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Recent eLetters

Displaying 1-10 letters out of 745 published

  1. Cautious anticoagulation strategy in patients with dialysis-requiring end-stage kidney disease.

    We read with interest this manuscript which demonstrated in a large clinical registry that patients with chronic kidney disease with indications for anticoagulation were often treated sub-therapeutically (1). A more aggressive approach was therefore advocated.

    We would like to point out that, while this study should be commended for including a large number of patients, it did not show data on the key clinical outcomes of stroke or bleeding. We feel, therefore, that a clear association cannot be made between low time in the therapeutic range (TTR) and any negative clinic outcome. In fact, paradoxically, our experience from a large tertiary cardiac and renal service differs. We agree with the authors that haemodialysis patients often have a suboptimal TTR, but we believe there is no convincing data implying that increased time spent in therapeutic range is beneficial in preventing embolic or thrombotic events (2).

    In addition, there is substantial evidence that haemodialysis patients are at significantly increased risk of major bleeding events, contributed to by uraemic platelet dysfunction, hypergastrinaemia and anticoagulation required for the extracorporeal circuit. This risk of major bleeding (bleeds into a critical organ, requiring transfusion or admission, or fatal) is increased compared with non-dialysis patients, and this risk has been shown to increase with the addition of antiplatelet treatment or oral anticoagulation (3).

    We would, therefore, advocate a cautious approach to anticoagulation in patients with dialysis-requiring end-stage kidney disease. Our policy is not to anticoagulate these patients in light of the fact that the significant bleeding risk per annum in our haemodialysis patients without addition anticoagulation is already nearly 4% (4). We believe there is an urgent need for clinical outcome data in order to better inform our clinical decision making in this complex patient group.

    References.

    References. 1. Yang et al. Heart online. 2016. doi:10.1136/heartjnl-2016-309266. 2. Chen et al. Circulation. 2016;133:265-272. 3. Holden et al. CJASN. 2008;3:105-110. 4. Nadarajah et al. Clin Nephrology 2015;85(5):274-9.

    Conflict of Interest:

    None declared

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  2. Considering genomic variants for cardiovascular disease prediction

    Dear Editor,

    I read with great interest the article by Morris et al entitled, "Marginal role for 53 common genetic variants in cardiovascular disease prediction" (1). The article analyzed a large sample of 11, 851 individuals from 7 prospective studies aimed at primary prevention of fatal or non-fatal coronary heart disease (CHD) or stroke.

    The study incorporated susceptibility variants for CHD and stroke into a genetic risk score (GRS), to match the two conditions predicted by a conventional risk score QRISK-2. Results for population-wide utility of the GRS, and estimates from a sequential screening strategy proposed for individuals at intermediate risk, were provided. The study extrapolated that 462 intermediate-risk individuals would need to be screened in order to prevent one coronary heart disease or stroke event in 10 years.

    Based on these results, a GRS could become a novel method for determining which intermediate-risk individuals should be managed aggressively, if reclassified to high-risk. However, before these results are adopted in clinical practice, the following should be considered. First, the extrapolated estimates should be confirmed prospectively. Second, the 53 variants include 46 for CHD and 7 for stroke. The CHD variants are not necessarily found to associate with stroke, and vice versa. This may limit predictions for each disorder. Third, 46 CHD variants account for 10% of heritability, and do not capture the entire contribution of genetics estimated at 40-60% (3). Fourth, the GRS included 29 variants unique for CHD, as well as 17 additional variants that also associate with CHD risk factors, such as cholesterol, blood pressure, and diabetes (3); these risk factors are already accounted for in QRISK2 and are not providing independent information. Fifth, the GRS did not incorporate 10 additional variants recently discovered (4). Reclassification and discrimination analyses should be redone with only 29 variants (then adding in the 10 new variants) in population-wide analysis and for intermediate-risk individuals. Finally, a weak effect on mortality was reported. This is likely due to the GRS being developed using case- control prevalence and not incidence.

    Overall, there is still work to be done before these excellent results can be implemented.

    References

    1. Morris RW, Cooper JA, Shah T, Wong A, Drenos F, Engmann J, et al. Marginal role for 53 common genetic variants in cardiovascular disease prediction. Heart. 2016 Jun 30. 2. Kullo IJ, Jouni H, Austin EE, Brown SA, Kruisselbrink TM, Isseh IN, et al. Incorporating a Genetic Risk Score Into Coronary Heart Disease Risk Estimates: Effect on Low-Density Lipoprotein Cholesterol Levels (the MI- GENES Clinical Trial). Circulation. 2016 Mar;133(12):1181-8. 3. Deloukas P, Kanoni S, Willenborg C, Farrall M, Assimes TL, Thompson JR, et al. Large-scale association analysis identifies new risk loci for coronary artery disease. Nat Genet. 2013 Jan;45(1):25-33. 4. Nikpay M, Goel A, Won HH, Hall LM, Willenborg C, Kanoni S, et al. A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease. Nat Genet. 2015 Oct;47(10):1121-30.

