This excellent short review article (1)is written by someone who has
a self declared interest in the manufacturer of the "laser balloon"
(Cardiofocus Inc, 500 Nickerson Road, Suite 500-200. Marlborough,
Massachusetts). It is unsurprising therefore to see that he gives the
cryoballoon, a rival technology, short shrift by dismissing it as "having
problems". In fact there are published data showing that it is probably
the...
This excellent short review article (1)is written by someone who has
a self declared interest in the manufacturer of the "laser balloon"
(Cardiofocus Inc, 500 Nickerson Road, Suite 500-200. Marlborough,
Massachusetts). It is unsurprising therefore to see that he gives the
cryoballoon, a rival technology, short shrift by dismissing it as "having
problems". In fact there are published data showing that it is probably
the most successful approach to PAF so-far invented (2). Acute success was
achieved in over 98% of 924 patients. The one year freedom from PAF rate
is over 70% discounting recurrences inside a 3 month blanking period.
Clinical pulmonary vein stenosis was 0.17%. Persistent phrenic nerve palsy
beyond 1 year occurred in only 0.37%. It is also a very simple technique
not involving any ancillary technology such as angioscopy and no
additional certification is required (In the UK laser training and
certification of both operator and laboratory is usually necessary to use
laser equipment). Also oesophageal temperature monitoring and power
adjustments are unnecessary. The simplicity of the technique has seen an
enthusiastic and growing uptake of the cryoballoon and several thousand
procedures have now been performed. The cryoballoon has brought PAF in
from the cold and is unlikely to be displaced in the near future by the
laser balloon which still does not have an established position in modern
cardiology. However, further studies are needed comparing, for example,
equipment costs, effectiveness, clinical outcomes, complications and
procedure durations.
References
(1) Gerstenfeld EP. Have lasers finally found their niche in
interventional cardiology? Heart doi:10.1136/heartjnl-2011-301358
(2) Andrade JG, Khairy P, Guerra PG et al. Efficacy and safety of
cryoballoon ablation for atrial fibrillation; a systematic review of
published studies. Heart Rhythm 2011:8; 1444-51
I read with great interest the editorial written by Zaman et al. The
paper has also highlighted that it is very difficult in any ethnic group
to understand all unmeasured socioeconomic variables which affect overall
cardiovascular risk.
Some unmeasured variable potentially could be:
1) Level of education of parents in the family.
2) Profession of father and mother.
3) Financial...
I read with great interest the editorial written by Zaman et al. The
paper has also highlighted that it is very difficult in any ethnic group
to understand all unmeasured socioeconomic variables which affect overall
cardiovascular risk.
Some unmeasured variable potentially could be:
1) Level of education of parents in the family.
2) Profession of father and mother.
3) Financial status of the family.
4) Diet - Personal liking of fast food in the family. Very difficult to
measure, however previous research has shown that fast food is often
preferred in lower socio-economical class [1]. Also, generally speaking
Asian food can vary in its saturated fat content depending upon personal
preferences. This will directly affect cardiovascular risk in that
population.
5) Location - For example, do Asians in London have better lifestyles than
those living in Glasgow? And does this effect overall cardiovascular risk?
In my opinion, Asian community educational programmes geared to
healthy lifestyles would be imperative to overall reduce the burden of
cardiovascular disease in this group in the UK.
This could potentially include interactive sessions on -
1) Healthy Asian Cooking
2) Dancing (Bollywood/Hollywood)
3) Organised social group Country Walks
4) Talks on various diseases like Diabetes, Obesity, heart attack, risk
factors for it.
5) Lastly, they should also know the fact - They are at higher risk of
heart attack than any other ethnicity in the UK!
Hopefully, with education we can reduce the overall burden of CAD in
Asian population in the UK.
Reference:
1. Smoyer-Tomic K.E., Spence J.C., Raine K.D., Amrhein C., et al. The
association between neighborhood socioeconomic status and exposure to
supermarkets and fast food outlets (2008) Health and Place, 14 (4), pp.
740-754.
