We thank Ripley and colleagues for their interest in our paper and
agree that T1 mapping with CMR is an emerging imaging biomarker that is
increasingly being investigated for its potential role in hypertrophic
cardiomyopathy and cardiac hypertrophy in general. Convincing data have
been published concerning hypertensive heart disease(Hinojar et al.,
2015), hypertrophic and dilated cardiomyopathy (Puntmann et al., 2013),...
We thank Ripley and colleagues for their interest in our paper and
agree that T1 mapping with CMR is an emerging imaging biomarker that is
increasingly being investigated for its potential role in hypertrophic
cardiomyopathy and cardiac hypertrophy in general. Convincing data have
been published concerning hypertensive heart disease(Hinojar et al.,
2015), hypertrophic and dilated cardiomyopathy (Puntmann et al., 2013),
transthyretin amyloidosis (Fontana et al., 2014) and Anderson-Fabry
disease (Pica et al., 2014). We have not found any specific published data
examining the role of T1 mapping in distinguishing ventricular septal
bulge in an elderly population from other etiologies of hypertrophy. We
therefore decided not to include T1 mapping in our review (Canepa et al.,
2016) but concur that this technique may be potentially useful in the
evaluation of ventricular septal bulge.
Canepa, M., Pozios, I., Vianello, P. F., Ameri, P., Brunelli, C.,
Ferrucci, L., & Abraham, T. P. (2016). Distinguishing ventricular
septal bulge versus hypertrophic cardiomyopathy in the elderly. Heart,
102(14), 1087-1094. doi:10.1136/heartjnl-2015-308764
Fontana, M., Banypersad, S. M., Treibel, T. A., Maestrini, V., Sado,
D. M., White, S. K., ... Moon, J. C. (2014). Native T1 Mapping in
Transthyretin Amyloidosis. JACC: Cardiovascular Imaging, 7(2), 157-165.
doi:10.1016/j.jcmg.2013.10.008
Hinojar, R., Varma, N., Child, N., Goodman, B., Jabbour, A., Yu, C.-
Y., Puntmann, V. O. (2015). T1 Mapping in Discrimination of Hypertrophic
Phenotypes: Hypertensive Heart Disease and Hypertrophic Cardiomyopathy:
Findings From the International T1 Multicenter Cardiovascular Magnetic
Resonance Study . Circulation: Cardiovascular Imaging , 8 (12
).doi:10.1161/CIRCIMAGING.115.003285
Pica, S., Sado, D. M., Maestrini, V., Fontana, M., White, S. K.,
Treibel, T., Moon, J. C. (2014). Reproducibility of native myocardial T1
mapping in the assessment of Fabry disease and its role in early detection
of cardiac involvement by cardiovascular magnetic resonance. Journal of
Cardiovascular Magnetic Resonance?: Official Journal of the Society for
Cardiovascular Magnetic Resonance, 16(1), 99. doi:10.1186/s12968-014-0099-
4
Puntmann, V. O., Voigt, T., Chen, Z., Mayr, M., Karim, R., Rhode, K.,
Nagel, E. (2013). Native T1 Mapping in Differentiation of Normal
Myocardium From Diffuse Disease in Hypertrophic and Dilated
Cardiomyopathy. JACC: Cardiovascular Imaging, 6(4), 475-484.
doi:10.1016/j.jcmg.2012.08.019
Goorden et al aim to establish the optimal threshold to rule out
myocardial infarction using a high-sensitivity cardiac troponin I assay.
They report that a cardiac troponin I concentration <10 ng/L or a
change of <20 ng/L on serial testing had a negative predictive value
for the diagnosis of myocardial infarction of 99.8% and 98.7%
respectively [1]. Whilst we agree there are better appro...
Goorden et al aim to establish the optimal threshold to rule out
myocardial infarction using a high-sensitivity cardiac troponin I assay.
They report that a cardiac troponin I concentration <10 ng/L or a
change of <20 ng/L on serial testing had a negative predictive value
for the diagnosis of myocardial infarction of 99.8% and 98.7%
respectively [1]. Whilst we agree there are better approaches to rule out
myocardial infarction than using the 99th centile upper reference limit
[2,3], we have several concerns about the generalisability and application
of these thresholds in clinical practice.
