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Recent eLetters

Displaying 1-10 letters out of 635 published

  1. Dual atrioventricular nodes

    I read with great interest the "challenge" posed by the electrocardiographic recording in issue 7 of Heart for 2014. I also noted with interest that the authors suggest that Monckeberg provided the first account of such dual nodes in 1993 (their reference #1). Since Monckeberg was long since dead by that date, this must be some mistake! I think the appropriate date is 1913. It is certainly the case that Monckeberg was the first to describe this rare anatomic arrangement. Monckeberg's heart, however, was characterised by the presence of discordant atrioventricular connections, and double outlet right ventricle. Since then, dual atrioventricular nodes have been demonstrated in another heart with double outlet right ventricle, but in the setting of concordant atrioventricular connections (Br Heart J 1973; 35: 566-569). To the best of my knowledge, all other hearts subsequently published with dual atrioventricular nodes have either had isomerism of the atrial appendages (Smith et al, Cardiol Young 2006; 16: 437-454), or else discordant atrioventricular connections, as in the index case described by Monckeberg. Again, to the best of my knowledge, hearts have yet to be described with dual nodes located as shown in the cartoon provided by Paech and colleagues. It is possible that their patient, with hypoplastic left heart syndrome, could have had a so- called "atriofascicular tract", since that is the closest arrangement of which I am aware that fits their cartoon.The second node in these situations, however, is found anterolaterally within the right atrioventricular junction (Becker et al, Circulation 1978; 57: 870-879), rather than inferiorly as pictured in their cartoon. I wonder, therefore, what additional information they have to prove that their patient had dual atrioventricular nodes? On the basis of my own experience with assessing autopsied hearts, I would be very surprised to find the arrangement that they have depicted in a patient with hypoplastic left heart syndrome.

    Conflict of Interest:

    None declared

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  2. Vitamin D reduces risk of cardiovascular disease

    The paper by the JBS3 Board dismisses the role of vitamin D in reducing risk of cardiovascular disease (CVD) since large-scale randomized controlled trials (RCTs) have not demonstrated the benefit [1]. However, a more recent paper from the Women's Health Initiative calcium/vitamin D RCT did report a beneficial effect in significantly lowering low-density lipoprotein cholesterol and raising high-density lipoprotein cholesterol [2]. This finding was made on the basis of 600 participants who had serum 25-hydroxyvitamin D [25(OH)D] and cholesterol levels measured at time of enrollment and at the end of two years in the study. Serum 25(OH)D levels were 38% higher in the active arm (mean 60.8 nmol/L) than in the placebo arm after two years.

    Evidence from observational studies strongly supports a role of vitamin D in reducing risk of CVD. A meta-analysis of 19 observational studies of CVD risk with respect to 25(OH)D levels found a relative risk of 2.1 at 18 nmol/L, 1.6 at 30 nmol/L, 1.2 at 50 nmol/L, and 1.02 at 70 nmol/L [3]. The findings in Ref. 2 are in general agreement with the findings in this meta-analysis.

    The proper way to conduct vitamin D RCTs was outlined in a recent paper. The guidelines include starting with a 25(OH)D-health outcome relation, enrolling people with 25(OH)D levels near the low end of the relation, supplementing with sufficient vitamin D to raise 25(OH)D levels to the optimal level, then remeasuring 25(OH)D levels [4]. RCTs conducted on groups with mean 25(OH)D levels above 50 nmol/L generally do not find beneficial effects due to using too little vitamin D and having an uncertainty larger than the expected benefit.

    As to the suggestion that low 25(OH)D levels reflect or may be a consequence of lifestyle factors rather than being a causal risk factor, that is not correct. There will be two letters to the editor responding to Ref. 154 (Autier et al.) published shortly in Lancet Diabetes & Endocrinology pointing out that observational studies provide good evidence and that all types of vitamin D studies should be considered and evaluated using Hill's criteria for causality in a biological system.