Having read the three papers published around the RATPAC Trial (1,2,3), I have come to the conclusion there has been a major miscarriage of justice.
That miscarriage of justice relates to diagnostic equipment used in the standard treatment protocols for the hospitals involved in the RATPAC Trial (Beckman Access, Centaur CP and Roche E170).
Point of Care Testing (POCT) was not convincingly vindicated in this trial but the o...
Having read the three papers published around the RATPAC Trial (1,2,3), I have come to the conclusion there has been a major miscarriage of justice.
That miscarriage of justice relates to diagnostic equipment used in the standard treatment protocols for the hospitals involved in the RATPAC Trial (Beckman Access, Centaur CP and Roche E170).
Point of Care Testing (POCT) was not convincingly vindicated in this trial but the other equipment and methods were deemed by association of the data to be inadequate.
A cursory examination of the papers clearly shows :
1. The main reason for the improvement in patient discharge was the decision to change the time interval for testing cardiac markers from 12 hours (or 6 hours in one case) to 90 minutes.
2. The sensitivity of the equipment used for Troponin under the standard protocol was as good as the method used in the POCT protocol (Siemens Stratus)
3. Both POCT and Standard Care Equipment would have required a centrifuged sample so pre-analytical delay should have been the same.
4. The variability of results between sites was more about ED processes than the POCT protocol.
Therefore simply using the equipment used in the standard care setting for the 90 minute protocol would, in my opinion, have given basically the same outcomes. Point of care analysis per se was not a major player in this trial. This was all about changing timeframes and processes.
I therefore find the conclusion that "Point of care testing panel assessment increases successful discharge home and reduces median length of stay........" misleading.
The use of troponin alone by the standard protocol methods has been evaluated elsewhere (4,5) and with great success.
It is therefore not surprising that the economic assessment of the RATPAC trial found point of care testing to be expensive. It has been found in this case to be unnecessary. What was also unnecessary was the standard care guideline of a 12 hour delay, though that was the recommendation and guideline at the time, and the contributors were right to be using it. It is an old guideline and troponin methods have improved so much as to make that interval redundant.
What this paper highlights is not that POCT can improve turnaround in ED but that protocols need to be kept up to date with technological change and clinical research. This is easier said than done given the complexity of committees looking after guidelines and the conservative nature of change in a clinical setting.
I therefore declare a mistrial and absolve the Beckman Access, Roche E170 and Centaur CP of any inference of inadequacy and everyone else of any criticism for what is still a well planned, executed and valuable trial in showing that processes and procedures are more important than equipment and that variations are more about people and the conditions they work under.
REFERENCES:
1.Goodacre, SW et al "The Randomised Assessment of Treatment using Panel Assay of Cardiac Markers (RATPAC) trial : a randomised controlled trial of point-of-care cardiac markers in the emergency department" Heart 2011 97:190-196; doi:10.1136/hrt.2010.203166
2. Fitzgerald, P et al "Cost-Effectiveness of Point-of-care Biomarker Assessment for Suspected Myocardial Infarction : The Randomised Assessment of Treatment Panel Assay of Cardiac Markers (RATPAC) Trial" Acad Emerg Med 2011;18(5):488-495
3. Bradburn, M et al "Interhospital Variation in the RATPAC trial (Randomised Assessment of Treatment Panel Assay of Cardiac Markers). Emerg Med J 2011; May 26
doi: 10.1136/emj.2010.108522
4. Keller, T et al "Sensitive Troponin I in Early Diagnosis of Acute Myocardial Infarction" NEJM 2009;361:868-877
5. Reichlin, T et al "Early Diagnosis of Myocardial Infarction with Sensitive Cardiac Troponin Assays" NEJM 2009;361:858-867
to the editor:
Spratt and colleagues describe two cases in which they state that
performing a Computed Tomography coronary angiography (CTCA) prior to
alcohol septal ablation (ASA) may aid in the selection of the appropriate
septal branch for ablation and patients suitable for ASA (1).