First, the authors compared diagnostic sensitivity and specificity to
identify thresholds for cardiac troponin I with similar diagnostic
performance to the reference standard. When used in conjunction with a
separate rule in threshold, we believe the optimal threshold to rule out
myocardial infarction should prioritise sensitivity alone to ensure a high
negative predictive value.
Second, the prevalence of myocardial infarction was low (8%;
114/1490) and included a significant proportion of patients with ST-
segment elevation myocardial infarction (2%; 23/1490) where rule-out
strategies based on cardiac biomarkers are inappropriate. Inclusion of
these patients will overestimate the negative predictive value of the
proposed rule out threshold. Furthermore, the negative predictive value
will be lower in hospitals with a higher prevalence of myocardial
infarction.
Third, this analysis was restricted to patients where symptoms were
present for at least 3 hours, limiting the clinical applicability of the
derived rule out thresholds as patients presenting early are at increased
risk of misdiagnosis and are precisely the population in whom rule out
thresholds must be validated.
Fourth, the analysis assumes the thresholds used for the reference
standard are optimal. The recommended rule in threshold for cardiac
troponin T is 14 ng/L (99th centile upper reference limit [4]) and the
limit of detection (5 ng/L) has been proposed to rule out myocardial
infarction. Goorden et al did not apply these thresholds in their
analysis, and as such the thresholds derived for cardiac troponin I are
challenging to interpret and may not be relevant to current clinical
practice.
In the absence of external validation and whilst these uncertainties
remain we would caution against the use of these thresholds in clinical
practice.
References
[1] Goorden SMI, van Engelen, RA, Wong LSM et al. A novel troponin I
rule-out value below the upper reference limit for acute myocardial
infarction. Heart Published Online First: 11th April 2016.
doi:10.1136/heartjnl-2015-308667
[2] Shah AS, Anand A, Sandoval Y, Lee KK, Smith SW, Adamson PD,
Chapman AR et al. High-sensitivity cardiac troponin I at presentation in
patients with suspected acute coronary syndrome: a cohort study. Lancet.
2015 Dec 19;386(10012):2481-8.
[3] Pickering JW, Greenslade JH, Cullen L et al. Validation of
presentation and 3 h high-sensitivity troponin to rule-in and rule-out
acute myocardial infarction. Heart. Published online first: 8th March
2016. doi:10.1136/ heartjnl-2015-308505
[4] Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White
HD et al; Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition
of Myocardial Infarction. Third universal definition of myocardial
infarction. Circulation. 2012 Oct 16;126(16):2020-35.
Conflict of Interest:
AA has received speaker fees from Abbott Laboratories. ASVS has acted as a consultant for Abbott Laboratories. NLM has acted as a consultant for Abbott Laboratories, Beckman-Coulter, Roche, and Singulex. The other authors declare no competing interests.
Nehme and coworkers tested out the effect of air versus oxygen on
myocardial injury in ST-elevation myocardial infarction (STEMI).1 When
administered in the first 12 hours after STEMI oxygen was associated with
a dose-dependent increase in troponin and creatine kinase. In 2015 the
same group of investigators published a study in Circulation showing that
air instead of oxygen supplementation in STEMI led to improved outco...
Nehme and coworkers tested out the effect of air versus oxygen on
myocardial injury in ST-elevation myocardial infarction (STEMI).1 When
administered in the first 12 hours after STEMI oxygen was associated with
a dose-dependent increase in troponin and creatine kinase. In 2015 the
same group of investigators published a study in Circulation showing that
air instead of oxygen supplementation in STEMI led to improved outcome.
The conclusions of these two studies seem to be that supplemental oxygen
therapy in patients with STEMI but without hypoxia may increase early
myocardial injury and is associated with larger myocardial infarct size
assessed at 6 months.
In 1980 we were the first to suggest that due to production of oxygen free
radicals air could be better than oxygen supplementation during
reoxygenation.2 During the next 30 years we performed a series of studies
demonstrating that air compared to 100% oxygen caused significantly less
oxidative stress and less myocardial and kidney injury, and resulted in
higher survival rates in newborn infants needing resuscitation at birth.
In animal studies we demonstrated that 100% oxygen induced injury or
inflammation of several organs as the brain and heart.3,4 We also have
worked intensively with the basic mechanisms explaining such findings.
