We thank Dr San Roman and colleagues for their comment on our
editorial. They suggest that all cases with endocarditis should be
referred to a reference center because the specialist expertise to monitor
their progress may not be available at general hospitals.
The typical length of intravenous antibiotic therapy for patients
with endocarditis is 4-6 weeks and beds in most cardiac centers are
limited so that...
We thank Dr San Roman and colleagues for their comment on our
editorial. They suggest that all cases with endocarditis should be
referred to a reference center because the specialist expertise to monitor
their progress may not be available at general hospitals.
The typical length of intravenous antibiotic therapy for patients
with endocarditis is 4-6 weeks and beds in most cardiac centers are
limited so that it is necessary to manage their use carefully. Some
patients are unlikely to need cardiac surgery, for example those with
uncomplicated endocarditis caused by fully sensitive oral streptococci or
those with right-sided endocarditis. It should be safe to manage these
at a general hospital provided there are close links with the cardiac
center including case-discussions by telephone and review of
echocardiography via a shared archive. Other patients, after a period of
inpatient medical therapy with or without surgical intervention, can be
managed by the reference center as outpatients with close monitoring of
continued intravenous therapy and periodic evaluation for persistent
infection or complications. Clearly local variations in practice should
evolve including specialists from the surgical center visiting the general
hospital, temporary transfer to the cardiac center for a day for a
transoesophageal echocardiogram if indicated and formulation of a
management plan. If close links between the center and the general
hospital are not feasible and if sufficient beds are available then
management of all cases at the center is reasonable.
The key to optimal treatment implicit in both our editorial and the
comment by Dr San Roman et al is that endocarditis requires specialist
involvement at presentation and at all stages of inpatient and subsequent
outpatient care.
I read with interest a study by Balt et al. (1) concluding that among
patients who underwent alcohol septal ablation (ASA) for hypertrophic
obstructive cardiomyopathy (HOCM) only 7% of patients experienced
malignant tachyarrhythmia (VT/VF) in the first post-ASA month, while no
VT/VF were observed later. I wish to support their study and comment on
our own experience dealing with this topic.
Based on multi-centre and mult...
I read with interest a study by Balt et al. (1) concluding that among
patients who underwent alcohol septal ablation (ASA) for hypertrophic
obstructive cardiomyopathy (HOCM) only 7% of patients experienced
malignant tachyarrhythmia (VT/VF) in the first post-ASA month, while no
VT/VF were observed later. I wish to support their study and comment on
our own experience dealing with this topic.
Based on multi-centre and multi-national European study (2), we know that
the development of ventricular arrhythmias early after ASA is not rare and
the early post-ASA period can be compared to the same period after acute
myocardial infarction. We found in-hospital VT/VF requiring immediate
electrical cardioversion in 1% of cases. Therefore, patients after ASA
require close ECG monitoring for at least five post-procedural days (2).
However, among patients with early post-procedural VT/VF there were no
further adverse clinical events. Thus, one may speculate that most of
early post-ASA ventricular arrhythmias are related to the procedure and
have no further clinical consequences (2).
A major concern associated with ASA is potentially increased risk of
sudden cardiac death in long-term follow-up. Recently, several studies
have demonstrated post-ASA survival similar to the expected survival of
age- and sex-matched general population (3-4). Moreover, causes of deaths
were determined with predominance of non-cardiac death (4).
Therefore, authors of the recent paper in the Heart should be
congratulated on further evidence of relative long-term safety of ASA.
1. Balt JC, Wijffels MC, Boersma LV, Wever EF, Ten berg JM.
Continuous rhythm monitoring for ventricular arrhythmias after alcohol
septal ablation for hypertrophic cardiomyopathy. Heart 2014 Jul 29.pii:
heartjnl-2014-305593.
2. Veselka J, Lawrenz T, Stellbrink C, et al. Low incidence of procedure-
related major adverse cardiac events after alcohol septal ablation for
symptomatic hypertrophic obstructive cardiomyopathy. Can J Cardiol
2013;29:1415-21.
3. Jensen MK, Prinz C, Hortskotte D, et al. Alcohol septal ablation in
patients with hypertrophic obstructive cardiomyopathy: low incidence of
sudden death and reduced risk profile. Heart 2013;99:1012-7.
4. Veselka J, Krejci J, Tomasov P, Zemanek D. Long-term survival after
alcohol septal ablation for hypertrophic obstructive cardiomyopathy: A
comparison with general population. Eur Heart J 2014;35: 2040-5.