    References 1.JBS3 Board. Joint British Societies' consensus recommendations for the prevention of cardiovascular disease (JBS3). Heart 2014;100:ii1-ii67

    2. Schnatz PF, Jiang X, Vila-Wright S, et al. Calcium/vitamin D supplementation, serum 25-hydroxyvitamin D concentrations, and cholesterol profiles in the Women's Health Initiative calcium/vitamin D randomized trial. Menopause. 2014 Mar 3. [Epub ahead of print]

    3. Wang L, Song Y, Manson JE, et al. Circulating 25-hydroxy-vitamin D and risk of cardiovascular disease: A meta-analysis of prospective studies. Circ Cardiovasc Qual Outcomes. 2012;5:819-29.

    4. Heaney RP. Guidelines for optimizing design and analysis of clinical studies of nutrient effects. Nutr Rev. 2014;72:48-54.

    Conflict of Interest:

    I receive funding from Bio-Tech Pharmacal (Fayetteville, AR), the Sunlight Research Forum (Veldhoven) and the UV Foundation (McLean, VA).

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  3. Pre-procedural fasting for coronary interventions: is it time to change practice?

    Patients undergoing invasive cardiac procedures are routinely fasted for varying periods of time even though there is no clearly applicable evidence-base to support current practices. We read with great interest the study by Hamid et al exploring the occurrence of emergency endotracheal intubation and peri-procedural aspiration pneumonia following elective and planned inpatient percutaneous coronary intervention (PCI) in their practice.1 This is the first published study in the peer-reviewed literature that specifically addresses the issue of fasting prior to any cardiac procedure. Considering that it involved retrospective analysis of existing data, the wider applicability of the results may be limited, but their paper would crucially serve to raise awareness amongst the profession on this issue.

    The custom of fasting patients prior to cardiac procedures appear to have evolved from fasting guidelines for general anaesthesia (GA) in the operating theatre. Induction of GA results in depression of cough and swallow reflexes, which can predispose individuals to aspiration of gastric contents. There is a theoretical risk that conscious sedation may depress the cough and swallow reflexes similar to GA. It is interesting to read that the Cardiology teams at the authors' host institutions have 'abandoned' the non-evidence based practice of fasting patients prior to PCI and observed no adverse patient outcomes, although these patients had varying amounts of intravenous sedation.

    In a Cochrane review in 2003 it was concluded that there is no evidence to suggest a shortened fluid fast results in increased risk of aspiration or related morbidity compared with the traditional 'nil by mouth from midnight' policy for patients undergoing GA.2 Although there have been some recent small studies on fasting, the evidence base to determine the optimal period of pre-procedural fasting has been exceedingly slow to develop. Recent European anaesthetic guidelines have recommended clear fluid intake to be continued for up to two hours prior to GA.3 Similar recommendations have been made by the Association of Anaesthetists of Great Britain and Ireland, and the American Society of Anesthesiologists. There are no consensus guidelines on the optimal period of fasting required prior to the wide spectrum of invasive cardiac procedures that may involve local anaesthetic, conscious sedation or GA. This probably reflects the poor evidence base. As a result, practice is largely based on often poorly-referenced local guidelines that differ between institutions.

    It is incredible how, within a specialty as evidence-based as Cardiology, we have managed to accumulate such little evidence on appropriate fasting (indeed if at all needed) prior to any cardiac procedure. The study by Hamid et al is refreshing, however a more robust evidence base would be crucial to 1) establish best practice and 2) promote consistency of such practice within the Cardiology community. Is there any rationale in advising patients to fast at all prior to cardiac procedures under local anaesthetic (eg. diagnostic left and right heart catheterisation or implantation of a loop recorder) where there is a negligible risk of complication involving peri-procedural intubation? How long should patients fast prior to cardiac procedures such as pacemaker implantation or lead revision under conscious sedation (if at all)? There is a crucial and ever-pressing need for well-designed, multicentre prospective randomised controlled trials and engagement within the international cardiology community to attempt to address these questions.