Visualisation of a dominant septal perforator and its course in the
myocardium with CTCA has been described previously (2). Importantly,...
to the editor:
Spratt and colleagues describe two cases in which they state that
performing a Computed Tomography coronary angiography (CTCA) prior to
alcohol septal ablation (ASA) may aid in the selection of the appropriate
septal branch for ablation and patients suitable for ASA (1).
Visualisation of a dominant septal perforator and its course in the
myocardium with CTCA has been described previously (2). Importantly, CTCA
has three important limitations being that it is unable to visualise due
to limitation of resolution smaller proximal septal branches that can be
the target vessel, that it is unable to visualise the perfusion area of
the septum and that it cannot display the area of maximal flow
acceleration. The combination of coronary angiography and contrast
echocardiography has been shown to be superior for these purposes (3) and
we therefore believe that performing additional CTCA prior to ASA does not
give extra information.
reference
1) Spratt JC, Langrish JP. Identifying the target septal perforator prior
to alcohol septal ablation in hypertrophic obstructive cardiomyopathy: a
new application for computed tomography coronary angiography. Heart 2011;
97: 1718-1719.
2) Brinjikji W, Harris SR, Froemming AT, Christensen KN, Lachman N, Araoz
PA. Descriptive anatomy of the dominant septal perforators using Dual
Source CT angiography. Clin Anat 2010; 23(1): 70-8.
3) Faber L, Seggewiss H, Gleichmann U. Percutaneous septal myocardial
ablation in hypertrophic obstructive cardiomyopathy: Results with respect
to intraprocedural myocardial contrast echocardiography. Circulation 1998;
98: 2415-2421.
To the Editor
Daniell [1] reports a case of syncope after "pill-in-the-pocket" treatment
with propafenone. He mentions the CYP2D6 metabolism of propafenone and the
possible interaction with CYP2D6 inhibitors. We would like to further
illustrate the potential risks of propafenone in CYP2D6 poor metabolisers
with the case of a 70 year-old woman who died from sudden cardiac arrest
after taking 600 mg of propafenone orally for...
To the Editor
Daniell [1] reports a case of syncope after "pill-in-the-pocket" treatment
with propafenone. He mentions the CYP2D6 metabolism of propafenone and the
possible interaction with CYP2D6 inhibitors. We would like to further
illustrate the potential risks of propafenone in CYP2D6 poor metabolisers
with the case of a 70 year-old woman who died from sudden cardiac arrest
after taking 600 mg of propafenone orally for the treatment of atrial
fibrillation (AF).
The patient was seen on an outpatient basis following a cerebrovascular
accident. An ECG showed AF with a rapid ventricular rate. The QTC interval
was 430 msec. An echocardiography showed moderate left ventricular
hypertrophy (LVH) with left atrial enlargement. Left and right ventricular
systolic function and size were normal. She was taking gliclazide (160 mg
daily) for diabetes and verapamil (240 mg daily) for hypertension. After
three weeks of therapeutic anticoagulation, she received a single oral
dose of 600 mg propafenone. She was in sinusal rhythm by the next day.
Anticoagulation was maintained. A few months later, asymptomatic AF
justified another single dose of propafenone 600 mg orally. The ECG was
similar to the previous episode. She developed two hours later, a malaise
with profound weakness, sweating, pallor, nausea and vomiting. On arrival,
the emergency services noted cardiac arrest with asystole. Cardio-
pulmonary resuscitation failed.
No specific cause of death could be found. The autopsy showed moderate LVH
(<14mm) but no coronary abnormalities. A small scar of myocardial
infarction was noted on the lateral wall of the left ventricle. No
pulmonary embolism, ischemic or hemorrhagic stroke was found. However, PCR
showed homozygosity for CYP2D6*4 resulting in poor drug metabolism.
In the absence of Q wave or anamnestic angina, it is unlikely that the
small past infarction played a major role in sudden death. LVH is a known
risk factor for ventricular arrhythmia but it is mainly reported when the
septum is thicker than 14 mm. A contributory proarrhythmic adverse effect
of propafenone was suggested. Dose-related proarrhythmic effects such as
ventricular tachycardia, flutter, ventricular fibrillation and torsade de
pointes have been described [2].