Based on these and other studies international recommendations for newborn
resuscitation were changed in 2010 from starting with 100% oxygen to air.
We have always been surprised that colleagues in adult medicine
apparently have not been aware of these results. The mechanisms of
reoxygenation injury are probably similar in adults as in newborn. We are
therefore delighted that Nehme et al1 and Stub et al performed their
studies, although 30 years after we challenged the present oxygen dogma.
It is therefore with surprise we don't find any references in their
publications 1 to our basic experimental and clinical studies. Thirty
years of extensive research with internationally acknowledged
translational results have not been credited by the authors, reviewers as
well as the editors responsible for publishing these results.
We truly believe that now is the time when adult medicine should recognize
progress in neonatal medicine which has helped unravel pathophysiological
mechanisms that have improved the survival and quality of life of human
beings independently of their age.
References
1. Nehme Z, Stub D, Bernard S, et al. Effect of supplemental oxygen
exposure on myocardial injury in ST- elevation myocardial infarction.
Heart 2016;102: 444-51
2. Saugstad OD, Aasen AO. Plasma hypoxanthine concentrations in pigs. A
prognostic aid in hypoxia. Eur Surg Res 1980;12:123-9.
3. Saugstad OD, Ramji S, Vento M. Resuscitation of depressed newborn
infants with ambient air or pure oxygen: a meta-analysis. Biol Neonate
2005;87:27-34
4. Saugstad OD. Resuscitation of newborn infants: from oxygen to room air.
Lancet 2010;376:1970-1
Midregional pro-atrial natriuretic peptide and N-terminal pro-B natriuretic peptide for pediatric heart failure diagnosis
Running title
Natriuretic peptides for pediatric HF diagnosis
Guo-Ming Zhang,1 Zhi-De Hu2
1 Department of Laboratory Medicine, Shuyang People's Hospital, Shuyang, China
2 Department of Laboratory Medicine, The General Hospital, Jinan Military Command Region of PLA, Jinan, Shandong, China
Correspondence to...
Midregional pro-atrial natriuretic peptide and N-terminal pro-B natriuretic peptide for pediatric heart failure diagnosis
Running title
Natriuretic peptides for pediatric HF diagnosis
Guo-Ming Zhang,1 Zhi-De Hu2
1 Department of Laboratory Medicine, Shuyang People's Hospital, Shuyang, China
2 Department of Laboratory Medicine, The General Hospital, Jinan Military Command Region of PLA, Jinan, Shandong, China
Correspondence to
Dr Zhi-De Hu, Department of Laboratory Medicine, the General Hospital of Jinan Military Command Region, Jinan, Shandong, P.R. China; hzdlj81@163.com
To the Editor,
We read with interest the paper from Hauser et al. published recently in Heart [1]. To evaluate the diagnostic values of serum midregional pro-atrial natriuretic peptide (MR-proANP), soluble ST2 (sST2), growth differentiation factor-15 (GDF-15), midregional pro-adrenomedullin (MR-proADM) and N-terminal pro-B natriuretic peptide (NT-proBNP) for pediatric heart failure (HF), the investigators enrolled 114 pediatric HF patients and 89 controls. Diagnostic values of these biomarkers were evaluated using receiver-operating characteristic (ROC) curve analysis and logistic regression model. They found that both MR-proANP and NT-proBNP were useful for HF diagnosis, while the diagnostic values of GDF-15, MR-proADM and sST2 were limited.
Although the diagnostic values of MR-proANP and NT-proBNP have been well documented in adult HF patients [2, 3], their diagnostic values for pediatric HF patients remains largely unknown. Because the causes, signs and symptoms of pediatric HF differs substantially from its adult counterpart, the conclusion derived from adult HF cannot be applied in pediatric patients. Therefore, it is necessary and valuable to investigate the diagnostic values of NT-proBNP and MR-proANP for pediatric HF. The work performed by Hauser et al. is novel and interesting. However, some of the findings in this study need extra attention.