    References

    1. Hamid T, Aleem Q, Lau Y, et al. Pre-procedural fasting for coronary interventions: is it time to change practice? Heart 2014. doi: 10.1136/heartjnl-2013-305289. [Epub ahead of print]

    2. Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications. Cochrane database of systematic reviews 2003; CD004423. doi:10.1002/14651858.CD004423 [online]

    3. Smith I, Kranke P, Murat I, et al. Perioperative fasting in adults and children: guidelines from the European Society of Anaesthesiology. European journal of anaesthesiology 2011;28: 556-69.

    Conflict of Interest:

    None declared

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  4. Under-representation of Frail or Medically Compromised Hypertensive Older People in the Paper

    Under-representation of Frail or Medically Compromised Hypertensive Older People in the Paper Gulistan Bahat*, Asli Tufan, Mehmet Akif Karan

    Department of Internal Medicine, Division of Geriatrics, Istanbul Medical School, Istanbul University, Capa, 34390, Istanbul, Turkey

    Last name of authors: Bahat, Tufan, Karan

    Corresponding author: Gulistan Bahat Address: Istanbul University, Istanbul Medical School, Department of Internal Medicine, Capa, 34390, Istanbul, Turkey Telephone: + 90 212 414 20 00-33204 Fax: + 90 212 532 42 08 E-mail address: gbahatozturk@yahoo.com

    Dear Editor,

    We have read the article by Briasoulis et al. on effect of antihypertensive treatment in patients over 65 years of age with great interest [1]. They comprehensively reviewed prospective randomized trials and assessed the effects of antihypertensive treatment on cardiovascular, all-cause mortality, stroke and heart failure in patients over 65 years of age.By the way of 18 clinically relevant studies, they concluded that treatment to blood pressure target of 150/80 mm Hg or to blood pressure reduction of >25/10 mm Hg effectively decreases all-cause mortality, cardiovascular mortality, stroke and heart failure in patients over 65 years of age.

    However, elderly constitute a rather heterogeneous population and study recommendations could only be generalized to a given population if the given study participants are real and good representative of the population they recommend for. Departures from representativeness are amplified with increasing age. Progressively older adults who do participate in studies, may be progressively less representative of the group they are intended to reflect -as more non-representatively vigorous and robust. Consequently, the older the age, the greater the disparity may be between what is recommended based on 'evidence' and what is best for the patient [2].

    The randomized trials that showed benefit from the treatment of hypertension in older adults included relatively fit patients [3]. Accordingly, older adults who are frail may not benefit from antihypertensive therapy. There are some recent reports pointing out this problem. In a study of 2340 adults >65 years in 2012, among frail adults, there was no association between blood pressure and mortality. Moreover, a higher blood pressure was associated with a lower risk of death among the most frail (ie, those who could not walk the distance at all) [4]. Another exampe is that, in a study of 1562 Latino adults aged 60 -101 years, the relationship between systolic blood pressure and mortality was reported to vary by self-reported walking speed. Higher systolic blood pressure was associated with an elevated risk of mortality in fast walkers while not in slow walkers [5].

    We conclude that Briasoulis et al.'s conclusion could not be generalized to the elderly >65 years of age due to under-representation of frail or medically compromised patients that are rather prevalent in this age group . We think that their conclusion should be considered in view of this important limitation.