The learning points that Luther and colleagues have raised from this
case are well made. Brief limb-jerking is not uncommon during syncope and
such 'convulsive syncope' may lead to an incorrect diagnosis of epilepsy
and/or unnecessary referral to a neurology service. This misdiagnosis is
not uncommon in people with inherited cardiac conditions such as long QT
syndromes; it may delay appropriate asse...
The learning points that Luther and colleagues have raised from this
case are well made. Brief limb-jerking is not uncommon during syncope and
such 'convulsive syncope' may lead to an incorrect diagnosis of epilepsy
and/or unnecessary referral to a neurology service. This misdiagnosis is
not uncommon in people with inherited cardiac conditions such as long QT
syndromes; it may delay appropriate assessment and treatment and leave
people at risk.
Clinical guidelines on transient loss of consciousness, such as those
from NICE [1], recommend that a 12-lead ECG is recorded as part of the
initial assessment, with automated interpretation or interpretation by a
healthcare professional competent in identifying relevant abnormalities,
including QT abnormalities. The supine ECG in figure 1 shows clear
evidence of substantial QT prolongation. The rhythm recording during an
episode of syncope illustrates very well the potential benefit of the
early use of implanted event recorders in people whose syncopal episodes
are not sufficiently frequent to allow confident documentation of
symptomatic episodes with an external recorder [2].
The learning point that has not been made, and that must not be
overlooked, is the importance of referring such patients and their
families to an inherited cardiac conditions service with a view to genetic
testing of the proband and to relevant phenotypic screening and/or genetic
testing of first-degree relatives. This can allow identification of other
affected family members at risk of sudden cardiac death from which they
could be protected with appropriate treatment [3].
1. National Institute for Health and Care Excellence. Transient loss
of consciousness ('blackouts') management in adults and young people.
2010. Available at: http://www.nice.org.uk/guidance/cg109
2. Davis S, Westby M, Pitcher D, Petkar S. Implantable loop recorders
are cost-effective when used to investigate transient loss of
consciousness which is either suspected to be arrhythmic or remains
unexplained. Europace 2012; 14:402-9.
3. Priori SG, Wilde AA, Horie M et al. HRS/EHRA/APHRS Expert
Consensus Statement on the Diagnosis and Management of Patients with
Inherited Primary Arrhythmia Syndromes. Available at:
http://www.escardio.org/communities/EHRA/publications/consensus-
documents/Documents/diagnosis-management-patients-inherited-primary-
arrhythmia-syndromes.pdf.
We read with interest the recent article on survival by stroke volume
index (SVI) in patients with low-gradient (LG) normal ejection fraction
(EF) severe aortic stenosis (AS), which demonstrated lower SVI is
incrementally associated with mortality [1].
The authors discuss a putative mechanism of low stroke volume
secondary to concentric remodeling which results in reduced LV cavity
size. This, is turn, impedes...
We read with interest the recent article on survival by stroke volume
index (SVI) in patients with low-gradient (LG) normal ejection fraction
(EF) severe aortic stenosis (AS), which demonstrated lower SVI is
incrementally associated with mortality [1].
The authors discuss a putative mechanism of low stroke volume
secondary to concentric remodeling which results in reduced LV cavity
size. This, is turn, impedes LV diastolic filling, culminating in
diminished systolic function despite EF. The authors quote evidence of
systolic impairment, e.g. reduced longitudinal strain, in similar cohorts
with preserved EF [2]. In the current study, the subgroup with lowest SVI,
and therefore presumed most severe systolic impairment despite EF >50%,
demonstrated the thickest relative wall measurements. We believe this
observation helps to explain the apparent paradox between significant
myocardial dysfunction and preservation of EF in this cohort and in the
wider 'heart failure with preserved ejection fraction' context. Recent
mathematical modeling of LV contraction has shown that both myocardial
shortening and end-diastolic wall thickness are determinants of EF [3].
Essentially, absolute LV wall thickening, as defined by the absolute
difference between wall thickness at end-systole and end-diastole, may be
nearly normal in patients with concentric LV hypertophy (LVH) because
absolute systolic thickening will be augmented in response to increased
end-diastolic LV wall thickness. As a result, the endocardial displacement
and EF will also be normal, as the external LV volume remains fairly
static throughout the cardiac cycle [4] and the absolute wall thickening
may appear to compensate for any contractile strain abnormality.
