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Recent eLetters

Displaying 1-10 letters out of 736 published

  1. T1 Mapping with CMR: an emerging clinical biomarker.

    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, 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.

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  2. Microcirculation impairment in acute coronary syndrome: It is not always the same story

    We read with great interest the elegant work of Kasula et al. recently published on Heart [1]. The Authors showed that fractional flow reserve (FFR) may be an effective tool to discriminate the long-term functional outcome after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) [1]. This retrospective study included exclusively ACS patients for whom FFR evaluation resulted "flow limiting" (<0.80). All patients were treated with PCI and the main finding of the study was that FFR value after PCI was able to discriminate those at higher risk of adverse events. The Authors concluded that FFR reliably estimates baseline ischemia and its subsequent reduction post-PCI in patients with ACS. We totally agree with the significance of the post-PCI FFR assessment, but any comment regarding the FFR role in the determination of baseline ischemia in ACS patients should not be taken for granted. Recently, Lee et al. showed that deferring the treatment of intermediate coronary stenosis based only on the FFR value, without taking into account the features of coronary microcirculation, exposes the patient to an increase of adverse events [2]. Kasula et al. did not report the long-term outcome of patients for whom FFR result was "no flow limiting" [1]. Accordingly, the conclusion that "FFR alone may be an invaluable tool in identifying ischemia producing lesions" is methodologically incorrect. It is well established that microvascular disfunction may be the result of: i) pre-existing condition (e.g. microvascular angina), ii) chronic damage (e.g chronic kidney disease [3]), iii) acute injury (e.g. ACS) or iv) a mix of these. Therefore, the impairment in the coronary microcirculation may differ significantly across ACS patients. Some patients show a partial impairment that allows an effective adenosine action and then a proper FFR determination. Contrarily, other patients have an extensive damage and FFR assessment may result misleading. For this reason, in our opinion, it seems important to focus our attention on ACS patients with "no flow limiting" FFR assessment. In these cases, the simultaneous assessment of the coronary microcirculation (e.g. index of microcirculatory resistance) may help physicians in the decision-making process [4].

    References

    1. Kasula S, Agarwal SK, Hacioglu Y, et al. Clinical and prognostic value of poststenting fractional flow reserve in acute coronary syndromes. Heart. 2016 Aug 4 doi: 10.1136/heartjnl-2016-309422 2. Lee JM, Jung JH, Hwang D, et al. Coronary Flow Reserve and Microcirculatory Resistance in Patients With Intermediate Coronary Stenosis. J Am Coll Cardiol. 2016 15;67(10):1158-69 3. Tebaldi M, Biscaglia S, Fineschi M, et al. Fractional flow reserve evaluation and chronic kidney disease: Analysis from a multicenter Italian registry (the FREAK study). Catheter Cardiovasc Interv. 2015 Dec 31. doi: 10.1002/ccd.26364 4. Tebaldi M, Biscaglia S, Pecoraro A, et al. Fractional flow reserve implementation in daily clinical practice: A European survey. Int J Cardiol. 2016 15;207:206-7.

    Conflict of Interest:

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  3. Re Larsson et al, Chocolate consumption adn risk fo myocardial infarction: a propspective stusy and meta-analysis

    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 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.

    Conflict of Interest:

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  4. Re:It is important to distinguish between HFrEF and HFpEF when interpreting these data

    We would like to thank Dr Cunnington for his interest in our study and raising some potentially interesting points . We do not have a breakdown of patients with heart failure ( HF) who had either preserved (HFpEF) or reduced ejection fraction (HFrEF) . Since beta-blockers only have a licensed indication for HFrEF on the basis of an echocardiogram , we do not believe that this is likely to be a relevant factor within our dataset . The relative prevalence of hypertension within our cohort was 13.3% verses 11.6% ,and for diabetes was 47.4% verses 41.9% respectively for HF alone verses HF with COPD . Hence the assertion made regarding a higher putative comorbidity is not supported by the data presented here . Consequently prescribing of ACEI/ARB in HF with COPD was not confounded by comorbidity due to treatment for either diabetes or hypertension . The higher use of ACEI/ARB without beta-blocker in HF with COPD compared to HF alone is more likely to reflect a reticence of physicians to prescribe add on therapy with beta-blockers in the presence of airflow obstruction due to fears of bronchoconstriction . As such we remain confident in the strength of our conclusions regarding underuse of beta-blockers in HF with COPD .

    Conflict of Interest:

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  5. Impact of Beta-blocker on The Outcome of Takotsubo Cardiomyopathy

    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.

    Conflict of Interest: None declared

    Conflict of Interest:

    None declared

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  6. It is important to distinguish between HFrEF and HFpEF when interpreting these data

    In this interesting article, Lipworth and colleagues report that beta -blockers are underused in patients with heart failure (HF) and COPD, compared to those with HF alone. However, they do not quote the proportion of "HF" patients within their dataset who had HF with reduced ejection fraction (HFrEF; left ventricular ejection fraction (LVEF) <40%) and HF with preserved ejection fraction (HFpEF; LVEF >50%). This distinction is important, as beta-blockers are only recommended in HF guidelines for patients with HFrEF (1), owing to a lack of trial data to support their efficacy in patients with HFpEF.

    Furthermore, patients with HFpEF tend to have a higher prevalence of co-morbidities compared to patients with HFrEF, including COPD, hypertension and diabetes (2). Thus, it is possible that "HF and COPD" patients in this dataset may have a higher proportion of HFpEF to HFrEF, in comparison to patients with "HF alone", and the rates of ACE/ARB prescribing may be increased in this group owing to treatment of hypertension and diabetes rather than HF. These considerations may therefore confound the strength of the authors' conclusions regarding underuse of beta-blockers in patients with HF and COPD.

    References

    1. Ponikowski P, Voors AA, Anker SD et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2016; DOI: 10.1093/eurheartj/ehw128.

    2. Ather S, Chan W, Bozkurt B et al. Impact of non-cardiac comorbidities on morbidity and mortality in a predominantly male population with heart failure and preserved versus reduced ejection fraction. J Am Coll Cardiol 2012;59:998-1005.

    Conflict of Interest:

    None declared

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  7. Hypertrophic cardiomyopathy and the potential influence of etomidate on postoperative outcomes.

    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.

    Conflict of Interest:

    None declared

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  8. Does loneliness and social isolation really increase the risk of CHD and stroke? Pooled results based on quality effect model

    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 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.

    Conflict of Interest:

    None declared

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  9. Midregional pro-atrial natriuretic peptide and N-terminal pro-B natriuretic peptide for pediatric heart failure diagnosis

    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.

    Conflict of Interest:

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  10. Fontan conversion is a dated approach to the Failing Fontan

    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 Thorac Surg. 2016;101(4):1574-6.

    Conflict of Interest:

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