Propafenone's first-pass liver metabolism is mainly related to CYP2D6, two
minor pathways being CYP1A2 and CYP3A4. CYP2D6 is subjected to
polymorphism and studies in CYP2D6 intermediate and poor metabolisers (PM)
have shown that Cmax is increased by nearly 50% and 150% respectively
compared to extensive metabolisers after a single oral dose.
Pharmacodynamics mirror pharmacokinetics with a prolongation of the PR
interval in PM [3].
The PM CYP2D6 genotype and the interaction between propafenone and
verapamil, a strong inhibitor of CYP3A4, may have led to increased
propafenone bioavailability. This, taken together with her previous
myocardial infarction and moderate LVH, might have increased the patient's
susceptibility to the dose-dependant proarrhythmogenic effects of
propafenone.
The benefit of the "pocket pill" strategy proposed for cardiac arrhythmia
[4] in vulnerable patients might well be hampered by pharmacogenetic
and/or drug-drug interactions leading to unexpected and unfavourable
issues. Determining the genotype or phenotype of patients treated with
drugs that have narrow therapeutic margins (such as class I
antiarrhythmics) may allow the prescription of an adapted dose regimen for
CYP2D6 PM.
References
1. Daniels HW. Syncope following "pill-in-the-pocket" treatment of atrial
fibrillation with propafenone plus quinidine. Heart 2011;97:1626.
2 Capucci A, Boriani G. Propafenone in the treatment of cardiac
arrhythmias. A risk-benefit appraisal. Drug Safety 1995; 12: 55-72.
3. Zhou SF. Polymorphism of human cytochrome P450 2D6 and its clinical
significance: Part I. Clin Pharmacokinet 2009;48:689-7234.
4. Alboni P, Botto GL, Baldi N, Luzi M, Russo V, Gianfranchi L et al.
Outpatient treatment of recent-onset atrial fibrillation with the "pill-in
-the-pocket" approach. N Engl J Med 2004; 351: 2384-91
I read with interest Harinstein et al's review of clinical assessment
in acute heart failure syndromes (AHFS) . Initial assessment of AHFS
included evaluation of important prognostic factors which influence
treatment such as the presence of atrial fibrillation, acute pulmonary
oedema and renal function. This is in accordance with the 6 axis model
described by Professor Gheorghiade. An important factor in the 6 axis
model...
I read with interest Harinstein et al's review of clinical assessment
in acute heart failure syndromes (AHFS) . Initial assessment of AHFS
included evaluation of important prognostic factors which influence
treatment such as the presence of atrial fibrillation, acute pulmonary
oedema and renal function. This is in accordance with the 6 axis model
described by Professor Gheorghiade. An important factor in the 6 axis
model which has been neglected is the role of blood pressure in the
presentation and evaluation of AHFS. Blood pressure plays a critical role
in the prognosis of acute heart failure and should be a central
consideration in management decisions. Previous work by Prof Gheorghiade
describes the central role of blood pressure in acute heart failure. Blood
pressure is an independent predictor of mortality and morbidity in heart
failure. AHFS can present with low, normal and high blood pressure and
each of these groups have different pathophysiology and respond
differently to treatment. It is important to distinguish between them in
the evaluation of AHFS. High blood pressure in AHFS tends to be due to a
reactive hypertension caused by high sympathetic tone whereas low blood
pressure reflects poor cardiac output . Studies have shown that elevated
systolic blood pressure (SBP) is common in patients hospitalized with
AHFS. These patients have a lower post-discharge mortality, lower rates of
rehospitalisation and shorter duration of stay that those with low
systolic blood pressure. However they also have a increased risk of morbid
events. It is hypothetised that blood pressure may distinguish those with
early or mid stage disease (high SBP) from those with advanced disease
(low SBP) . Congestive symptoms were more likely in high blood pressure
at admission however during discharge low SBP had more congestive
symptoms. Patients with high blood pressure may respond to heart failure
treatment differently to low SBP however high blood pressure in AHFS is
underrepresented in clinical trials of heart failure drugs. Use of ACE
inhibitors and Beta blockers in these patients may have beneficial anti-
hypertensive effect whereas they are less used in heart failure with
hypotension. Hypotension may represent low cardiac output and maintaining
adequate blood pressure is a treatment priority in the management of these
types of AHFS. High SBP had better response to treatment however the re-
hospitalisation rates and risk of morbid events were similar to low SBP.