The development of concentric LVH ventricle may be viewed as a
compensatory response that normalises contractile stress and total
contractile force. However, if contractile stress remains reduced, the
contractile force will be inadequate and result in a fall in stroke volume
despite the preserved EF. In order to understand the apparent discrepancy
in SV and EF, one must distinguish between contractile strain and stress
and the relationship between end-diastolic wall thickness and EF.
The authors elected to investigate SV indexed to body surface area.
However, it would be interesting to know whether correcting EF for the
presence of concentric LVH (EFc), as described in mathematical modeling
studies of the LV [3], would be a useful prognostic marker in this cohort
of patients. After all, EFc is potentially an even more relevant
allometric indexed value given the importance of end-diastolic wall
thickness in patients with concentric LVH and systolic impairment but
preserved EF.
References:
[1] Eleid MF, Sorajla P, Michelena HI, et al. Survival by stroke
volume index in patients with low-gradient normal EF severe aortic
stenosis. Heart. Published Online First: 12 September 2014. Doi:
10.1136/heartjnl-2014-306151
[2] Adda J, Mielot C, Giorgi R, et al. Low-flow, low-gradient severe
aortic stenosis despite normal ejection fraction is associated with severe
left ventricular dysfunction as assessed by speckle-tracking
echocardiography: a multicenter study. Circ Cardiovasc Imaging 2012; 5: 27
-35.
[3] Maciver DH. A new method for quantification of left ventricular
systolic function using a corrected ejection fraction. Eur J Echocardiogr
2011; 12: 228-34.
[4] Emilsson K, Brudin L, Wandt B. The mode of left ventricular
pumping: is there an outer contour change in addition to atrioventricular
plane displacement? Clin Physiol 2001; 21: 437-446.
Acknowledgements:
NIHR Bristol Biomedical Research Unit in Cardiovascular Medicine.
The views expressed are those of the authors and not necessarily
those of the National Health Service, National Institute for Health
Research, or Department of Health.
We are intrigued by the article by Priest et al. The importance of genomics has been clearly identified and the article beautifully describes the role of genetics in cardiovascular medicine but concentrates on inherited arrthymias, cardiomyopathies and occasional pharmacogenomics profiling. We suggest they have failed to consider the large, unrecognized need for genomics in adults patients with congenital heart conditions....
We are intrigued by the article by Priest et al. The importance of genomics has been clearly identified and the article beautifully describes the role of genetics in cardiovascular medicine but concentrates on inherited arrthymias, cardiomyopathies and occasional pharmacogenomics profiling. We suggest they have failed to consider the large, unrecognized need for genomics in adults patients with congenital heart conditions.
More than 90% of patients with congenital heart conditions now survive to adulthood and yet as neonates/children there was restricted availability of genetic testing and limited techniques. When such patients attend the adult clinic they want to know the inheritance risk of their condition. Yet there is an additional potential to, risk stratify other family members for syndromic as well as isolated congenital cardiac defects. Multiple studies have shown that that congenital cardiac defects demonstrate family clustering which then have a higher incidence of inheritance 1 The genomic wide association study (GWAS) was the first to identify the locus for the common congenital heart condition of atrial septal defect (the locus demonstrated to be a defect at chromosome 4p16)2. We know ASD???s run in families but in addition there is a familial ASD sub group who are at risk for late complete heart block. Such ???personalized??? medicine, guided by genomics, help discriminate which family members to screen and who to keep under long term follow up. For example, the presence of left ventricular outflow tract obstruction in an index case may help to identify bicuspid aortic valve in 1st degree family members which has important long-term clinical implications for morbidity and mortality
The current paediatric guidelines (AHA) suggest gene testing for infants born with interrupted aortic arch type B, truncus arteriosus, aortic arch anomalies, ToF with absent pulmonary valve and other conotruncal anomalies3. There is an absence of guidance in respect of gene testing in the adult patient and yet simply testing for 22q11 deletion in ALL conotruncal abnormalities finds a proportion (5.8%) who have the deletion (despite no phenotypic features) ??? clearly important given the 50% inheritance risk 4.
We have been able to offer congenital heart disease patients medical and surgical services to improve their quality of life leading to survival beyond adulthood but limited focus on genetics. There may be more to offer ??? for example, the genes that cause Noonan-related disorders are those that affect the RAS pathway to increase growth ??? i.e. they are potentially tumour-predisposing genes. These individuals are at risk of neoplasia.
