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Recent eLetters

Displaying 1-10 letters out of 663 published

  1. Low risk of malignant arrhythmias and sudden cardiac death after alcohol septal ablation

    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.

    Conflict of Interest:

    None declared

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  2. Please don't forget the family

    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 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.

    Conflict of Interest:

    None declared

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  3. Re:RESOLVE could not verify the VERIFY study: response from Berry & Oldroyd

    We write in response to the letter from Nijjer et al published in Heart on October 23rd 2013 subsequently removed and then reinstated in a revised form in October 1st 2014.

    The original letter (published 15 Oct 2013) was in response to correspondence from Fan et al (University School of Medicine, Shanghai, China) commenting on a paper published online in Heart from the Davies group in Sept 2013 describing changes in iFR following percutaneous coronary intervention. Fan et al point out that the RESOLVE study of which ourselves, Nijjer and Davies are co-authors reported a "poor correlation" (their words) between iFR as first described by the Davies group in the ADVISE study and FFR, the use of which has been shown in two important randomised controlled trials to improve clinical outcomes in patients with stable ischaemic heart disease. At no point in their letter do Fan et al refer to the VERIFY study. Nevertheless, in the reply from Nijjer and Davies, after an opening paragraph of questionable relevance to the topic under discussion, they go on to make several claims about the VERIFY study, all of which are inaccurate and in our view, deliberately misleading.

    1. "VERIFY when re-analysed independently using the validated iFR algorithms was not as originally presented and the findings of Berry et al. could not be substantiated"

    All of the raw VERIFY data were provided to an independent core laboratory in the University of Columbia, New York and utilized in the RESOLVE analysis. In fact the correlation coefficient between iFR and FFR was 0.70 in VERIFY using the methodology described in the original ADVISE paper and 0.66 in RESOLVE (Fig 1a) using the proprietary Imperial College algorithm for which Davies holds the intellectual property and which has been licensed to Volcano Corporation (a multinational medical device company). In other words, if anything, the correlation is worse in RESOLVE not better. Furthermore we have the RESOLVE core lab analysis of the VERIFY dataset and the mean difference in iFR values between the two different methodologies is -0.007 which is less than the mean difference between repeated measures of either parameter and therefore represents no difference at all. It would appear that, in this case, it is not us who are 'entrenched into a cherished concept'.

    2. "...the VERIFY authors paid little attention to the accuracy of their iFR wave free period and instead chose to define diastole to include a part of systole (Figure 1)..."

    The sampling frequency of the physiological systems used to record coronary pressure data is generally 100Hz. This means individual data points can be recorded at 10ms intervals. The apparent discrepancy in the Figure referred to represents no more than 5ms and cannot possibly account for the differences between ADVISE and VERIFY. We have also reanalyzed the data after altering the end-point of the so-called "wave free period" by as much as 50ms and this makes no difference to the relationship between iFR and FFR.

    3."Unique patient numbers appear overstated and misrepresented in the VERIFY manuscript"

    Davies has confirmed to us that he believes the retrospective dataset used in VERIFY contains duplicate records. In fact the dataset includes 88 patients who had iFR and FFR measurements made before and after PCI and although this represents 2 data points for each of these patients, they are not duplicates. In any event the post PCI data from these patients was not included in the RESOLVE analysis (personal communication Dr Allen Jeremias).

    Since the publication VERIFY, the iFR paradigm has changed. The "optimal" iFR treatment threshold recommended in ADVISE was 0.83, then it became 0.89, then 0.90 and now there is a hybrid protocol (0.86-0.93). Clearly, these changes are relevant to how individual patients might be treated with stents or bypass surgery or neither. One of the main results from VERIFY was that iFR was reduced by adenosine (see figure 3 in the original paper Berry C et al J Am Coll Cardiol 2013; 61: 1421-7. "iFR during rest and hyperaemia (with intravenous adenosine).

    This result directly conflicts with ADVISE, the title page of which describes iFR as an "Adenosine-independent index of stenosis severity" which, patently, it is not. The hybrid approach now proposed is in fact dependent on using adenosine in a considerable proportion of patients. Our study was the first to show the adenosine dependence of iFR and this result has been replicated in several other studies (e.g. Redwood S et al British Cardiovascular Intervention Society 2014).

    Finally, we wish to address the accusation that "... in the excitement and haste of rapidly reporting VERIFY, some oversights may have understandably occurred." In VERIFY, which was an international multicentre study, we met our timelines for data acquisition and reporting, but there was no excitement or haste. These assumptions, like several others before, are incorrect.

    Conflict of Interest:

    Prof Berry is a signatory to institutional agreements for consultancy and a research grant between the University of Glasgow and St Jude Medical. Prof Oldroyd has acted as a Consultant for Volcano Corp. and St Jude Medical.

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  4. Survival by stroke volume index in patients with low-gradient normal EF severe aortic stenosis: insights into myocardial function and dysfunction.

    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.

    Conflict of Interest:

    None declared

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  5. Clinical Genomics and the adult with congenital heart disease: new opportunities"

    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.

    Conflict of Interest:

    None declared

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  6. Re:Pre-procedural fasting for coronary interventions: is it time to change practice?

    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 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

    Conflict of Interest:

    None declared

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  7. Role of late gadolinium enhancement cardiovascular magnetic resonance in the risk stratification of hypertrophic cardiomyopathy (HCM) - but what about 'apical' HCM?

    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

    Conflict of Interest:

    None declared

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  8. Correspondence: sudden death is associated both with epilepsy and with use of antiepileptic medications

    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

    Conflict of Interest:

    None declared

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  9. The role of Left Ventricle in the Autograft Complication after ROSS operation

    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.

    Conflict of Interest:

    None declared

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  10. Epistenocardiac pericarditis can be an electrocardiographic challenge!

    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.

    Conflict of Interest:

    None declared

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