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Recent eLetters

Displaying 1-10 letters out of 671 published

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

    To the Editor,

    We thank the authors for their letter. The question is raised whether our study is able to distinguish between the effect of using antiepileptic medications (AEMs) and epilepsy on SCD risk. We studied SCD risk among AEM users (with and without epilepsy).1 We show in multiple ways that AEM use increases SCD risk, independently from epilepsy and other confounders. Notably, SCD risk in non-epilepsy patients using AEMs was 2.3 (1.01-5.2), while SCD risk in all patients using AEMs was also 2.3 (1.4-3.9), with correction for epilepsy and confounders. Additionally, we show among epilepsy patients (who were all AEM users) that uncontrolled seizures determined SCD risk. Epilepsy patients with controlled seizures (=stable epilepsy) had an SCD risk of 1.6 (0.7-4.1), while epilepsy patients with uncontrolled seizures had an SCD risk of 6.4 (2.4-17.4). Therefore, we believe that SCD is associated with both epilepsy and AEM use. Another question is raised whether sudden unexpected death in epilepsy (SUDEP) could be an alternative diagnosis for SCD. We have previously studied SCD risk in epilepsy in a large population-based study, with ECG- documentation of ventricular fibrillation (VF).2 In that study, 1.4% of all cases (n=1019) had epilepsy. In the current study, SCD was defined by established clinical criteria. Here we found epilepsy in 1.5% of SCD cases (n=926). Thus, proportions of epilepsy are comparable between the populations. For this reason we assume that SCD misclassification is minimal. If SUDEP would be misclassified as SCD, one would expect the proportion of epilepsy to be higher.

    Importantly, autopsy-negative sudden death (the hallmark of SUDEP) does not help to exclude cardiac causes of sudden death. Potentially fatal arrhythmia syndromes (e.g., Idiopathic VF, Brugada Syndrome, Long QT syndrome) are often accompanied by negative autopsy.

    The OR for Gabapentine is indeed based on small numbers, however significant. Although residual bias cannot be excluded, we would like to underline that diabetes and stroke were no major confounders in this association.

    In conclusion, we believe that SUDEP has both cardiac and non-cardiac causes. Acknowledging that SCD is part of SUDEP is the first step in the battle against sudden death in epilepsy.

    REFERENCES 1. Bardai A, Blom MT, van Noord C, Verhamme KM, Sturkenboom MC, Tan HL. Sudden cardiac death is associated both with epilepsy and with use of antiepileptic medications. Heart Published Online First: 16 Jul 2014 doi:10.1136/heartjnl-2014-305664 2. Bardai A, Lamberts RJ, Blom MT, Spanjaart AM, Berdowski J, van der Staal SR, Brouwer HJ, Koster RW, Sander JW, Thijs RD, Tan HL. Epilepsy is a risk factor for sudden cardiac arrest in the general population. PLoS One. 2012;7:e42749

    Conflict of Interest:

    None declared

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  2. Instantaneous Wave-free Ratio: a Word of Caution or Reliable Parameter?

    Changqing Yang Guoxin Fan, Xiaolong Qi, Shisheng He, Tongji Hospital, Tongji University School of Medicine Shanghai China

    TO THE EDITOR: We take great interest in the paper (1) by Nijjer et al with regard to instantaneous wave-free ratio (iFR) assessing improvement in coronary haemodynamics after percutaneous coronary intervention (PCI). However, we have some concerns about the invasive, pressure-only index, iFR.

    iFR, a novel resting index without hyperemia, is calculated over five heartbeats as the ratio of distal to proximal coronary pressures during the diastolic. The assumption is that the resistance during a particular part of diastole will be as low as the average resistance during the complete heart cycle in hyperemia and not be influenced by adenosine infusion.2