Better treatment response in high SBP gave physician a false sense of
security that these patients were not as ill as hypotensive AHFS. This
may have resulted in less aggressive management. There were lower rates of
left ventricular function assessment and aldosterone use in high SBP.
Acute heart failure is often inadequately managed in hospitals resulting
in poor prognosis and re-hospitalisation. One of the factors influencing
good management is careful evaluation of blood pressure. The role of this
important factor is often poorly understood and underestimated. Yet it is
a clinical feature which makes a substantial difference to treatment
response.
Harinstein M E, Flaherty J D, Fonarow G C, Mehra M R, Lang R M,
Raymond K J, Cleland J G, Knight B P, Pang P S, Bonow R O, GHEORGHIADE M
Clinical assessment of acute heart failure syndromes: emergency department
through the early post-discharge period Heart 2011 97:1607-1618;
doi:10.1136/hrt.2011.222331
Gheorghiade M, Abraham W T, Albert N M, Greenberg B H, O'Connor C,
Yancy C W, Young J B, Fonorow G C, Systolic Blood Pressure at Admission,
Clinical Characteristics, and Outcomes in Patients Hospitalized With Acute
Heart Failure JAMA. 2006;296(18):2217-2226. doi: 10.1001/jama.296.18.2217
Gheorghiade M, Abraham WT, Albert NM, et al., OPTIMIZE-HF
Investigators and Coordinators. Systolic blood pressure at admission,
clinical characteristics, and outcomes in patients hospitalized with acute
heart failure. JAMA. 2006;296(18):2217-2226.
Flaherty JD, Bax JJ, De Luca L, et al., Acute Heart Failure Syndromes
International Working Group. Acute heart failure syndromes in patients
with coronary artery disease early assessment and treatment. J Am Coll
Cardiol. 2009;53(3):254-263
Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure
syndromes: current state and framework for future research.
Circulation.2005;112:3958
Further to Kenny et al's response to our editorial view (1) of their
original paper (2), we completely agree that long-term surveillance after
coarctation stenting is required to detect complications but would re-
iterate that this must also apply to balloon dilation and surgical repairs
too. Given that these patients will need life-long follow up and continued
imaging it is important that such imaging carries a low risk to...
Further to Kenny et al's response to our editorial view (1) of their
original paper (2), we completely agree that long-term surveillance after
coarctation stenting is required to detect complications but would re-
iterate that this must also apply to balloon dilation and surgical repairs
too. Given that these patients will need life-long follow up and continued
imaging it is important that such imaging carries a low risk to the
patient and is sensitive to vascular complications that may arise both at
the site of repair and at the aortic valve and ascending aorta.
While MRI scanning cannot detect circumferential stent fracture, it
occurs in the setting of a resistant lesion and by its very occurrence is
accompanied by a recurrent gradient that is detectable on echocardiography
or MRI velocity scanning. Current MRI imaging sequences are now able to
provide good wall definition even with stainless steel stents and as MRI
becomes more widely available should allow a reduction in the need for CT
scanning in this setting just to detect aneurysm formation. We use CT now
only when urgency dictates and MRI is not readily available for logistic
reasons.
As Kenny et al acknowledge, the assessment of coarctation by MRI
scanning is comprehensive and without any risks from radiation and we
believe should become the preferred modality supplemented by interval
echocardiography and clinical examination.
1. Rosenthal E, Bell A. Optimal imaging after coarctation stenting.
Heart 2010; 96:1169-71.
2. Chakrabarti S, Kenny D, Morgan G, et al. Balloon expandable stent
implantation for native and recurrent coarctation of the aorta :
prospective computed tomography assessment of stent integrity, aneurysm
formation and stenosis relief. Heart 2010; 96:1212-16.
