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Recent eLetters

Displaying 1-10 letters out of 670 published

  1. Re:Considerations on the poor discriminatory power of the FRANCE-2 risk score

    We thank Diaz and colleagues for their positive comments on the methodology used to develop the France-2 TAVI score. We also share their opinion that its discrimination limits the accurate identification of patients who are likely to die shortly after TAVI. This should, however, be balanced by the good calibration. We agree that "the creation of an efficient and reliable predictive model for TAVI seems to be of the biggest challenges". Nevertheless, the means to reach this goal is not easy and deserves comment. Although surgical risk scores achieve good overall predictive performance, they mix low- and high-risk patients. Their discrimination and/or calibration decreases when applied to high-risk patients, even with the Euroscore II (1). A particularity of the elderly population is the frequent alteration of functional and/or cognitive capacities which may have an impact on outcome. A simple bedside clinical evaluation favourably compares with current risk scores (2). A promising approach is to include variables related to frailty in risk scores. In a series of 152 patients aged 70 years or over undergoing valvular or coronary surgery, the addition of an indice of disability (Nagi scale) and frailty (5-meter gait speed) increased the c-index from 0.68 to 0.73 when using the STS-PROMM score to predict early morbidity and morbidity (3). A model was recently developed from 2137 patients to predict 6-month poor outcome after TAVI (4). The 10 factors of this model included a mini-mental status exam and 6-minute walk test and achieved a c-index of 0.64 in the validation sample. Therefore, additional variables may increase the discrimination of predictive models, but to a moderate extent. Their incremental predictive value should be assessed in larger series and weighed against the time needed to systematically collect additional geriatric indices. At the present time, it remains difficult to define a core of variables allowing for a reliable prediction of early outcome after TAVI or surgery. Waiting for high-performance scoring systems in the elderly, if any, current evidence supports patient selection through clinical judgement in a Heart Team taking into account available risk scores but knowing their limitations, as recommended in recent guidelines.

    References 1. Barili F, Pacini D, Capo A, et al. Does EuroSCORE II perform better than its original versions? A multicentre validation study. Eur Heart J 2013;34:22-9. 2. Laurent M, Fournet M, Feit B, et al. Simple bedside clinical evaluation versus established scores in the estimation of operative risk in valve replacement for severe aortic stenosis. Arch Cardiovasc Dis 2013;106:651- 60. 3. Afilalo J, Mottillo S, Eisenberg MJ, et al. Addition of frailty and disability to cardiac surgery risk scores identifies elderly patients at high risk of mortality or major morbidity. Circ Cardiovasc Qual Outcomes 2012;5:222-8. 4. Arnold SV, Reynolds MR, Lei Y, et al. Predictors of poor outcomes after transcatheter aortic valve replacement: Results from the PARTNER (Placement of Aortic Transcatheter Valve) trial. Circulation 2014;129:2682 -90.

    Conflict of Interest:

    Dr. Iung has received consultant fees from Abbott, Boehringer Ingelheim, Bayer, Valtech, and speaker's fees from Edwards Lifesciences. Dr. Himbert has received proctoring fees from Edwards Lifesciences and Medtronic. Dr. Vahanian is member of Advisory Board for Medtronic, Abbott, Valtech, and Boehringer Ingelheim, and has received speaker's fees from Edwards Lifesciences and Siemens.

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  2. "Type 2" myocardial infarction: Evidence-based or guesswork diagnosis

    I read with great interest the recently published article by the authors Baron et al [1] on October 20, 2014 in the journal ahead of print regarding "type 2" myocardial infarction (MI) in clinical practice. One of the important findings in this large study is the outsized variation in the incidence of "type 2" MI between the reporting sites in SWEDEHEART registry. "Type 2" MI was almost nonexistent in some sites (0.2%) and as high as 13% of patients with MI in other sites. The main reasons for these variations, in my opinion, are that the existing definition of acute "type 1" MI is inadequate and that the definition of "type 2" MI is unclear and not evidence-based [2]. Substantial numbers of patients classified as "type 2" MI in this study have in reality no MI [2]. One of the clinical entities, which erroneously diagnosed as acute MI is takotsubo syndrome (TS). TS has a clinical presentation, ECG changes and infarction biomarker rise and/or fall resembling that of MI. TS is absolutely not MI and its histopathological features are distinct from MI. The term "type 2" MI has emerged during the last few years to describe MI secondary to an "ischemic imbalance". The diagnosis of supply and/or demand imbalance is a very subjective one and based rather on guesswork than on scientific evidence. Furthermore the conditions, which cause the presumed "decreased oxygen supply" as anemia, or respiratory failure and the conditions with supposed "increased oxygen demand", may act as a trigger factor for TS. The second finding in the study is that patients with"type 2" MI were predominantly elderly women, had more comorbidities, smaller extent of myocardial necrosis MI and more normal coronary arteries. These findings are actually characteristic features of TS. Moreover, the inclusion of an indistinct and non-evidence-based diagnosis as "type 2" MI in SWEDEHEART registry, where the second "E" in the word is standing for "Evidence-based care", is an important limitation of the study. On the contrary to what the authors of the study believe, the true incidence of "type 2" MI, if such a diagnosis would be present, might have been overestimated in the study because it has certainly incorporated many patients with TS. For further detail about the above-mentioned arguments, the reader is referred to [2].