    Nevertheless, assumption is assumption, whilst numerical equation makes sense. Fluid-dynamics equation elucidates that iFR is able to predict the severity of stenosis (e.g. a 70% long LAD stenosis) only when friction is the predominant cause of energy loss within the stenosis.(2) That is to say, a short 50% left main stenosis, in which separation and turbulent flow are responsible for the energy loss, creates a negligible resting gradient with an extremely large hyperemic gradient. In the recent Resolve registry (3), a poor correlation was found between iFR and fractional flow reserve (FFR). Only if iFR was <_0.82 as="in=" _24="of=" the="_1539="_1539"" patients="patients" could="could" hyperemia="hyperemia" be="be" omitted="omitted" to="to" achieve="achieve" a="a" _95="_95" certainty="certainty" making="making" correct="correct" decision="decision" whether="whether" or="or" not="not" revascularize.="revascularize." so="so" our="our" question="question" raised="raised" again="again" is="is" ifr="ifr" equivalent="equivalent" ffr="ffr" _4="_4" it="it" even="even" instantaneously="instantaneously" measured="measured" name="name" suggests="suggests" totally="totally" independent="independent" pharmacological="pharmacological" vasodilatation="vasodilatation" because="because" calculated="calculated" an="an" average="average" value="value" and="and" strongly="strongly" influenced="influenced" by="by" hyperemia.2="hyperemia.2" we="we" really="really" appreciate="appreciate" this="this" prospective="prospective" observational="observational" study="study" applying="applying" assess="assess" improvement="improvement" coronary="coronary" haemodynamics="haemodynamics" after="after" pci.="pci." found="found" that="that" change="change" intervention="intervention" _0.20="_0.20" _0.21="_0.21" was="was" similar="similar" _0.22="_0.22" _0.15="_0.15" p="p" surely="surely" based="based" on="on" data="data" presented="presented" might="might" used="used" objectively="objectively" document="document" following="following" pci="pci" manner="manner" ffr.1="ffr.1" however="however" may="may" have="have" highly="highly" variable="variable" measurement="measurement" clinical="clinical" practice="practice" almost="almost" unachievable="unachievable" create="create" true="true" resting="resting" condition="condition" obscure="obscure" determine="determine" what="what" extent="extent" some="some" present.="present.">

    1 Nijjer SS, et al. Improvement in coronary haemodynamics after percutaneous coronary intervention: Assessment using instantaneous wave- free ratio. Heart. 2013

    2. Pijls NH. Fractional flow reserve to guide coronary revascularization. Circ J. 2013; 77: 561-569.

    3. A. J. Resolve: A multicenter study to evaluating the diagnostic accuracy of ifr compared to ffr. J Am Coll Cardiol. 2013;

    4. Fan GX and Xu YW. Is the instantaneous wave-free ratio equivalent to fractional flow reserve? J Am Coll Cardiol. 2013; 62: 943.

    Conflict of Interest: None declared

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  3. Does TCPC power loss really affects exercise capacity?

    We read with interest the article by Khiabani et al.[1], where the authors suggested TCPC power loss could affect exercise performance in Fontan patients. Using indexed Power Loss, "iPL", instead of unadjusted PL, they report higher iPL correlated with worse exercise. We believe that this approach is misleading leading to wrong conclusions.

    iPL was:

    iPL=PL/(pQ^3/BSA^2 )

    where PL, p, Q, and BSA are the TCPC power loss, blood density, TCPC flow, and body surface area. The justification for using iPL is that it "accounts for differences in flow and BSA between different patients[1]". However, this may not be true. While the authors state iPL is a flow- independent resistance index [2], there are no data supporting it is independent of BSA. This is critically important, because if iPL is dependent on BSA, then using iPL to correlate against exercise parameters that are themselves dependent on BSA, would mandate 'self correlation'. Using another dimensionless parameter, Reynolds number (Re), as an example, one can propose to correlate Re with exercise. Since Re directly depends on blood flow velocity, and velocity indeed changes with exercise, a compulsory correlation would be uncovered without being clinically useful.

    The problem with iPL is indexing by BSA^2. Since BSA is not directly relating to fluid flow, BSA should not be used in dimensional analysis of flow physics. To illustrate this, while patient age is empirically related to body size and blood flow, it would be erroneous to use age as a time dimension in a dimensional analysis of TCPC flow physics. A more appropriate choice would be using anatomic length measurements such as diameter of major blood vessels.

    Without knowing iPL is independent of BSA, the correlation between iPL and peak VO2 does not convincingly support the study conclusion. Another study which did not use the authors' iPL found no correlation between power loss and exercise capacity[3]. Others have shown TCPC power loss represents a fraction of total systemic power[4], making it questionable whether power loss is physiologically significant. We encourage the authors to use alternative metrics, and reassess the correlation between TCPC power loss and exercise capacity.

    References

    1 Khiabani RH, Whitehead KK, Han D, Restrepo M, Tang E, Bethel J, Paridon SM, et al. Exercise capacity in single-ventricle patients after Fontan correlates with haemodynamic energy loss in TCPC. Heart 2014

    2 Dasi LP, Pekkan K, Katajima HD, Yoganathan AP. Functional analysis of Fontan energy dissipation. J Biomech 2008, 41: 2246-2252

    3 Bossers SS, Cibis M, Gijsen FJ, Schokking M, Strengers JL,

    Verhaart RF, Moelker A, et al. Computational fluid dynamics in Fontan patients to evaluate power loss during simulated exercise. Heart 2014, 100: 696-701

    4 Kung E, Baretta A, Baker C, Arbia G, Biglino G, Corsini C, Schievano S, et al. Predictive modeling of the virtual Hemi-Fontan operation for second stage single ventricle palliation: Two patient- specific cases. Journal of Biomechanics 2013, 46: 423-429

    Conflict of Interest:

    None declared

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  4. 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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  5. "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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  6. 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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  7. 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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  8. 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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  9. 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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  10. 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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