    References 1. Cardiac risk factors and prevention: Effects of antihypertensive treatment in patients over 65 years of age: a meta-analysis of randomised controlled studies. Briasoulis A, Agarwal V, Tousoulis D, Stefanadis C. Heart 2014;100:317-323. 2. Golomb BA, Chan VT, Evans MA, Koperski S, White HL, Criqui MH. The older the better: are elderly study participants more non-representative? A cross-sectional analysis of clinical trial and observational study samples. BMJ Open. 2012;2:pii e000833. 3. Egan BM. Section Editors: Bakris GL, Kaplan NM, Schmader KE. Treatment of hypertension in the elderly patient, particularly isolated systolic hypertension. http://www.uptodate.com/contents/treatment-of-hypertension-in-the-elderly- patient-particularly-isolated-systolic- hypertension?source=search_result&search=hypertension+elderly&selectedTitle=1%7E150#H14493503 (accessed on March 6, 2014). 4. Odden MC, Peralta CA, Haan MN, Covinsky KE. Rethinking the association of high blood pressure with mortality in elderly adults: the impact of frailty. Arch Intern Med 2012; 172:1162. 5. Odden MC, Covinsky KE, Neuhaus JM, Mayeda ER, Peralta CA, Haan MN. The association of blood pressure and mortality differs by self-reported walking speed in older Latinos. J Gerontol A Biol Sci Med Sci. 2012;67:977 -83.

    Conflict of Interest:

    None declared

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  5. Ultrasound cardiac calcium assessment.

    We read with interest, and we congratulate the authors for it, the nice paper by Kalsch et al, which demonstrates that aortic valve calcification (AVC) by computed tomography (CT), builds on Framingham score for risk stratification of future cardiovascular events. These are important data for preventive strategies, obtained in a wide and prospective study of healthy asymptomatics. In the discussion, the authors state that "Detection of degenerative aortic valve disease by assessing the prevalence of AVC can easily be performed by echocardiography" and that both echo and CT "provide a high degree of accuracy and reproducibility of AVC, with a higher degree of sensitivity provided by echocardiography but with less specificity than cardiac CT.". This difference can be understood in light of the known inability of ultrasound to differentiate between severe fibrosis and calcification, which inflates sensitivity but increases false-positive rate as long as calcium is the only endpoint; we want to stress that this "limitation" might also represent an advantage of ultrasound compared to CT, since fibrosis may also represent a marker of disease which is worth to detect. In a very recent paper from our group, too recent to be cited in the current paper, entitled "Aortic valve sclerosis as a marker of coronary artery atherosclerosis; a multicenter study of a large population with a low prevalence of coronary artery disease", Rossi A et al demontrated that the presence of AV sclerosis/calcification at echocardiography gives a patient 20 times (OR 21.8, 95CI 6.6-71.9, p <0.0001) the probability of angiographically obstructive CAD (in patients undergoing diagnostic coronary angiography before mitral surgery) after correction for the most relevant clinical factors. These data add to a wealth of literature demonstrating relevant value of heart valve sclerosis/calcification at ultrasound to predict coronary disease or coronary calcium or cardiovascular events, as also seen in prospective studies, such as the cardiovascular health or MESA study. CT has been fundamental to demonstrate the highly predictive value of coronary calcium and then that cardiac valve calcifications do relate to coronary calcium, also predicting cardiovascular events incrementally to Framingham score. Now it's time to prospectively test echocardiography, an incredibly easy, low-cost and radiation-free method, to investigate the potential of ultrasound cardiac calcium to risk-reclassify asymptomatic subjects. Thanks

    Nicola Gaibazzi Andrea Rossi Pompilio Faggiano

    Conflict of Interest:

    None declared

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  6. Bicuspid aortopathy: searching for the answer in "non- progressors"

    Evaldas Girdauskas1, Michael A. Borger2

    1- Department of Cardiac Surgery, Central Hospital Bad Berka, Germany 2- Department of Cardiac Surgery, Heart Center Leipzig, University Leipzig, Germany

    Keywords: bicuspid aortic valve, aortic aneurysm, aortopathy

    Corresponding author: Evaldas Girdauskas, MD, PhD (Address: Department of Cardiac Surgery, Central Hospital Bad Berka, Robert-Koch- Allee 9, 99437 Bad Berka, Germany. Tel.: +49 3645851101; Fax: +49 3645853510 E-mail address: egirdauskas@web.de)

    We read with a great interest the manuscript by Detaint and co- authors published in the last issue of Heart [1]. The authors should be congratulated for their efforts to shine some light on the controversial issue of bicuspid aortic valve (BAV)-associated aorthopathy in their current longitudinal echocardiographic study. Indeed, there are some novel and intriguing findings in this manuscript which may deserve a more extensive commentary.