Congenital (paediatric) cardiologists are good at recognizing and gene testing ???syndromic??? patients, but there remain patients seen in the adult clinics who were never tested as children. Furthermore, ???non syndromic??? patients with congenital heart conditions, may have recognizable features (phenotype or association of conditions) to a geneticist who would then suggest an appropriate gene panel. We urge the close collaboration of the congenital cardiologist and geneticist in the adult congenital heart clinic. and geneticist to guide not only inheritance risk, but cascade screening and perhaps predict future risks. ???Genomics in the adult congenital heart practice. Indeed!
Reference:
1. Burn J, Brennan P, Little J, Holloway S, Coffey R, et al. Recurrence risks in offspring of adults with major heart defects: results from first cohort of British collaborative study. Lancet. 1998; 351:311???316.
2. Heather J. Cordell, Jamie Bentham, Ana Topf et al ???Genome-wide association study of multiple congenital heart disease phenotypes identifies a susceptibility locus for atrial septal defect at chromosome 4p16??? Nat Genet. Jul 2013; 45(7): 822???824
3. Pierpont ME1, Basson CT, Benson DW Jr et al ???Genetic basis for congenital heart defects: current knowledge: a scientific statement from the American Heart Association Congenital Cardiac Defects Committee, Council on Cardiovascular Disease in the Young: endorsed by the American Academy of Pediatrics??? Circulation. 2007 Jun 12;115(23):3015-38
4.Beauchesne LM, Warnes CA, Connolly HM, Ammash NM, Grogan M, et al. Prevalence and clinical manifestations of 22q11.2 microdeletion in adults with selected conotruncal anomalies. J Am Coll Cardiol. 2005;45:595???598.
We read with interest the comments from Wijeyeratne et al (1) regarding our paper. They commend our study (2) for questioning the need for fasting prior to percutaneous cardiac procedures and highlight the lack of evidence either for or against the necessity to fast in this scenario. We agree with their comments and fully accept the limitations of our retrospectively analysed data. While we don???t exp...
We read with interest the comments from Wijeyeratne et al (1) regarding our paper. They commend our study (2) for questioning the need for fasting prior to percutaneous cardiac procedures and highlight the lack of evidence either for or against the necessity to fast in this scenario. We agree with their comments and fully accept the limitations of our retrospectively analysed data. While we don???t expect our paper to result in an immediate major practice shift in cardiology, we certainly hope that it will raise awareness of this issue.
As they point out, patients might be instructed to fast, drink fluids only or not fast at all (for varying periods of time) prior to the exactly the same procedure performed in different institutions. There are no guidelines and only scant evidence to guide practice. One can see how this inconsistency in practice has arisen.
There are understandable concerns that if patients are not fasted, then their risk of complications may increase. However, these concerns are probably overstated and indeed, it is possible that harm may be more likely to occur in fasted patients.
We agree that concerns regarding a possible increased risk of pulmonary aspiration in non-fasted patients are probably unfounded. Patients who undergo primary percutaneous coronary intervention (PPCI) for acute ST elevation MI (STEMI) are not fasted and there is no reported excess of peri-procedural pulmonary aspiration on the British Cardiovascular Intervention Society (BCIS) national registry. An open label study by Kwon et al (3) reported that no patient (fasted vs non- fasted) undergoing cerebral angiography had pulmonary aspiration. A prospective study by Agrawal et al (4) demonstrated that there was no association between adverse events and not being fasted in children undergoing pre-procedural sedation in emergency department.
When patients are not fasted, we suspect radial access is easier and there appears to be less sedation-induced blood pressure drop. We believe that allowing patients to freely eat and drink before their scheduled procedure makes them less anxious as described by some patients: ???They are having a procedure, not an operation???. In centres that routinely fast their patients, delays may occur if a patient hadn???t fasted for long enough before their scheduled procedure time or if they had inadvertently broken their fast. This may prolong inpatient stay and increase costs.
We concur that more studies are required and our group is currently designing a larger, multi-center prospective study aiming to compare the two practices (fasting versus non-fasting prior to percutaneous cardiac procedures). We suspect that our findings from that larger study will provide further evidence that pre-procedural fasting is not required.
KEYWORDS:
Interventional Cardiology; Quality of Care and Outcomes, Pre Procedural
fasting.