To the Editor: We read with interest the paper by van Engelen et
al.,1 analysing the prevalence of 22q11.2 deletion syndrome (22q11.2DS) in
adults with tetralogy of Fallot (TOF) and with pulmonary
atresia(PA)/ventricular septal defect (VSD). We agree with the experience
that many adult patients with TOF have not been tested for 22q11.2DS in
the past, so that awareness of the syndrome is needed among clinicians who
care ad...
To the Editor: We read with interest the paper by van Engelen et
al.,1 analysing the prevalence of 22q11.2 deletion syndrome (22q11.2DS) in
adults with tetralogy of Fallot (TOF) and with pulmonary
atresia(PA)/ventricular septal defect (VSD). We agree with the experience
that many adult patients with TOF have not been tested for 22q11.2DS in
the past, so that awareness of the syndrome is needed among clinicians who
care adults with congenital heart defects (CHDs). Nevertheless, we
disagree to introduce as general practice the large-scale screening of all
TOF patients irrespective of their clinical phenotype. Personal experience
in paediatric patients with 22q11.2DS has evidenced that the deletion is
virtually never found in non-syndromic patients with conotruncal defects.2
In addition, it has been evidenced that distinct subtypes of conotruncal
heart defects are likely to be found in association with 22q11.2DS. In
regard to TOF, patients with 22q11.2DS have often right/cervical aortic
arch with/without aberrant left subclavian artery, hypoplasia or absence
of the infundibular septum, absence of the pulmonary valve, and hypoplasia
and discontinuity of the pulmonary arteries.2 Among children with TOF and
PA, the 35% is carrying a 22q11.2DS, and distinctive recognizable patterns
of CHDs include major aorto-pulmonary collateral arteries, sometimes with
discontinuity of the pulmonary arteries.2
The review of the literature about clinical characteristics of adults with
22q11.2DS is showing that extracardiac anomalies can help clinician to
suspect 22q11.2DS.3 Particularly, previous series reported that facial
anomalies can be detected in 99-100% of the cases, ranging from subtle to
characteristic. Additional evidenceable signs include hypernasal speech
(90%), intellectual disability of any degree and/or learning difficulties
(93-97%). The rare occurrence of extremely mild clinical expression of
22q11.2DS in a parent of an affected child can now be explained with the
molecular mechanisms of genetic compensation (presence of a 22q11.2
deletion on one chromosome and 22q11.2 duplication on the other allele of
chromosome 22).4
In conclusion, the search for 22q11.2DS is important in adult patients
with TOF and with PA/VSD, since recognition of the syndrome has clinical
and reproductive implications, but genetic testing, in our opinion, should
be reserved to patients with associated "classic" or "subtle" extracardiac
anomalies, and to those with distinct anatomic cardiac subtypes.
M.Cristina Digilio,1 Bruno Marino,2 Bruno Dallapiccola1
1 Medical Genetics, Bambino Gesu' Paediatric Hospital, IRCCS, Rome, Italy;
2 Department of Pediatrics, Pediatric Cardiology, La Sapienza University,
Rome, Italy
Correspondence to Dr M.Cristina Digilio, Medical Genetics, Bambino
Gesu' Paediatric Hospital, IRCCS, Piazza S.Onofrio 4, 00165 Rome, Italy;
mcristina.digilio@opbg.net
REFERENCES
1. van Egelen K, Topf A, Keavney BD, et al. 22q11.2 deletion syndrome is
under-recognized in adult patients with tetralogy of Fallot and pulmonary
atresia. Heart 2010;96:621-4.
2. Marino B, Digilio MC, Toscano A, et al. Anatomic patterns of
conotruncal defects associated with deletion 22q11. Genet Med 2001;3:45-8.
3. Fung WLA, Chow EWC, Webb GD, Gatzoulis MA, Bassett AS. Extracardiac
features predicting 22q11.2 deletion syndrome in adult congenital heart
disease. Int J Cardiol 2008;131:51-8.