In this study, no pre-designed inclusion and exclusion criteria were adopted to enroll entire study cohort consecutively, and controls in this study were patients without heart disease undergoing phlebotomy. Therefore, this is a two-gate design study with alternative diagnosis controls [4]. The major limitation of this type of design is that the specificities of index tests may be biased, depending on the type of alternative diagnosis included. It seems that the controls in this study do not have risk factors, symptoms and signs of HF, and clinicians do not need biomarkers to distinguish between them and patients with HF.
It would be better to consecutively enroll all subjects using well defined criteria (one-gate design). Under such a case, the controls are subjects who also have clinical presentations of HF, and the entire cohort represent a target population in whom MR-proANP and NT-proBNP should be tested.
Taken together, the work performed by Hauser et al. provides us new insight into the diagnostic values of MR-proANP and NT-proBNP for pediatric HF. However, due to the design weakness, further well designed studies are needed to rigorously evaluate the diagnostic values of MR-proANP and NT-proBNP for pediatric HF
Conflicts of interest
The authors stated that there are no conflicts of interest regarding the publication of this article.
Acknowledgements
None
References
1 Hauser JA, Demyanets S, Rusai K, et al. Diagnostic performance and reference values of novel biomarkers of paediatric heart failure. Heart 2016.
2 Hu Z, Han Z, Huang Y, et al. Diagnostic power of the mid-regional pro-atrial natriuretic peptide for heart failure patients with dyspnea: a meta-analysis. Clin Biochem 2012;45:1634-9.
3 Roberts E, Ludman AJ, Dworzynski K, et al. The diagnostic accuracy of the natriuretic peptides in heart failure: systematic review and diagnostic meta-analysis in the acute care setting. BMJ 2015;350:h910.
4 Rutjes AW, Reitsma JB, Vandenbroucke JP, et al. Case-control and two-gate designs in diagnostic accuracy studies. Clin Chem 2005;51:1335-41.
We read with interest the paper by Dhillon and colleagues which
provided a high quality propensity matched observational study of
perioperative outcomes in patients with hypertrophic cardiomyopathy
(HCM).1 This study showed no difference in what they defined as 'hard
outcomes' such as myocardial infarction, stroke and death. They did
however show an increased incidence of composite end points (10%; p= 0.03)
such as post-...
We read with interest the paper by Dhillon and colleagues which
provided a high quality propensity matched observational study of
perioperative outcomes in patients with hypertrophic cardiomyopathy
(HCM).1 This study showed no difference in what they defined as 'hard
outcomes' such as myocardial infarction, stroke and death. They did
however show an increased incidence of composite end points (10%; p= 0.03)
such as post-operative congestive heart failure (CHF) (1%) and readmission
rates (7%).
One interesting point that we would like to raise is the
significantly higher use of etomidate in the HCM cohort (p= 0.002).
Understandably, etomidate was chosen in many cases for its rapid onset and
stable haemodynamic properties. This was likely reflected in the
significantly lower incidence of intra-operative tachycardia and
hypotension in HCM patients. However the use of etomidate is not without
controversy, with several studies have linked its use as a single dose
induction agent to post operative acute adrenal insufficiency.2,3
The use of etomidate may be a significant confounding factor in this
study. Previous groups have demonstrated similar types of adverse outcomes
with the use of etomidate; Komatsu and colleagues found substantially
increased incidence of post-operative adverse events and even mortality
when compared to the current paper.2 These differences may be related to a
lower rates of etomidate use by Dhillon and colleagues.
Given that there is currently a great deal of controversy surrounding
the use of etomidate it would be beneficial to see a breakdown of outcomes
in the subgroup that received etomidate. If the increased incidence of
adverse outcomes were related to the use of etomidate, then non-cardiac
surgery performed on HCM patients in experienced centres may no longer be
'high risk'.
References:
1. Dhillon A, Khanna A, Randhawa M, Cywinski J, Saager L,
Thamilarasan M, Lever H & Desai M (2016). Perioperative outcomes of
patients with hypertrophic cardiomyopathy undergoing non-cardiac surgery.
Heart. 0: 1-6.
2. Komatsu R, You J, Mascha E, Sessler D, Kasuya Y & Turan A
(2013). Anaesthetic induction with etomidate, rather than propofol, is
associated with increased 30-day mortality and cardiovascular morbidity
after noncardiac surgery. Anaesth Analg. 117(6): 1329-37.
