subjects. Clin Sci
(Lond) 2003;105(2):161-5.
(7) Behling A, Moraes RS, Rohde LE, Ferlin EL, Nobrega AC, Ribeiro JP.
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I was very pleased to see Professor Vano's editorial[1] and the
reference to our Publication,[2] on this topic. He
makes the important point that interventional cardiologists are at greater
risk from radiation exposure than most other medical specialists. Of
course, interventional procedures are also a potential source of quite
serious radiation detriment to patients, so it is important to apply thes...
I was very pleased to see Professor Vano's editorial[1] and the
reference to our Publication,[2] on this topic. He
makes the important point that interventional cardiologists are at greater
risk from radiation exposure than most other medical specialists. Of
course, interventional procedures are also a potential source of quite
serious radiation detriment to patients, so it is important to apply these
very valuable procedures in a proper manner.
ICRP Publication 85 discusses these topics in some detail. Your
readers may be interested in knowing that a set of PowerPoint slides
supporting and summarising the main features of the report is available
for downloading at no cost and no registration from our website, at http://www.icrp.org/educational_area.htm.
References
(1) Vano E. Radiation exposure to cardiologists: how it could be reduced. Heart 2003;89:1123-1124 .
(2) International Commission on Radiological Protection. ICRP Publication 85. Avoidance of radiation injuries from medical interventional procedures. Annals ICRP 2000;30(2). Oxford: Pergamon, Elsevier Science Ltd.
Dear Editor
Pell considers the provision of AEDs in public places an inappropriate use of health service funding because at present there is a lack of evidence both of clinical effectiveness and cost effectiveness to support this strategy.[1]
The basis for this assertion centres on the lack of clinical trials of the use of AEDs in this situation, or a lack of comparative or baseline data in published descript...
The Editor
I thank Dr Cook for his comments regarding cardiac nomenclature used to describe nuclear images.
I feel that his comments are justified.
Yours Sincerely
Avijit Lahiri
Dear Editopr
Campbell et al. describe a study of ischaemic heart disease (IHD) and HFE gene mutations in a population where there is a high prevalence of both. They find no association between IHD and HFE genotype.
In discussing these results they conclude that this is the largest study to date of the prevalence of the HFE gene mutations in a randomly selected mainland UK or Irish population. We a...
Dear Editor
Drs Sabharwal and Lahiri are to be congratulated on their review. And their pictures, particularly the one chosen for the cover illustration, are exquisite. The labelling of this image, however, illustrates a fundamental problem with the way that nuclear cardiologists currently describe the heart, as we pointed out in our recent Editorial published in Heart.[1]
The image that is described...
Dear Editor
I read with great interest the editorial by JE Sanderson,[1] which focuses on the current controversy about the term of "diastolic heart failure".[2-5]
There is now evidence that in patients with symptoms and signs of heart failure without overt evidence of impaired left ventricular systolic function, delayed relaxation and/or abnormal stiffness are almost constant regardless of the severity of s...
Dear Editor
We read with interest the article by Nielsen et al.[1] One of the interesting findings of that study is the rather low rates of ACE inhibitor use (16% and 8% respectively for hospitalized and community dwelling heart failure patients, and 1.7% for patients with heart disease but no heart failure). The fact that the study was done conducted between 1993 and 1996 partly explains these low rates. H...
Dear Editor
We sincerely appreciate the comments by Tetsuya Sato et al. concerning our report of transient apical ballooning associated with apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated, using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients have extensive myocardial stunning as the result of sympathetic denervation. Reduction of MIBG accumulation, suggestive...
Dear Editor
Like all medals, also flecainide has two faces. One is that of a fast and efficient antiarrhythmic drug, the other one being that of a drug with a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of ventricular fibrillation in a neonate suffering from supraventricular tachycardia (SVT), likely due to the pro...
Dear Editor
We greatly appreciate Dr Nobrega’s interest in our recent publication on the acute effects of pyridostigmine on post-exercise heart rate recovery in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic threshold, our more complete analysis of submaximal exercise demonstrated no differences between the effects of pyridostigmine 30 mg and pl...
Dear Editor
I was very pleased to see Professor Vano's editorial[1] and the reference to our Publication,[2] on this topic. He makes the important point that interventional cardiologists are at greater risk from radiation exposure than most other medical specialists. Of course, interventional procedures are also a potential source of quite serious radiation detriment to patients, so it is important to apply thes...
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