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Recent eLetters

Displaying 1-10 letters out of 678 published

  1. Re:Physical Activity and Cardiorespiratory Fitness as Underappreciated Modulators of Obesity-Related Risk of Sudden Cardiac Death

    We thank Laukkanen et al. for their interest in our recent report titled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" (1). We agree that regular moderate physical activity reduces the risk of sudden cardiac death (SCD) and all-cause mortality. Physical activity, but not fitness, was captured in the ARIC study via questionnaires. However, adjustment for this variable in our multivariable analysis did not change the results of the study. In the analysis for BMI, after adjustment for physical activity in addition to all variables in our Model 2, the HR (95% CI) for SCD were 1, 1.24 (0.75-2.04), 1.05 (0.59-1.85), and 1.42 (0.76-2.68) among non- smokers with BMI of 18.5-24.9, 25-29.9, 30-34.9 and 35+, respectively (p for trend 0.45). In the analysis for waist-hip-ratio, after additional adjustment for physical activity in our Model 2, the HR (95% CI) for SCD were 1, 0.98 (0.53-1.81), 1.45 (0.86-2.43), and 1.93 (1.13-3.30) among non -smokers with waist-hip-ratio of reference (<0.8 in women, <0.95 in men), high category 1, 2 and 3, respectively (p for trend 0.005). REFERENCES 1. Adabag S, Huxley RR, Lopez FL, Chen LY, Sotoodehnia N, Siscovick D, Deo R, Konety S, Alonso A, Folsom AR. Obesity related risk of sudden cardiac death in the atherosclerosis risk in communities study. Heart. 2015;101:215-21

    Conflict of Interest:

    None declared

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  2. NICE guidance for the investigation of recent-onset chest pain

    The paper by Patterson et al (1) illustrates why the NICE and ESC guidelines (2,3) recommend no non-invasive testing in patients presenting with undifferentiated chest pain in whom a non-cardiac cause is suspected or the probability of coronary artery disease (CAD) is judged to be very low (NICE <_10 esc="esc" _15.="_15." table="table" _5="_5" shows="shows" there="there" were="were" _351="_351" such="such" patients="patients" of="of" whom="whom" _24="_24" subsequently="subsequently" diagnosed="diagnosed" with="with" cad.="cad." even="even" if="if" we="we" accept="accept" that="that" the="the" chest="chest" pain="pain" in="in" all="all" these="these" false="false" negative="negative" cases="cases" was="was" fact="fact" caused="caused" by="by" myocardial="myocardial" ischaemia="ischaemia" this="this" is="is" equivalent="equivalent" to="to" a="a" diagnostic="diagnostic" sensitivity="sensitivity" _93="_93" for="for" clinical="clinical" judgment="judgment" ruling="ruling" out="out" coronary="coronary" disease="disease" better="better" than="than" could="could" be="be" achieved="achieved" exercise="exercise" electrocardiography="electrocardiography" or="or" perfusion="perfusion" imaging="imaging" low="low" risk="risk" population="population" _4.="_4." _="_" p="p">

    It is unclear from the manuscript exactly how ???the subsequent CAD diagnosis??? was determined and how sound was that determination. There were only 11 hospital admissions with ???angina??? so it presumably involved some form of non-invasive testing in most cases. The fact that CAD was ???excluded??? or ???inconclusive??? in nearly all (>90%) of these patients is entirely predictable given the initial clinical diagnosis of non-cardiac chest pain or low probability CAD. This begs the question what contribution the testing made to patient care? Certainly, the tests were unhelpful in failing to prevent 6 MACE events, although it is hard to know whether this 1.7% event rate should be seen as a cause for ???alarm???.

    Finally, Patterson et al warn against using the NICE guidance to ???justify excluding (low risk) patients from further investigation if CAD is still suspected based on all available clinical information???. There was no intention that the guideline should be used in this way but a more selective approach to investigation than apparently used by Patterson et al is surely needed to address increasing concerns about the overuse of noninvasive diagnostic tests in patients with chest pain (5).

    References

    1. Patterson CM, Nair A, Ahmed N, Bryan L, Bell D, Nicol ED. Clinical outcomes when applying NICE guidance for the investigation of recent-onset chest pain to a rapid-access chest pain clinic population. Heart 2015;101:113-118

    2. Chest pan of recent onset: Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. NICE guidelines [CG95] Published date: March 2010. http://www.nice.org.uk

    3. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A, et al. 2013 ESC guidelines on the management of stable coronary artery disease: The Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013; 34(38):2949-3003

    4. Detrano R, Gianrossi R, Mulvihill D, Lehman K, Dubach P, Colombo A, Froelicher V. Exercise-induced ST segment depression in the diagnosis of multivessel coronary disease: a meta analysis. J Am Coll Cardiol 1989;14:1501-8.