3. Chan C, Mitchell A & Shorr A (2012). Etomidate is associated
with mortality and adrenal insufficiency in sepsis: A meta-analysis. Crit
Care Med. 40(11): 2945-2953.
We read the educational review on distinguishing ventricular septal
bulge (VSB) versus hypertrophic cardiomyopathy (HCM) by Canepa et al[1]
with great interest. The authors recognise the increasingly established
role of cardiovascular magnetic resonance (CMR) in the assessment of this
difficult diagnostic dilemma. They describe the gold standard role of CMR
in the quantification of myocardial mass,...
We read the educational review on distinguishing ventricular septal
bulge (VSB) versus hypertrophic cardiomyopathy (HCM) by Canepa et al[1]
with great interest. The authors recognise the increasingly established
role of cardiovascular magnetic resonance (CMR) in the assessment of this
difficult diagnostic dilemma. They describe the gold standard role of CMR
in the quantification of myocardial mass, myocardial fibrosis with late
gadolinium enhancement and the morphological and functional imaging of
mitral valve abnormalities.
T1 mapping with CMR is an emerging clinical biomarker for the
quantification of myocardial disease. The technique is easily measured,
highly reproducible and has recently translated into the clinical
pathway[2]. With the addition of gadolinium based contrast agent the
extracellular volume (ECV) can also be estimated. T1 mapping is clinically
able to identify early phenotypic expression of HCM with both increased
native T1 and higher ECV[3] and has been shown to distinguish between
early phenotypic expression of athlete hearts vs HCM[4]. We would highly
recommend T1 mapping techniques to be performed on all patients undergoing
CMR which will aid the differentiation of VSB vs HCM.
Dr David P. Ripley
Dr Subhi E. Akleh
Dr Alison F. Lee
References:
1. Canepa M, Pozios I, Vianello PF, et al. Distinguishing ventricular
septal bulge versus hypertrophic cardiomyopathy in the elderly. Heart
2016;102(14):1087-94.
2. Sado DM, White SK, Piechnik SK, et al. Identification and assessment of
Anderson-Fabry disease by cardiovascular magnetic resonance noncontrast
myocardial T1 mapping. Circ Cardiovasc Imaging 2013;6(3):392-8.
3. Puntmann VO, Voigt T, Chen Z, et al. Native T1 mapping in
differentiation of normal myocardium from diffuse disease in hypertrophic
and dilated cardiomyopathy. JACC Cardiovasc Imaging 2013;6(4):475-84.
4. Swoboda PP, McDiarmid AK, Erhayiem B, et al. Assessing Myocardial
Extracellular Volume by T1 Mapping to Distinguish Hypertrophic
Cardiomyopathy From Athlete's Heart. J Am Coll Cardiol 2016;67(18):2189-
90.
re Larsson et al, Chocolate consumption and risk of myocardial
infarction: a prospective study and meta-analysis.
The findings of Larsson et al are fascinating and in line with earlier
reports of cardio-protective effects of chocolate consumption, especially
of dark chocolate. Having noticed this in the literature, a colleague and
I were inspired to measure the vitamin D con...
re Larsson et al, Chocolate consumption and risk of myocardial
infarction: a prospective study and meta-analysis.
The findings of Larsson et al are fascinating and in line with earlier
reports of cardio-protective effects of chocolate consumption, especially
of dark chocolate. Having noticed this in the literature, a colleague and
I were inspired to measure the vitamin D content of dark chocolate, since
it was known that curing cocoa beans in the sun was associated with some
fungal growth and that fungi synthesize vitamin D2, as evidenced in
mushrooms, sometimes irradiated with UV for food fortification, and or-ur
pilot study demonstrated remarkably high vitamin D2 content of the various
dark chocolate samples examined. The reported benefits may, therefore, be
due in part to the contained vitamin D2, since similar protection is
currently being found with better vitamin D status, or supplementation. I
would be interested to know, therefore, whether the cohorts reported upon
happen to have measurements of serum 25(OH)D available that could be
assessed for variation with chocolate consumption, and cardiovascular
events, which would be of great interest, either way.