Reference:
1. Wijeyeratne YD, Wendler R, Spray D, Bunce N;Preprocedural fasting
for coronary interventions: is it time to change practice?Heart
2014;100:13
2. Hamid T, Aleem Q, Lau Y, Singh R, McDonald J, Macdonald JE, Sastry
S, Arya S, Bainbridge A, Mudawi T, Balachandran K. re-procedural fasting
for coronary interventions: is it time to change practice? Heart. 2014
Apr;100(8):658-661
3. Kwon OK, Oh CW, Park H, Bang JS, BaeHJ, Han MK, Park SH, Han MH,
Kang HS, Park SK, Whang G, Kim BC, Jin SC; Is fasting necessary for
elective cerebral angiography? AJNR Am J Neuroradiol. 2011 May;32(5):908-
910
4. Agrawal, D., Manzi, S.F., Gupta, R. et al. Preprocedural fasting
state and adverse events in children undergoing procedural sedation and
analgesia in a pediatric emergency department. Ann Emerg Med. 2003; 42:
636-646
We read with great interest the article by Ismail et al, (1) looking
at the role of late gadolinium enhancement (LGE) cardiac magnetic
resonance in the risk stratification of patients with hypertrophic
cardiomyopathy (HCM). We would like to congratulate the authors for
delineating the interesting findings that the amount of myocardial
fibrosis was a strong univariable predictor of sudden cardiac death (SCD)
albeit the e...
We read with great interest the article by Ismail et al, (1) looking
at the role of late gadolinium enhancement (LGE) cardiac magnetic
resonance in the risk stratification of patients with hypertrophic
cardiomyopathy (HCM). We would like to congratulate the authors for
delineating the interesting findings that the amount of myocardial
fibrosis was a strong univariable predictor of sudden cardiac death (SCD)
albeit the effect was not maintained after adjusting for LV-EF.
Interestingly, in this study of consecutive referrals of patients
with suspected/known HCM to a single large tertiary centre, 18% of the
patient cohort had apical HCM phenotype. Traditionally, apical HCM has
been considered a rarer variant of HCM, with a prevalence of approximately
7% in previous studies, with known more benign prognosis and lower risk of
SCD (2).
Anecdotally, in our large tertiary CMR Unit we see a similar 18% of
apical HCM phenotype in patients with suspected/known HCM (as in the
current study), suggesting the disease variant is perhaps not as rare as
initially thought. This could be explained by the higher diagnostic value
of CMR vs echo in detecting apical HCM. (3)
It would be very interesting to clarify to which extent the findings
of this study can be fully applicable to patients with apical HCM. It is
not uncommon to find a significant amount of late gadolinium myocardial
enhancement (replacement fibrosis) in the hypertrophied apical segments.
Does this carry the same risk as demonstrated in Ismail et al.(1), in a
cohort with intrinsic more benign prognosis? Would this yet be another
reason in favor of considering apical HCM as a separate entity? (4)
Acknowledgements
NIHR Bristol Biomedical Research Unit in Cardiovascular Medicine.
The views expressed are those of the authors and not necessarily
those of the National Health Service, National Institute for Health
Research, or Department of Health.
References
1. Ismail TF, Jabbour A, Gulati A, Mallorie A, Raza S, Cowling TE,
et al. Role of late gadolinium enhancement cardiovascular magnetic
resonance in the risk stratification of hypertrophic cardiomyopathy. Heart
[Internet]. 2014 Jun 24 [cited 2014 Aug 12];heartjnl-2013-305471-.
Available from: http://heart.bmj.com/content/early/2014/06/24/heartjnl-
2013-305471.full?hwshib2=authn%3A1407961738%3A20140812%253Aae52e5ce-0f8e-
43c3-a6eb-c194a4650ad2%3A0%3A0%3A0%3AF2LsLqYFBrKXczCM8MPT0g%3D%3D
2. Eriksson MJ, Sonnenberg B, Woo A, Rakowski P, Parker TG, Wigle
ED, et al. Long-term outcome in patients with apical hypertrophic
cardiomyopathy. J Am Coll Cardiol [Internet]. Journal of the American
College of Cardiology; 2002 Feb 20 [cited 2014 Aug 12];39(4):638-45.