    The authors were able to demonstrate the fastest aortic dilatation rate at the ascending aortic level and smaller baseline aortic diameter being predictor of rapid aortic progression. Importantly, no correlation was found between aortic dilatation rate and BAV morphology as well as basic aortic phenotype. Typical morphology of BAV (i.e., L-R BAV fusion pattern) was independently associated with the baseline dilatation of the entire aortic root, which may reflect specific patterns of transvalvular flow in this BAV subtype [2].

    The BAV population analyzed in this study is quite distinct from the "typical" surgical BAV population and these differences should be highlighted. First of all, 113/353 (32%) BAV patients without raphe were identified in the current study. In our experience, it is rather rare to find a BAV without raphe during aortic valve replacement (AVR) surgery. Similarly, BAV without raphe was identified in only 7% patients in the surgical series by Sievers and co-authors [3]. Another major difference is the low proportion of patients with a BAV stenosis in the study (i.e., 14% of the study population). Calcific stenosis is the most common fate of congenital BAV (i.e., accounts for up 85% of surgically treated patients [4]) which is clearly underrepresented in the current series. As opposed to this, the authors revealed significant (i.e., at least moderate) BAV insufficiency in 123/353 (35%) study patients. Therefore, BAV cohort analyzed in this manuscript may represent a specific referral pattern of the tertiary care center. How many patients underwent AVR surgery during study period? Were these patients excluded from further echocardiographic follow-up? Is there any role of the variable "AVR surgery" in the progression of aortic diameters?

    Was there a subgroup of BAV patients with the maximal progression of aortic diameters at the level of the sinuses of Valsalva? There is some evidence in the literature that patients with so-called "root phenotype" (i.e., Valsalva sinuses > ascending aorta) may represent a predominantly congenital form of BAV disease which is associated with a higher risk of adverse aortic events [5]. What was the proportion of BAV patients in the subgroup of "sinuses phenotype" which showed stable aortic diameters at follow-up echocardiography?

    However, the most intriguing question from this manuscript - why did aortic diameters remain stable in nearly half of the BAV patients? Is this only a function of limited echocardiographic follow-up interval (i.e., aortopathy would progress over longer follow-up periods) or a real phenotypic difference in BAV patients? Provided that it is a real phenotypic difference- what are the predictors of non-progressive aortopathy in BAV disease? Obviously, this issue was not the main focus of the current manuscript and no specific analysis has been performed. However, based on the presented data, risk stratification for aortic events based on BAV morphology and baseline aortic diameter would be inadequate. A higher level of complexity in determinants of BAV-associated aortopathy has been proposed by the authors. In our opinion, this question will be impossible to address without knowing the precise haemodynamic profile of transvalvular flow in these BAV patients. Moreover, the presented data underscore still significant gaps in knowledge in the development of BAV aortopathy.

    References

    1. Detaint D, Michelena HI, Nkomo VT, Vahanian A, Jondeau G, Sarano ME. Aortic dilatation patterns and rates in adults with bicuspid aortic valves: a comparative study with Marfan syndrome and degenerative aortopathy. Heart. 2014;100:126-34.

    2. Mahadevia R, Barker AJ, Schnell S, Entezari P, Kansal P, Fedak PW, Malaisrie SC, McCarthy P, Collins J, Carr J, Markl M. Bicuspid Aortic Cusp Fusion Morphology Alters Aortic 3D Outflow Patterns, Wall Shear Stress and Expression of Aortopathy. Circulation. 2013 Dec 17.

    3. Sievers HH, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg. 2007;133:1226-33.

    4. Sabet HY, Edwards WD, Tazelaar HD, Daly RC. Congenitally bicuspid aortic valves: a surgical pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional cases. Mayo Clin Proc. 1999;74:14-26.

