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We believe that we have identified a methodological issue related to
the procedure that Pieters et al. [1] used to combine studies using
different types of regression models. In some studies heart rate
variability parameters were modeled as a linear model but in others they
were modeled as log-linear (i.e., where the outcome was log-transformed).
To combine effect estimates from these two types of models, the authors
co...
We believe that we have identified a methodological issue related to
the procedure that Pieters et al. [1] used to combine studies using
different types of regression models. In some studies heart rate
variability parameters were modeled as a linear model but in others they
were modeled as log-linear (i.e., where the outcome was log-transformed).
To combine effect estimates from these two types of models, the authors
converted the effect estimate into a "percent change" for an increment of
10 ug/m3.
We consider that the procedure Pieter et al. [1] used to compute
percent change from un-transformed model to be incorrect. For a log-linear
model of an outcome, y, regressed on exposure x and adjusted for
covariates, z, the percent change of the expected value of y, E(y), is:
E((y2-y1)/y1) = exp(b(x2-x1))-1. But it cannot be computed for a simple
linear model because it includes the intercept (a) and covariates:
{E(y(x2))-E(y(x1))}/E(y(x1)) = b(x2-x1)/[a+bx1+cz].
Because the value of these covariates z depends on each subject in
the study, percent change from an untransformed model cannot be computed
and used in a meta-analysis. Replacing the mean value of the outcome with
the value of the entire linear predictor in the denominator, as Pieters et
al. [1] did, is not correct because it assumes that none of the covariates
have an effect on the outcome. Effectively, they have computed the
difference and standardized it by the mean value of the outcome.
We also found that the same conversion procedure in Pieters et al.[1]
has been used in others studies [e.g., 2, 3, 4], also yielding spurious
estimates of percent change. In summary, effect estimates derived from
regression models using different functional forms for outcomes cannot be
combined and used in a meta-analysis.
References:
[1] Pieters N, Plusquin M, Cox B, Kicinski M, Vangronsveld J, Nawrot
TS. An epidemiological appraisal of the association between heart rate
variability and particulate air pollution: a meta-analysis. Heart (British
Cardiac Society) 2012; 98(15): 1127-35.
[2] Schneider A, Neas LM, Graff DW, et al. Association of cardiac and
vascular changes with ambient PM2.5 in diabetic individuals. Part Fibre
Toxicol 2010a; 7: 14.
[3] Rich DQ, Kipen HM, Huang W, et al. Association between changes in air
pollution levels during the Beijing Olympics and biomarkers of
inflammation and thrombosis in healthy young adults. JAMA : the journal of
the American Medical Association 2012; 307(19): 2068-78.
[4] Lipsett MJ, Tsai FC, Roger L, Woo M, Ostro BD. Coarse particles and
heart rate variability among older adults with coronary artery disease in
the Coachella Valley, California. Environ Health Perspect 2006; 114(8):
1215-20.
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 pa...
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
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.
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.
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.
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
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
bigg...
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.
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...
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.
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.
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 al...
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.
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
stratif...
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.
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...
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
We believe that we have identified a methodological issue related to the procedure that Pieters et al. [1] used to combine studies using different types of regression models. In some studies heart rate variability parameters were modeled as a linear model but in others they were modeled as log-linear (i.e., where the outcome was log-transformed). To combine effect estimates from these two types of models, the authors co...
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 pa...
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,...
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...
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 bigg...
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...
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
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 stratif...
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...
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