Available from:
http://content.onlinejacc.org/article.aspx?articleid=1127753
3. Moon JCC, Fisher NG, McKenna WJ, Pennell DJ. Detection of apical
hypertrophic cardiomyopathy by cardiovascular magnetic resonance in
patients with non-diagnostic echocardiography. Heart [Internet]. 2004 Jun
[cited 2014 Aug 18];90(6):645-9. Available from:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1768283&tool=pmcentrez&rendertype=abstract
4. Maron BJ, Haas TS, Kitner C, Lesser JR. Onset of apical
hypertrophic cardiomyopathy in adulthood. Am J Cardiol [Internet]. 2011
Dec 15 [cited 2014 Aug 13];108(12):1783-7. Available from:
http://www.sciencedirect.com/science/article/pii/S0002914911024301
We read with interest the recent paper by Bardai et al1(1), which
reports that epilepsy and antiepileptic drugs (AEDs) were independently
associated with sudden cardiac death (SCD). We are unconvinced that such a
clear distinction between disease and drug effects can be made in this
study as all people with epilepsy were by definition taking AEDs. We
believe this is why SCD risk in those with epilepsy (Table 2) and in AED...
We read with interest the recent paper by Bardai et al1(1), which
reports that epilepsy and antiepileptic drugs (AEDs) were independently
associated with sudden cardiac death (SCD). We are unconvinced that such a
clear distinction between disease and drug effects can be made in this
study as all people with epilepsy were by definition taking AEDs. We
believe this is why SCD risk in those with epilepsy (Table 2) and in AED
users with epilepsy (Table 3) was the same: OR 2.8 (95% CI: 1.4, 5.3). It
is unclear whether these numbers reflect disease effects, drug effects, or
both.
It is reported that people with epilepsy are at increased risk of SCD, yet
in this population there is a major diagnostic alternative: sudden
unexpected death in epilepsy, an autopsy-negative mostly seizure-related
type of sudden death with cardiac and non-cardiac causes.(2) We do not
believe that sudden death in people with epilepsy can be assumed to be of
cardiac origin (versus, for example, neurogenic respiratory depression)
without documentation of a cardiac mechanism of death (e.g. by ECG).
Carbamazepine and gabapentin were the only individual AEDs associated with
increased SCD risk. The authors attribute this to the supposed sodium
channel blocking properties of these drugs, but we believe that indication
bias cannot be excluded. Carbamazepine is the drug of choice in people
with focal seizures and stroke is a leading cause of this type of
epilepsy, particularly in the elderly.(3) An important indication for
gapabentin is diabetic chronic neuropathic pain.(4) It is possible that a
worse cardiovascular status rather than sodium channel blocking properties
explains the higher SCD risk in users of these AEDs. Despite the use of a
large database, many numbers are small, so the demonstrated significant
effect for sodium channel blocking AEDs but not for non-sodium channel
blocking AEDs may reflect limited sample size rather than differences in
effect. There was a consistent trend; all reported AED ORs were greater
than the null value.
This paper is important in that it confirms that epilepsy in the community
is associated with an increased risk of sudden natural death. Future
studies with additional documentation of death mechanisms, correction for
indication bias and larger sample size are needed to explain the cause of
this excess risk and clarify the role of AEDs.
1. Bardai A, Blom MT, van Noord C, et al. Sudden cardiac death is
associated both with epilepsy and with use of antiepileptic drugs. Heart.
2014 Jul 16. doi: 10.1136/heartjnl-2014-305664.
2. Shorvon S, Tomson T. Sudden unexpected death in epilepsy. Lancet 2011;
378(9808):2028-2038.
3. Ryvlin P, Montavont A, Nighoghossian N. Optimizing therapy of seizures
in stroke patients. Neurology 2006;67(12 Suppl 4):S3-9.
4. Moore RA, Wiffen PJ, Derry S, et al. Gabapentin for chronic neuropathic
pain and fibromyalgia in adults. Cochrane Database Syst Rev. 2014 Apr 27.
doi: 10.1002/14651858.CD007938.pub3
We have read the interesting article from Luciani and colleagues [1]
documenting the outcomes into the second decade after the Ross procedure
in infants and children from the Italian Paediatric Ross Registry.
Conclusion concisely stated the Ross procedure was a low risk palliative
procedure for aortic valve abnormalities at the expense of valve-related
reoperation.
We have read the interesting article from Luciani and colleagues [1]
documenting the outcomes into the second decade after the Ross procedure
in infants and children from the Italian Paediatric Ross Registry.
Conclusion concisely stated the Ross procedure was a low risk palliative
procedure for aortic valve abnormalities at the expense of valve-related
reoperation.