Barbara J Boucher BSc. MD, FRCP. bboucher@doctors.org.uk
References
Chocolate consumption and cardiometabolic disorders: systematic review and
meta-analysis. BMJ 2011;343:d4488; Response, by Timms PM et al
Dietary vitamin D?--a potentially underestimated contributor to
vitamin D nutritional status of adults? Cashman KD, Kinsella M, McNulty
BA, Walton J, Gibney MJ, Flynn A, Kiely M.
Br J Nutr. 2014 Jul 28;112(2):193-202.
The vitamin D activity of cacao shell: The effect of the fermenting
and drying of cacao on the vitamin D potency of cacao shell. II. The
origin of vitamin D in cacao shell. Knapp AW. Biochem J. 1935
Dec;29(12):2728-35.
The article by Isogai et al. published in Heart (1) discuss the use
of beta-blockers in patients diagnosed and admitted with takotsubo
cardiomyopathy (TTC).
Although no effective guidelines have been prescribed for the
treatment of TTC, it is suggested that a parable could be drawn by
comparing the use of beta-blocker and angiotensin-converting-enzyme
inhibitors in these patients with that of control subjects a...
The article by Isogai et al. published in Heart (1) discuss the use
of beta-blockers in patients diagnosed and admitted with takotsubo
cardiomyopathy (TTC).
Although no effective guidelines have been prescribed for the
treatment of TTC, it is suggested that a parable could be drawn by
comparing the use of beta-blocker and angiotensin-converting-enzyme
inhibitors in these patients with that of control subjects as well as
those suffering from coronary artery disease. Beta-blockers were
considered more likely to be prescribed to control subjects and patients
diagnosed with coronary artery disease than to patients diagnosed with
TTC. Interestingly, TTC and coronary artery disease patients received
angiotensin-converting-enzyme inhibitors / angiotensin receptor blockers
more often than control subjects. The concluding suggestion that the 5
year mortality is similar in both disease groups and higher than control
subjects furthers our debate on this topic. The large International
Takotsubo Registry reported a 5.6% mortality per-patient year (2) and the
use of angiotensin-converting- enzyme inhibitors or angiotensin receptor-
blockers was associated with improved survival rates. However, evidence
establishing a marked survival benefit with beta-blocker use has yet to be
documented. The pathogenesis of TTC is yet to be fully understood. A
popular hypothesis suggests the involvement of a catecholamine-mediated
mechanism. Although all these trials essentially compared the outcome of
TTC with matched cohorts of patients with coronary artery disease, a
relevant suggestion elucidates the role of an inflammatory and energetic-
metabolic pathway as a possible pathophysiological mechanism (3). We
retrospectively described a collective of 114 consecutive patients
diagnosed with TTC between January 2003 and September 2015 at our
institution. Our data showed that the use of beta-blocker was associated
with improved survival rates over mean follow-up of 5 years (4). These
novel findings necessitate the need for a standardized treatment regimen
in TTC patients. We recommend the urgent need of randomized trials to
clearly define treatment approaches and management strategies in takotsubo
cardiomyopathy thus enabling the practice of evidence-based medicine
within guidelines.
References
1. Isogai T, Matsui H, Tanaka H, et al. Early beta-blocker use and in
-hospital mortality in patients with Takotsubo cardiomyopathy. Heart
2016;102(13):1029-1035. 2 . Templin C, Ghadri JR, Diekmann J, et al.
Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N
Engl J Med 2015;373(10):929-938. 3. Eitel I, von Knobelsdorff-Brenkenhoff
F, Bernhardt P, et al. Clinical characteristics and cardiovascular
magnetic resonance findings in stress (takotsubo) cardiomyopathy. JAMA
2011;306(3):277-286. 4. Becher T, El-Battrawy I, Baumann S, et al.
Characteristics and long- term outcome of right ventricular involvement in
Takotsubo cardiomyopathy. Int J Cardiol 2016;220:371-375.
Loneliness and social isolation may lead to CHD and stroke? Valtorta
et al. answered this question in a recent meta-analysis [1]. After pooling
evidence based on 16 cohorts, they found that poor social relationships
increase the risk of CHD and stroke. However, do things really like this?
Maybe not.
The problem is the random-effect (RE) model they used, which may lead to
overconfident and biased re...
Loneliness and social isolation may lead to CHD and stroke? Valtorta
et al. answered this question in a recent meta-analysis [1]. After pooling
evidence based on 16 cohorts, they found that poor social relationships
increase the risk of CHD and stroke. However, do things really like this?