    5. Ladapo JA, Blecker S, Douglas PS. Physician decision making and trends in the use of cardiac stress testing in the United States: An analysis of repeated cross-sectional data. Ann Intern Med 2014;161:482-490

    Conflict of Interest:

    I chaired the NICE guideline group: Chest pan of recent onset: Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. NICE guidelines [CG95] Published date: March 2010. http://www.nice.org.uk

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  3. What about the actual history of the chest pain

    I am rather surprised that the authors did not take into account more clinical features of the history in their model.(1) Pleuritic features and relief when sat up suggest pericarditis, whilst there are of course specific features that suggest reflux oesophagitis; timing is important, as pain lasting less than a minute is really not suggestive of ischaemic disease.

    The authors state 'we included consenting adults aged >25 years who presented to the ED within 24h of experiencing chest pain suspected to be cardiac in origin by the initial treating physician' and thus I take this to assume they trusted the history of the initial physician as one that suggested cardiac disease - even then, I assume 'cardiac' means ischaemic, not pericarditic or indeed dissection-type of pain.

    Similar work to this paper has been done in stable angina, where the description of angina pain as typical is associated with coronary outcomes.(2) Clearly unstable angina lacks the exertional component of stable angina and is thus harder perhaps from simple history-taking alone to be sure of a diagnosis, but that does not mean chest pain descriptors (character, site, duration) don't play a diagnostic, and hence potentially prognostic role in unstable angina.

    1. Body R, Carley S, McDowell G, Pemberton P, Burrows G, Cook G, Lewis PS, Smith A, Mackway-Jones K. The Manchester Acute Coronary Syndromes (MACS) decision rule for suspected cardiac chest pain: derivation and external validation. Heart 2014;100:18 1462-1468

    2. Zaman MJ, Junghans C, Sekhri N, et al. Presentation of stable angina pectoris among women and South Asian people. CMAJ 2008;179:659-67

    Conflict of Interest:

    None declared

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  4. what was the prevalence of concordant ST segment deviation in type 1 AMI with LBBB?

    The 6.3% prevalence of left bundle branch block(LBBB) among 17,488 subjects with type 1 acute myocardial infarction(AMI) translates into 1101 subjects with this manifestation of AMI(1). This represents a golden opportunity to document the prevalence of concordant ST segment deviation in those 1101 subjects so as to enable a comparison to be made with the study which reported a low prevalence of acute coronary occlusion in patients with LBBB who did not have concordant ST segment deviation(2). An even more important comparison would be a documentation of the sensitivity and specificity of concordant ST segment deviation for type 1 AMI in those 1101 subjects vs the documentation of 16.7% sensitivity and 88.6% specificity in the 120 subjects evaluated by Brown et al(3) References (1)Baron T., Hambraeus K., Sundstrom J et al Type 2 myocardial infarction in clinical practice Heatr 2015;101:101-106 (2)McMahon R., Siow W., Bhindi R et al Left bundle branch block without concordant ST changes is rarely associated with acute coronary occlusion International Journal of Cardiology 2013;167:1339-1342 (3) Brown AJ., Hoole SP., McCormick LM et al Left bundle branch block with acute thrombotic occlusion is associated with increased myocardial jeopardy score and poor clinical outcomes in primary percutaneous coronary activations Heart 2013;99:774-778

    Conflict of Interest:

    None declared

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  5. manchseter medical society

    The documentation of a rising incidence of cardiac resynchronisation therapy(CRT)-related infection(1) calls for a reappraisal of the Class 1 level A recommendation for the use of this modality(2), given the fact that the recommendation antedated the ground breaking introduction of angiotensin-neprilysin inhibition in subjects with comparable severity of systolic heart failure(3). In that study a significant(p < 0.001) reduction in mortality and hospitalisation for heart failure was documented in subjects randomised to angiotensin-neprilysin inhibition vs counterparts randomised to optimum dose enalapril with comparable background therapy(3). Over and above the risk of infection(1), CRT has the added disadvantage of unpredictability of response(4), and, in 36% of cases, poor retention on mean follow up of 2.5 years(5). Accordingly, to justify CRT in the unique subgroup of symptomatic systolic heart failure subjects with left bundle branch block(QRS duration > 150 ms) and sinus rhythm(2) that modality will have to be shown to be superior to angiotensin-neprilysin inhibition when the latter is used in a comparable group of subjects , both groups being on comparable background therapy. References (1) Harrison JL., Prenedergast BD., Sandoe JAI Guidelones for diagnosis management and prevention of implantable cardiac electronic device infection Heart 2014 doi 10.1136/heartjnl-2014-306873 (2) Brignole M., ASuricchio A., Baron Equivas G et al 2013 ESC guidelines on cardiac pacing and cardiac resynchronisation therapy Europace 2013;15:1070-1118 (3) McMurray JJV., Packer M., Desai AS et al Angiotensin-neprilysin inhibition versus enalapril in heart fdailure 2014;371;993-1004 (4) Clelenad J., Freemantle N., Ghio S et al Predicting the long term effects of cardiac resynchronisation therapy on mortality from baseline variables and early response J Am Coll Cardiol 2008;52:430-444 (5) Knight B., Desai A., Coman J Faddis M., Yong P Long term retention of cardiac resynchronisation therapy J Am Coll Cardiol 2004;44:72-77