4. Carelle-Calmels N, Saugier-Veber P, Girard-Lemaire F, et al. Genetic
Compensation in a Human Genomic Disorder. N Engl J Med 2009;360:1211-6.
The full National Heart Failure Audit report[1] and a recent
editorial in the Lancet endorse the report's conclusion that it 'provides
a powerful incentive to reorganize heart failure care in the UK'.[1,2] The
suggested solution is to provide specialist care similar to that given to
people after heart attacks citing that such specialized units 'could do
for heart failure what coronary care units have done for myocardial...
The full National Heart Failure Audit report[1] and a recent
editorial in the Lancet endorse the report's conclusion that it 'provides
a powerful incentive to reorganize heart failure care in the UK'.[1,2] The
suggested solution is to provide specialist care similar to that given to
people after heart attacks citing that such specialized units 'could do
for heart failure what coronary care units have done for myocardial
infarction.'[2] There is no mention of how primary care could be involved
and there is only a passing reference to rehabilitation.
Since 2004 general practitioners in the UK have been rewarded for
maintaining heart failure registers through the quality and outcomes
framework of the GMS contract. In many parts of the UK there are community
based heart failure specialist nurses who make an important contribution
in caring for patients with heart failure - providing lifestyle advice and
supervising the gradual titration of beneficial drugs such as angiotensin
converting inhibitors and beta blockers. It would make sense to link these
community-based services with the services in hospitals. The forward in
the audit report acknowledges that 'it is vital that there is close
collaboration between primary and secondary care if the improved outlook
for heart failure patients is to be realised'. [1]
The benefits of nurse led secondary prevention clinics for coronary heart
disease in primary care are proven[3]and a recent updated Cochrane review
of exercise in heart failure has demonstrated improved outcomes.[4] It is
possible to link clinics in primary care with cardiac rehabilitation
programmes [5] and commissioners can now access new NHS support for
cardiac rehabilitation to design better services for heart
failure.(http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/Browsable/DH_117504)
Hasnain Dalal, Peninsula Medical School (Primary Care), Truro, TR1
3HD
Jenny Wingham, Royal Cornwall Hospitals Trust, Truro
Patrick Doherty, York St John University
Robert JP Lewin, University of York, York
Rod S Taylor,Penisula Medical School(Primary Care), Exeter
Reference List
(1) NHS Information Centre and the British Society for Heart
Failure. National Heart Failure Audit 2010. 2010.
Ref Type: Report
(2) Crunch time for heart failure care in England and Wales. Lancet
2010; 376(9758):2041.
(3) Campbell NC, Thain J, Deans HG, Ritchie LD, Rawles JM, Squair
JL. Secondary prevention clinics for coronary heart disease: randomised
trial of effect on health. BMJ 1998; 316(7142):1434-1437.
(4) Davies EJ, Moxham T, Rees K, Singh S, Coats AJ, Ebrahim S et al.
Exercise training for systolic heart failure: Cochrane systematic review
and meta-analysis. Eur J Heart Fail 2010; 12(7):706-715.
(5) Dalal HM, Evans PH. Achieving national service framework
standards for cardiac rehabilitation and secondary prevention. BMJ 2003;
326(7387):481-484
Conflict of Interest:
All authors except Patrick Doherty are members of the REACH HF Study Group which has received funding from the NIHR as a Programme Development Grant to conduct research in heart failure and cardiac rehabilitation
Remarkably, chest radiography was notable by its absence from the
"mandatory fields for completion" in the 2008-2009 national heart failure
audit(1) notwithstanding the documentation that clinical markers of
congestion have high positive predictive value(PPV) for validation of
acute heart failure(2). According to one review, pulmonary vascular
redistribution is associated with a PPV of 75% and a negative predictive
valu...
Remarkably, chest radiography was notable by its absence from the
"mandatory fields for completion" in the 2008-2009 national heart failure
audit(1) notwithstanding the documentation that clinical markers of
congestion have high positive predictive value(PPV) for validation of
acute heart failure(2). According to one review, pulmonary vascular
redistribution is associated with a PPV of 75% and a negative predictive
value(NPV) of 52% for the presence of acute heart failure.