Maybe not.
The problem is the random-effect (RE) model they used, which may lead to
overconfident and biased results [2, 3]. Because under RE model, large
studies were given more weight while the study quality was ignored [2].
Moreover, RE model is proved to link with underestimated coverage
probability [3]. To solve these limitations, a widely accepted model
called quality effect (QE), proposed by Doi et al. [4] has been gradually
valued.
In order to see if poor social relationships really increase the risk of
CHD and stroke, we might re-pool the evidence by QE model [4]. We use the
information of risk of bias summarized in Figure 2 and assume low risk of
bias to be 2 score, high risk of bias 0 score, and unclear risk of bias 1
score to quantification estimator of quality. By doing so, the quality of
each included study can be measured as total score (also known as Qi in QE
model [4]).
Under QE procedure, interestingly, loneliness and social isolation no
longer lined with increased risk of CHD (RR=1.24; 95%CI: 0.97, 1.57) and
stroke (RR=1.26; 95CI%: 0.95, 1.68). That is to say, when taking quality
item into consideration, the pooled results no more statistical
significance. Then, can we still claim poor social relationships increase
the risk of CHD and stroke? Maybe we should treat the conclusion with
caution.
Conflicts: The authors declare no conflicts and interests.
Reference
1. Valtorta NK, Kanaan M, Gilbody S, et al. Loneliness and social
isolation as risk factors for coronary heart disease and stroke:
systematic review and meta-analysis of longitudinal observational studies.
Heart 2016; 102(13):1009-16.
2. DerSimonian R, Laird N. Meta-analysis in clinical trials.
Controlled Clinical Trials. 1986; 7:177-188.
3. Brockwell SE, Gordon IR. A comparison of statistical methods for
meta-analysis. Stat Med. 2001; 20(6): 825-840.
4. Doi SA, Barendregt JJ, Khan S, et al. Advances in the meta-
analysis of heterogeneous clinical trials II: The quality effects model.
Contemp Clin Trials. 2015; 45(Pt A): 123-129.
We read with great interest the report by van Melle et al. who
conducted a retrospective multi-centre European study to assess surgical
options for the failing Fontan [1]. Firstly, we would like to acknowledge
the effort made to bring together the results of these infrequently
performed, difficult interventions. However, we would also like to
highlight concerns with the conclusions reached from this historical mixed
regi...
We read with great interest the report by van Melle et al. who
conducted a retrospective multi-centre European study to assess surgical
options for the failing Fontan [1]. Firstly, we would like to acknowledge
the effort made to bring together the results of these infrequently
performed, difficult interventions. However, we would also like to
highlight concerns with the conclusions reached from this historical mixed
registry data.
The authors state that a late failing Fontan patient with poor ventricular
function is better off with a heart transplant, while preserved
ventricular function can be treated with conversion. It should be noted,
however, that heart transplantation here was performed mainly in children,
whilst conversion was predominantly indicated for right atrial dilatation
and intractable arrhythmia in young adults with atrio-pulmonary Fontans.
The atrio-pulmonary Fontan operation has not been performed for more than
a decade and patient numbers with this repair are diminishing [2]. As more
energy efficient circulations are developed, the substrate for arrhythmia
is evolving. It is improbable that these results can therefore be
generalised to make a case for future conversions.
Furthermore, as the authors acknowledge, the Fontan population is aging;
it is our experience that increasingly patients present in their thirties
and forties with failure of the circulation due to extra-cardiac disease,
most notably the liver [3,4]. Failure to identify, assess and address this
in patients with preserved ventricular function may increase the risk and
sometimes preclude the option of transplantation.
The role of Fontan takedown, as stated, has not been elucidated for the
late failing Fontan; we should question too whether there may be an
alternative way to balance the circulation, avoiding the Fontan in the
first place [5]. In the meantime, addressing listing criteria for late
failing Fontan and exploring utility of ventricular assist devices must be
the priority for the current population.
Fontan conversion may have a role in highly selected cases but should not
be regarded as a definitive option to timely transplantation for the
growing adult patient group. Extrapolating past results in a changing
surgical arena to current and future populations must be treated with
caution.