Contrary to prior evidence, autograft reoperation was more common
than homograft in their cohort, raising the concern about the autograft
failure in paediatric population. Besides the predictors which the authors
discussed, the interaction between the left ventricle (LV) and the
autograft is an essential associated factor.
Raedle-Hurst and associates [2] reported that elevation of LV
volumes, both systolic and diastolic, could still be noticed in patients
years after the Ross operation. Theoretically, the residual LV dilation
impairing the autograft annulus geometry, will change steady dynamics and
exhaust autograft wall structures. Therefore root dilation and valvular
regurgitation will exist more significant, translating into clinical
autograft failure.
In 2005, authors of the present study had reported younger age at
Ross procedure was predictive of late autograft dilatation [3]. However,
there was a potential confounding because patients who have Ross at an
early age usually presented with a severe valve abnormality and a severely
impaired LV.
Interestingly, Hoerer and colleagues [4] reported different findings
concerning the autograft complication. In their cohort, the autograft
annulus postoperatively tended to enlarge and regurgitation develops
predominantly in older children. A corollary to this observation is that
older patients have a more impaired LV which suffers from the haemodynamic
abnormality for a longer time.
These two findings seem to be ostensibly different, however, have one
common nature: the impaired LV, substantially highlighting the role of LV
in the development of autograft failure. All these evidence suggest LV may
be a potential key to reduce autograft complications. Hence there are more
information could be further illustrated by this study as the largest
multi-center paediatric cohort, including the baseline LV diameter and
function of the study population, the recovery of the impaired LV and
their potential relationship. Moreover, additional comments about this
issue would be helpful.
References
[1] Luciani GB, Lucchese G, Carotti A, et al. Two decades of
experience with the Ross operation in neonates, infants and children from
the Italian Paediatric Ross Registry. Heart 2014 0:heartjnl-2014-305873v1-
heartjnl-2014-305873; doi:10.1136/heartjnl-2014-305873
[2] Raedle-Hurst TM, Hosse M, Hoffmann S, et al. Ventricular
performance assessed by 2-dimensional strain analysis after Ross operation
versus aortic valve reconstruction. Ann Thorac Surg 2013;96:1567-73.
[3] Luciani GB, Favaro A, Casali G, et al. Ross operation in the
young: a ten-year experience. Ann Thorac Surg 2005;80:2271-7.
[4] Horer J, Kasnar-Samprec J, Charitos E, et al. Patient age at the
Ross operation in children influences aortic root dimensions and aortic
regurgitation. World J Pediatr Congenit Heart Surg 2013;4:245-52.
We enjoyed the image challenge published by Wu et al which
illustrates a case of contained left ventricular rupture [1]. In the
explanation, authors have excluded pericarditis based on the absence of
fever and characteristic pericarditis ECG findings. We would like to
emphasize that early post-infarction pericarditis ("epistenocardiac") is
notorious to cause atypical ECG changes which are often territorial to the
infarct...
We enjoyed the image challenge published by Wu et al which
illustrates a case of contained left ventricular rupture [1]. In the
explanation, authors have excluded pericarditis based on the absence of
fever and characteristic pericarditis ECG findings. We would like to
emphasize that early post-infarction pericarditis ("epistenocardiac") is
notorious to cause atypical ECG changes which are often territorial to the
infarct area [2-5]. One of our previous studies demonstrated that only
3.2% patients with epistenocardiac pericarditis present with classical
Stage-I pericarditic ECG changes [4]. Pericarditis in the presented case
should be correctly ruled out by the absence of a pericardial rub and the
presence of significant reciprocal ST-depressions in III and aVF on the
third ECG-tracing. Authors also point out that the key to the diagnosis
for left ventricular free wall rupture (LVFWR) is the presence of
pericardial effusion. In our opinion, the absence of pericardial effusion
has a very high negative predictive value for LVFWR, however the presence
of it (even hemorrhagic effusion) does not confirm the diagnosis as an
effusion may often accompany an 'effusive epistenocardiac pericarditis'
[2]. The hallmark to the echocardiographic diagnosis of LVFWR is the
actual visualization of wall-rupture and/or the classical color-doppler
findings with or without the use of an echo contrast [2].
References:
1.Wu H, Qian J, Ge J. Recurrent ST-segment elevation in infarct-associated
leads. Heart. 2014 Jul 29. pii: heartjnl-2014-306289. doi:
10.1136/heartjnl-2014-306289. (PMID: 25073887).