    5. Girdauskas E, Disha K, Secknus M, Borger M, Kuntze T. Increased risk of late aortic events after isolated aortic valve replacement in patients with bicuspid aortic valve insufficiency versus stenosis. J Cardiovasc Surg (Torino). 2013;54:653-9.

    Conflict of Interest:

    None declared

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  7. Don't forget radiotherapy

    This is an excellent article which will help many of us who have to manage patients who are undergoing cancer treatment.

    It must be remembered that many patients also undergo radiotherapy, as is acknowledged in the article. High dose radiotherapy to the thorax can cause heart failure, both systolic and restrictive, valvular dysfunction and coronary artery disease, which often presents many years later. In lymphoma survivors who have received such therapy, cardiovascular disease is the most common cause of death.

    A history of thoracic radiotherapy is important to elicit when assessing patients with cardiovascular symptoms. Such patients may present with symptoms of cardiac disease at a younger age than is typical, with few traditional risk factors, and are therefore potentially at higher risk of initial misdiagnosis.

    Conflict of Interest:

    None declared

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  8. Conclusions about elderly people need real elderly people

    We really appreciate the clarifications offered by Alexandros Briasoulis concerning his article, but in our opinion our claim about the importance of including in the meta-analysis information only (or mostly) from elderly patients remains well founded. In this regard, the Cochrane Hypertension Group encourages to accept only studies if 70% or more of the participants meet the definition, or individual patient data are available, or data of relevant patients are provided separately allowing specific inclusion of the population as defined (1). Moreover, the inclusion of INVEST trial (2) in the ACCF/AHA 2011 (3) cannot be claimed as a relevant argument to support proceeding in the same manner in the meta-analysis, because of the inherent low level of evidence showed by consensus. On the other hand, the INVEST trial has a very high risk of bias. It is an open trial and no information on the sequence generation nor the allocation concealment is provided.

    We agree with the author in the conclusion showed by the secondary analysis (4). But in fact this provides to us compelling evidence of the importance of separating the information between young and older people. Furthermore, it is not clear to us why these findings are said to be "in accordance" with the results of the sensitivity analysis performed by the author. According to the Discussion (1), the subgroup analysis of studies with patients over 70 years showed that "the beneficial effects of antihypertensive treatment remained significant in the first group of studies (treatment versus placebo group)" but the meta-analysis did not take into account blood pressure levels, thereby both papers seem to be focused on very different issues. Also, we have not been able to read in the last article cited (5) the assertion made on the J-curve association in patients above or below age of 65. In fact, this study did not compare different age subgroups any time but different blood pressure strata, and the mean age values in each 10-mm Hg blood pressure stratum were very similar (66-67 years).

    In short, if elderly age begins at 65, we need to found our practices on studies including real elderly people. Evidence based on the results of studies with patients of a mean age close to 65 is not trustworthy.

    (1) Gorricho J, Garjon J, Celaya MC, Muruzabal L, Montoya R, Lopez A, Malon MDM, Saiz LC. Blood pressure targets for the treatment of patients with hypertension and cardiovascular disease. Cochrane Database of Systematic Reviews 2013, Issue 1. Art. No.: CD010315. DOI: 10.1002/14651858.CD010315. (2) Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al. A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease. The International Verapamil- Trandolapril Study (INVEST): a randomized controlled trial. JAMA. 2003;290(21):2805-16. (3) Aronow WS, Fleg JL, Pepine CJ, et al. ACCF/AHA 2011 expert consensus document on hypertension in the elderly: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. Circulation. 2011;123:2434-2506. (4) Denardo SJ, Gong Y, Nichols WW, et al. Blood pressure and outcomes in very old hypertensive coronary artery disease patients: an international verapamil ST-Trandolapril (INVEST) substudy. Am J Med. 18 2010;123:719-26. (5) Messerli FH, Mancia G, Conti CR, et al. Dogma disputed: can aggressively lowering blood pressure in hypertensive patients with coronary artery disease be dangerous? Ann Intern Med. 2006;144:884-93.