    REFRENCES 1 Baron T, Hambraeus K, Sundstrom J, et al. Type 2 myocardial infarction in clinical practice. Heart 2014. 2 Y-Hassan S. In case of strict application, the third universal definition of myocardial infarction will erase takotsubo syndrome as a diagnosis. Inter J Cardiol 2014;176:1217-9.

    Conflict of Interest:

    None declared

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  3. Re:Re:Effect of incomplete revascularization

    Thank you for your response. However, since lesion calcification influenced incomplete revascularization, it would have been interesting to note its effect independant of incomplete revascularization on PCI outcomes.

    Conflict of Interest:

    None declared

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  4. Mitral regurgitation in Patients with Aortic Stenosis

    There are a number of studies looking at resolution of mitral regurgitation in patients undergoing aortic valve replacement and there is no reason to doubt that these findings will apply to patients undergoing Transcutaneous Aortic Valve Implantation (TAVI) as well. Mitral regurgitation secondary to abnormal leaflets i.e. a degree of Prolapse, in patients with aortic stenosis will NEVER get better with Aortic valve intervention alone. If the mitral is morphologically normal, a strong predictor of resolution after aortic valve intervention is rhythm. If the patient is in sinus rhythm, mitral regurgitation will improve. If however the patient is in atrial fibrillation and has an enlarged atrium, the mitral regurgitation will not improve and may even worsen after surgery. It is important that cardiology teams involved in heart valve intervention read the surgical literature - re-invention of the wheel is wasteful.

    Conflict of Interest:

    None declared

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  5. Re:Effect of incomplete revascularization

    Unfortunately, data with regards the presence of incomplete revascularization was available only in the Syntax study and thus this variable was not inserted in the multivariate model. Besides the aim of this analysis was to assess for clinical and anatomical variables that are available before percutaneous coronary intervention and are independent predictors of worse outcomes, since these variables can be used to stratify risk pre-procedure, and thus guide treatment.

    Conflict of Interest:

    None declared

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  6. Re:The role of Left Ventricle in the Autograft Complication after ROSS operation

    We thank the Authors for the careful analysis of our work and the kind comments. In general, a distinction needs to be made when analysing clinical outcome after the Ross procedure in paediatric age. Whereas the neonatal and infant population generally presents with either isolated (often recurrent) or complex, multilevel LVOTO, which may be associated with mitral valve disease and varying degrees of LV hypoplasia, the preschool and school age population generally requires the Ross procedure for isolated (congenital) aortic valve disease. Therefore, the former patient subgroup is characterized by high operative risk and reoperations on the left heart mostly due to technical (autograft) or concomitant (mitral, aortic arch) problems. On the contrary, in the latter group, hospital risk is negligible (less than 1%) and reintervention is generally caused by progressive autograft root dilation and/or dysfunction. In other words, the pre-school and school age child having the Ross procedure tends to behave similar to the grown-up or adult, as previously shown by Hazekamp and associates [1]. Practically, the concern raised by Li and colleagues applies only to older children. Indeed, in one of our previous works [2], as well as in the study by Horer and associates [3], attention was mostly focused on the older child and the young adult, as the infant population was modestly represented. Thus, differences in baseline demography (particularly mean age) might perhaps explain, at least in part, the apparent contradictory results of the multivariate analysis amongst different studies. In fact, we essentially agree with the point raised by the Authors, as in the older child and the grown-up presenting with aortic insufficiency, LV and anular dilation, recurrence or non regression of LV dilation after the Ross procedure may promote late autograft dilation and dysfunction. We regret not to be able to further support this hypothesis in the Italian Paediatric Ross Registry database [4] due to incompleteness of echocardiographic follow-up information.

    References:

    1. Hazekamp MG, Grotenhuis HB, Schoof PH, et al. Results of the Ross operation in a pediatric population. Eur J Cardiothorac Surg. 2005 Jun;27(6):975-9.

    2. Luciani GB, Favaro A, Casali G, et al. Ross operation in the young: a ten-year experience. Ann Thorac Surg 2005;80:2271-7.

    3. 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.

    4. 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

    Conflict of Interest:

    None declared

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  7. Re:Comments on: The infective endocarditis team: recommendations from an international working group

    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.

    Conflict of Interest:

    None declared

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  8. 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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  9. 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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  10. 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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