2.Spodick DH: The Pericardium: A Comprehensive Textbook, Marcel Dekker,
New York 1997. pp: 334-367.
3.Bruce MA, Spodick DH. Atypical electrocardiogram in acute pericarditis:
characteristics and prevalence. J Electrocardiol. 1980;13(1):61-66.
4.Krainin FM, Flessas AP, Spodick DH. Infarction-associated pericarditis.
Rarity of diagnostic electrocardiogram. N Engl J Med. 1984;311(19):1211-
1214.
5.Chhabra L, Chaubey VK, Spodick DH. Recurrent myocardial infarction or
Epistenocardiac pericarditis: how can surface ECG be useful in clinical
decision making? Hellenic J Cardiol. 2014. In Press.
We thank Dr San Roman and colleagues for their comment on our editorial. They suggest that all cases with endocarditis should be referred to a reference center because the specialist expertise to monitor their progress may not be available at general hospitals.
The typical length of intravenous antibiotic therapy for patients with endocarditis is 4-6 weeks and beds in most cardiac centers are limited so that...
I read with interest a study by Balt et al. (1) concluding that among patients who underwent alcohol septal ablation (ASA) for hypertrophic obstructive cardiomyopathy (HOCM) only 7% of patients experienced malignant tachyarrhythmia (VT/VF) in the first post-ASA month, while no VT/VF were observed later. I wish to support their study and comment on our own experience dealing with this topic. Based on multi-centre and mult...
Dear Editor
The learning points that Luther and colleagues have raised from this case are well made. Brief limb-jerking is not uncommon during syncope and such 'convulsive syncope' may lead to an incorrect diagnosis of epilepsy and/or unnecessary referral to a neurology service. This misdiagnosis is not uncommon in people with inherited cardiac conditions such as long QT syndromes; it may delay appropriate asse...
We read with interest the recent article on survival by stroke volume index (SVI) in patients with low-gradient (LG) normal ejection fraction (EF) severe aortic stenosis (AS), which demonstrated lower SVI is incrementally associated with mortality [1].
The authors discuss a putative mechanism of low stroke volume secondary to concentric remodeling which results in reduced LV cavity size. This, is turn, impedes...
We are intrigued by the article by Priest et al. The importance of genomics has been clearly identified and the article beautifully describes the role of genetics in cardiovascular medicine but concentrates on inherited arrthymias, cardiomyopathies and occasional pharmacogenomics profiling. We suggest they have failed to consider the large, unrecognized need for genomics in adults patients with congenital heart conditions....
Dear Editor;
We read with interest the comments from Wijeyeratne et al (1) regarding our paper. They commend our study (2) for questioning the need for fasting prior to percutaneous cardiac procedures and highlight the lack of evidence either for or against the necessity to fast in this scenario. We agree with their comments and fully accept the limitations of our retrospectively analysed data. While we don???t exp...
We read with great interest the article by Ismail et al, (1) looking at the role of late gadolinium enhancement (LGE) cardiac magnetic resonance in the risk stratification of patients with hypertrophic cardiomyopathy (HCM). We would like to congratulate the authors for delineating the interesting findings that the amount of myocardial fibrosis was a strong univariable predictor of sudden cardiac death (SCD) albeit the e...
We read with interest the recent paper by Bardai et al1(1), which reports that epilepsy and antiepileptic drugs (AEDs) were independently associated with sudden cardiac death (SCD). We are unconvinced that such a clear distinction between disease and drug effects can be made in this study as all people with epilepsy were by definition taking AEDs. We believe this is why SCD risk in those with epilepsy (Table 2) and in AED...
We have read the interesting article from Luciani and colleagues [1] documenting the outcomes into the second decade after the Ross procedure in infants and children from the Italian Paediatric Ross Registry. Conclusion concisely stated the Ross procedure was a low risk palliative procedure for aortic valve abnormalities at the expense of valve-related reoperation.
Contrary to prior evidence, autograft reoperat...
We enjoyed the image challenge published by Wu et al which illustrates a case of contained left ventricular rupture [1]. In the explanation, authors have excluded pericarditis based on the absence of fever and characteristic pericarditis ECG findings. We would like to emphasize that early post-infarction pericarditis ("epistenocardiac") is notorious to cause atypical ECG changes which are often territorial to the infarct...
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