    Conflict of Interest:

    None declared

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  6. Physical Activity and Cardiorespiratory Fitness as Underappreciated Modulators of Obesity-Related Risk of Sudden Cardiac Death

    We read with great interest the recent report, published in Heart, entitled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" by Adabag et al.1 Among a large cohort of middle-aged adults (n = 14,491 African American and white men and women; 55% female), baseline measures of obesity, including body mass index (BMI), waist circumference (WC), and waist-to- hip ratio (WHR), were related to the incidence of sudden cardiac death (SCD, 253 cases) over a 12.6 year follow up. BMI was indirectly associated with SCD through its adverse effects on cardiovascular risk factors, diabetes and heart disease, whereas abdominal obesity, measured by WHR, appeared to be the strongest predictor of SCD in non-smokers. In contrast, the relation between measures of obesity and SCD were inconsistent in current smokers, perhaps due to the relatively small number of SCD cases in this population subset. It was suggested that this finding may reflect the 'obesity paradox.' Although the ARIC investigators attempted to adjust for potential confounding variables to clarify the impact of obesity per se on SCD, there was no mention of physical activity or cardiorespiratory fitness (CRF), potential mortality modulators in SCD cohorts. Adherence to a regular exercise regimen (> 30 minutes/day) is strongly and independently associated with a lower risk of SCD in women.2 Numerous previous studies have also shown that low fitness is an independent predictor of mortality in normal-weight, overweight, and obese men and women, regardless of the risk factor profile.3 Similarly, we reported that CRF was inversely related to the risk of SCD in a population-based long-term follow-up study.4 Hu et al5 examined whether higher levels of physical activity can counter the elevated risk of death associated with excess adiposity. During a 24- year follow-up of 116,564 women (30-55 years of age) who free of known cardiovascular disease and cancer, there were 10,282 deaths. The relative risk of death of lean (BMI < 25 kg/m2)-active, lean-inactive, obese (BMI > 30 kg/m2)-active, and obese-inactive was 1.00, 1.55, 1.91, and 2.42, respectively. It was concluded that both increased adiposity and reduced physical activity are strong and independent predictors of death. In conclusion, we wonder whether the ARIC study included assessments of physical activity or CRF and, if so, why these variables were not considered in their multivariate adjusted model? Furthermore, we question whether the association between WHR and SCD would have persisted after adjusting for these variables. Collectively, these data and other recent reports,6 suggest that the deleterious health impact of obesity may be markedly overestimated, unless physical activity and CRF are appropriately accounted for.

    REFERENCES

    1.Adabag S, Huxley RR, Lopez FL, Chen LY, Sotoodehnia N, Siscovick D, Deo R, Konety S, Alonso A, Folsom AR. Obesity related risk of sudden cardiac death in the atherosclerosis risk in communities study. Heart. 2014 Nov 19.

    2.Chiuve SE, Fung TT, Rexrode KM, Spiegelman D, Mason JE, Stampfer MJ, Albert CM. Adherence to a low-risk, healthy lifestyle and risk of sudden cardiac death among women. JAMA 2011;306:62-69.

    3.Lavie CJ, McAuley PA, Church TS, Milani RV, Blair SN. Obesity and cardiovascular diseases: implications regarding fitness, fatness, and severity in the obesity paradox. J Am Coll Cardiol 2014;63:1345-54.

    4.Laukkanen JA, M?kikallio TH, Rauramaa R, Kiviniemi V, Ronkainen K, Kurl S. Cardiorespiratory fitness is related to the risk of sudden cardiac death: a population-based follow-up study. J Am Coll Cardiol 2010;56:1476- 83.

    5.Hu FB, Willett WC, Li T, et al. Adiposity as compared with physical activity in predicting mortality among women. N Engl J Med 2004;351:2694-703.

    6.Lee CD, Sui X, Blair SN. Combined effects of cardiorespiratory fitness, not smoking, and normal waist girth on morbidity and mortality in men. Arch Intern Med 2009;169:2096-101.

    Sae Young Jae, PhD, Department of Sport Science, University of Seoul, Seoul, South Korea.

    Sudhir Kurl, MD, Department of Medicine, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.

    Jari A. Laukkanen, MD, Department of Medicine, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland (jariantero.laukkanen@uef.fi).

    Barry A. Franklin, PhD, Preventive Cardiology and Cardiac Rehabilitation, William Beaumont Hospital, Royal Oak, MI, USA.

    Conflict of Interest:

    None declared

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  7. Comment on: An epidemiological appraisal of the association between heart rate variability and particulate air pollution: a meta-analysis

    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.

    Conflict of Interest:

    None declared

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  8. 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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  9. 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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  10. 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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