References
[1] van Melle JP, Wolff D, H?rer J et al. Surgical options after Fontan
failure. Heart. 2016 Apr 13.
[2] d'Udekem Y, Iyengar AJ, Galati JC et al. Redefining expectations of
long-term survival after the Fontan procedure: twenty-five years of follow
-up from the entire population of Australia and New Zealand. Circulation.
2014;130(11 Suppl 1):S32-8.
[3] Coats L, O'Connor S, Wren C et al. The single-ventricle patient
population: a current and future concern a population-based study in the
North of England. Heart. 2014;100(17):1348-53.
[4] Greenway SC, Crossland DS, Hudson M et al. Fontan-associated liver
disease: Implications for heart transplantation. J Heart Lung Transplant.
2016;35(1):26-33.
[5] D'Souza TF, Samuel BP, Hillman ND, Vettukattil JJ, Haw MP.
Biventricular Repair of Pulmonary Atresia After Fontan Palliation. Ann
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We thank Ripley and colleagues for their interest in our paper and agree that T1 mapping with CMR is an emerging imaging biomarker that is increasingly being investigated for its potential role in hypertrophic cardiomyopathy and cardiac hypertrophy in general. Convincing data have been published concerning hypertensive heart disease(Hinojar et al., 2015), hypertrophic and dilated cardiomyopathy (Puntmann et al., 2013),...
To the Editor,
Goorden et al aim to establish the optimal threshold to rule out myocardial infarction using a high-sensitivity cardiac troponin I assay. They report that a cardiac troponin I concentration <10 ng/L or a change of <20 ng/L on serial testing had a negative predictive value for the diagnosis of myocardial infarction of 99.8% and 98.7% respectively [1]. Whilst we agree there are better appro...
Nehme and coworkers tested out the effect of air versus oxygen on myocardial injury in ST-elevation myocardial infarction (STEMI).1 When administered in the first 12 hours after STEMI oxygen was associated with a dose-dependent increase in troponin and creatine kinase. In 2015 the same group of investigators published a study in Circulation showing that air instead of oxygen supplementation in STEMI led to improved outco...
We read with interest the paper by Dhillon and colleagues which provided a high quality propensity matched observational study of perioperative outcomes in patients with hypertrophic cardiomyopathy (HCM).1 This study showed no difference in what they defined as 'hard outcomes' such as myocardial infarction, stroke and death. They did however show an increased incidence of composite end points (10%; p= 0.03) such as post-...
Dear Editor,
We read the educational review on distinguishing ventricular septal bulge (VSB) versus hypertrophic cardiomyopathy (HCM) by Canepa et al[1] with great interest. The authors recognise the increasingly established role of cardiovascular magnetic resonance (CMR) in the assessment of this difficult diagnostic dilemma. They describe the gold standard role of CMR in the quantification of myocardial mass,...
Comment to the Heart Journal website
re Larsson et al, Chocolate consumption and risk of myocardial infarction: a prospective study and meta-analysis. The findings of Larsson et al are fascinating and in line with earlier reports of cardio-protective effects of chocolate consumption, especially of dark chocolate. Having noticed this in the literature, a colleague and I were inspired to measure the vitamin D con...
The article by Isogai et al. published in Heart (1) discuss the use of beta-blockers in patients diagnosed and admitted with takotsubo cardiomyopathy (TTC).
Although no effective guidelines have been prescribed for the treatment of TTC, it is suggested that a parable could be drawn by comparing the use of beta-blocker and angiotensin-converting-enzyme inhibitors in these patients with that of control subjects a...
Dear editor,
Loneliness and social isolation may lead to CHD and stroke? Valtorta et al. answered this question in a recent meta-analysis [1]. After pooling evidence based on 16 cohorts, they found that poor social relationships increase the risk of CHD and stroke. However, do things really like this? Maybe not. The problem is the random-effect (RE) model they used, which may lead to overconfident and biased re...
We read with great interest the report by van Melle et al. who conducted a retrospective multi-centre European study to assess surgical options for the failing Fontan [1]. Firstly, we would like to acknowledge the effort made to bring together the results of these infrequently performed, difficult interventions. However, we would also like to highlight concerns with the conclusions reached from this historical mixed regi...
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