Correspondingly, interstitial oedema is associated with PPV and NPV of 78%
and 53%, respectively(2). Accordingly the national heart failure audit
was a missed opportunity for evaluating the diagnostic accuracy of these
two radiographic parameters in the real world
References
(1) Cleland JG., McDonagh T., Rigby AS et al
The national heart failure audit for England and Wales 2008-2009
Heart 2011;97:876-886
(2)Gheorghiade M., Follath F., Ponikowski P et al
Assessing and grading congestion in acute heart failure: a scientific
statement from the Acute Heart Failure Committee of the Heart Failure
Association of the European Society of Cardiology and Endorsed by the
European Society of Intensive Care Medicine
European Journal of Heart Failure 2010;12:423-33
This excellent short review article (1)is written by someone who has a self declared interest in the manufacturer of the "laser balloon" (Cardiofocus Inc, 500 Nickerson Road, Suite 500-200. Marlborough, Massachusetts). It is unsurprising therefore to see that he gives the cryoballoon, a rival technology, short shrift by dismissing it as "having problems". In fact there are published data showing that it is probably the...
Dear Editor
I read with great interest the editorial written by Zaman et al. The paper has also highlighted that it is very difficult in any ethnic group to understand all unmeasured socioeconomic variables which affect overall cardiovascular risk.
Some unmeasured variable potentially could be:
1) Level of education of parents in the family. 2) Profession of father and mother. 3) Financial...
to the editor: Spratt and colleagues describe two cases in which they state that performing a Computed Tomography coronary angiography (CTCA) prior to alcohol septal ablation (ASA) may aid in the selection of the appropriate septal branch for ablation and patients suitable for ASA (1). Visualisation of a dominant septal perforator and its course in the myocardium with CTCA has been described previously (2). Importantly,...
To the Editor Daniell [1] reports a case of syncope after "pill-in-the-pocket" treatment with propafenone. He mentions the CYP2D6 metabolism of propafenone and the possible interaction with CYP2D6 inhibitors. We would like to further illustrate the potential risks of propafenone in CYP2D6 poor metabolisers with the case of a 70 year-old woman who died from sudden cardiac arrest after taking 600 mg of propafenone orally for...
I read with interest Harinstein et al's review of clinical assessment in acute heart failure syndromes (AHFS) . Initial assessment of AHFS included evaluation of important prognostic factors which influence treatment such as the presence of atrial fibrillation, acute pulmonary oedema and renal function. This is in accordance with the 6 axis model described by Professor Gheorghiade. An important factor in the 6 axis model...
Further to Kenny et al's response to our editorial view (1) of their original paper (2), we completely agree that long-term surveillance after coarctation stenting is required to detect complications but would re- iterate that this must also apply to balloon dilation and surgical repairs too. Given that these patients will need life-long follow up and continued imaging it is important that such imaging carries a low risk to...
To the Editor: We read with interest the paper by van Engelen et al.,1 analysing the prevalence of 22q11.2 deletion syndrome (22q11.2DS) in adults with tetralogy of Fallot (TOF) and with pulmonary atresia(PA)/ventricular septal defect (VSD). We agree with the experience that many adult patients with TOF have not been tested for 22q11.2DS in the past, so that awareness of the syndrome is needed among clinicians who care ad...
The full National Heart Failure Audit report[1] and a recent editorial in the Lancet endorse the report's conclusion that it 'provides a powerful incentive to reorganize heart failure care in the UK'.[1,2] The suggested solution is to provide specialist care similar to that given to people after heart attacks citing that such specialized units 'could do for heart failure what coronary care units have done for myocardial...
Remarkably, chest radiography was notable by its absence from the "mandatory fields for completion" in the 2008-2009 national heart failure audit(1) notwithstanding the documentation that clinical markers of congestion have high positive predictive value(PPV) for validation of acute heart failure(2). According to one review, pulmonary vascular redistribution is associated with a PPV of 75% and a negative predictive valu...
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