    Luis Carlos Saiz, Pharm D Pharmacotherapy Research Coordinator Navarre Health Service, Spain

    Juan Erviti, Pharm D, PhD Head of Unit, Drug Information Navarre Health Service, Spain

    Conflict of Interest:

    None declared

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  9. Pre-test probability in the new ESC guidelines or appropriateness criteria.

    We read with great interest the recent article by Bhattacharyya et. al.1 They state that a high proportion (71/250) of stress echocardiograms (SE) were performed on low risk patients and were inappropriate, concluding that implementation of diagnostic appropriateness criteria2 would reduce this.

    Appropriateness criteria2 published in 2011 reviewed clinical scenarios warranting SE and graded these on a scale of 1 to 9. Classifying patients into 3 categories, appropriate (grade 7-9), uncertain (grade 4-6) and inappropriate (grade 1-3). The 2013 ECS guidelines3 for investigation of stable coronary artery disease (CAD) recommends functional testing for patients with intermediate (15-85%) pre-test probability (PTP). However, Bhattacharyya et. al. do not elaborate on the PTP of patients in each classification. Thus, in accordance with new ESC guideline SE may have been appropriate in some of the patients classified as uncertain or inappropriate.

    Furthermore, a proportion of patients classified as inappropriate included previously revascularised patients with stable symptoms. Cardiologists may feel obliged to perform investigations on symptomatic previously revascularised patients, often with invasive coronary angiography, even if they are stable with a negative SE within the previous two years. To reduce the burden on SE, cardiac CT is a viable alternative that demonstrates grafts and proximal stent patency.

    Finally, NICE, ESC and ACC/AHA guidelines all differ in diagnostic guidelines, enabling cardiologists to use their experience and local expertise to select the most appropriate investigation for individual patients.

    Conflict of Interest:

    None declared

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  10. Re:Scaling cardiac dimensions to body size is crucial in the cardiovascular care of elite athletes

    Dear Professor Pressier,

    Thank you for your correspondence with respect to our study (1). We have read your paper (2) with interest and congratulate you on an important paper providing further empirical evidence to support more appropriate methods of generating body size independent cardiac indices. We are delighted your data demonstrated the importance of fat free mass something we and others have proposed empirically before and represented in previous review articles (3, 4). Your recent study is a very insightful contribution to this field and we hope others in the clinical field read this work and follow suit. We feel our additional comments in the meta- analysis support a revisionist approach to the use of cardiac indices.

    We would go further though and not stop at structural data and charge all interested groups to look at how key functional data are indexed. We have some empirical data published in respect of longitudinal tissue velocities (5) and we feel this work should be extended.

    References 1. Utomi V, Oxborough D, Whyte GP, Somauroo J, Sharma S, Shave R, et al. Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete's heart. Heart 2013;99:1727-1733. 2. Pressler A, Haller B, Scherr J, Heitkamp D, Esefeld K, Boscheri A, et al. Association of body composition and left ventricular dimensions in elite athletes. European Journal of Preventive Cardiology. 2012;19(5):1194 -204. 3. Batterham A, George K, Whyte G, Sharma S, McKenna W. Scaling cardiac structural data by body dimensions: a review of theory, practice, and problems. Int J Sports Med. 1999;20(8):495-502. 4. Dewey F, Rosenthal D, Murphy DJ, Froelicher V, Ashley E. Does size matter? Clinical applications of scaling cardiac size and function for body size. Circulation. 2008;117(17):2279-87. 5. Oxborough D, Batterham AM, Shave R, Artis N, Birch KM, Whyte G, et al. Interpretation of two-dimensional and tissue Doppler-derived strain (?) and strain rate data: is there a need to normalize for individual variability in left ventricular morphology? Eur J Echocardiogr. 2009;10(5):677-82.

    Conflict of Interest:

    None declared

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