    Conflict of Interest:

    None declared

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  3. "Definite Diagnosis of Spontaneous Coronary Artery Dissection: An Unsettled Issue"

    We read with great interest the manuscript by Faden et al. (1) entitled "A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium" when it was published online July 13. Using the Healthcare Cost and Utilization Project national database, the authors evaluated over 4 million pregnancy-related discharges, looking at the prevalence and outcomes of pregnancy-associated spontaneous coronary artery dissection (P-SCAD). By applying the International Classification of Diseases, 9th Revision (ICD-9) 79 cases of P-SCAD were identified, resulting in a prevalence of 1.81 per 100,000 pregnancies. Although this study stands out as the largest cohort thus far assessing P-SCAD, a few shortcomings should be highlighted. First, the methodology for P-SCAD search and identification included the ICD-9 medical code 412.12 represents a general definition of coronary artery dissection; there is no specific classification for SCAD in either the ICD -9 or in the recent ICD-10-CM (diagnosis code I25.42). Therefore, the 79 cases identified by the investigators may have included coronary artery dissections arising from other causes including atherosclerosis. The genuine classification of SCAD should be non-atherosclerotic. In addition, other ambiguous findings by angiography, such as thrombus, may also mimic SCAD (2). Prior study evaluating pregnant and postpartum women with myocardial infarction showed that its pathophysiology includes SCAD in 43% of cases, atherosclerosis in 27%, intracoronary thrombus in 17%, and normal coronary arteries in 11% (3). Second, despite its well-known limitations, invasive coronary angiography is still the main tool for recognizing this condition; other intravascular imaging such as intravascular ultrasound and optical coherence tomography have been recently used to enhanced its diagnostic accuracy. Of note, the pathognomonic appearance of SCAD on angiography--contrast dye staining of arterial wall with multiple radiolucent lumen--is less prevalent among all the findings, making the diagnostic ability of invasive angiography limited and challenging (5). In the present study by Faden et al. there is no mention about the angiographic findings of those patients, making the definite and final diagnosis of P-SCAD debatable. Had the authors reassessed all coronary invasive angiography, the ability to definitively diagnosis SCDA would have been improved; indeed, 10% of cases did not undergo invasive angiography, so the final diagnosis P-SCDA could only be extracted from the data set alone. Finally, when assessing the risk factors for P-SCAD, the authors demonstrated that chronic hypertension and lipid profile abnormalities were highly prevalent in relation to SCAD, which is in disagreement with prior studies showing that most patients had no risk factors for coronary artery disease (4). Likewise, a high rate of prior coronary angioplasty and, specifically, coronary artery bypass graft surgery (34%) in this cohort may suggest the inclusion of patients with coronary atherosclerosis.

    References:

    1. Faden MS, Bottega N, Benjamin A, Brown RN. A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium. Heart 2016;0:1-6. doi:10.1136/heartjnl-2016-309403.

    2. Cade JR, Abizaid A, Caixeta A. Organized Thrombus Mimicking Spontaneous Coronary Artery Dissection. JACC Cardiovasc Interv. 2014; 7(12):1458.

    3. Elkayam U, Jalnapurkar S, Barakkat MN, Khatri N, Kealey AJ, Mehra A, et al. Pregnancy-associated acute myocardial infarction: a review of contemporary experience in 150 cases between 2006 and 2011. Circulation. 2014;129(16):1695-702.

    4. Cade JR, Szarf G, de Siqueira ME, Chaves A, Andrea JC, Figueira HR, et al. Pregnancy-associated spontaneous coronary artery dissection: insights from a case series of 13 patients. Eur Heart J Cardiovasc Imaging. 2016 [Epud ahead of print].

    5. Saw J. Coronary angiogram classification of spontaneous coronary artery dissection. Catheter Cardiovasc Interv. 2014;84(7):1115-22.

    Conflict of Interest:

    None declared

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  4. A Case for Palliative PCI

    Dear Editor

    On reading the review on coronary revascularisation in the elderly by Cockburn et al (1) I must agree that more trials are needed to focus on the benefit of PCI in elderly populations.

    When assessing these patients, clinicians should consider the impact of symptom relief versus procedural risk. If a patient is experiencing recurrent and debilitating chest pain requiring frequent hospital admission then the risks of PCI, despite multiple comorbidities, could easily be rationalised when the benefit to the patient is clear. In such patients this "palliative PCI" approach, aiming to improve quality of life but not necessarily prolong it, should be at the forefront of the clinicians mind. Each patient should be assessed with consideration of the benefits to the individual and with a clear understanding of the values of the patient.

    An interesting additional consideration not mentioned in the review is the potential benefit of PCI in elderly patients in terms of cost to hospitals. Although complications and poor outcomes may be increased in this population, the burden of elderly patients deemed unfit for PCI presenting with recurrent admissions due to chest pain must be taken into account. I noted that in a paragraph on future research the authors mentioned further trials of PCI in elderly patients that looked at myocardial infarction and mortality as their primary outcomes. This may no longer be as relevant in elderly patients where quality of life is more important than quantity. A trial involving predominantly elderly patients assessing quality of life both before and after PCI as the primary outcome could be useful.

    References: 1.Cockburn J, Hildick-Smith D, Trivedi U, de Belder A. Heart 2016;0:1-9. doi:10.1136/heartjnl-2015-308999

    Conflict of Interest:

    None declared

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  5. Oxygen is toxic during reoxygenation in STEMI patients as well as in other clinical conditions

    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

    Conflict of Interest:

    None declared

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  6. Signficance of Inverse Prognostic Value of Post-PCI FFR in Patients with NSTEMI

    I read the article by Kasula and colleagues with great interest. I firmly believe that this is a novel finding and of great clinical significance (1).

    Utility of Fractional flow reserve (FFR) is firmly established in stable coronary artery disease but has been widely debated in patients with acute MI particularly in the culprit vessel (2, 3). FFR measurements require maximal coronary hyperaemia which may be less readily achieved in patients with acute coronary disease because of coronary microvascular dysfunction. This in turn may result in a falsely higher FFR value. This will be of particular concern while assessing FFR value post-PCI since coronary stenting of a 'hot' culprit lesion in acute coronary syndrome would inevitably carry risk of some distal embolization which may further exacerbate this issue. Since, microvascular obstruction carries a poor prognosis, a direct (in contrast to an inverse relationship) relationship between post-PCI FFR value and adverse outcome would have supported this theoretical limitation of FFR in patients with MI (4). However, it was reassuring to see that these concerns appear unfounded in the current study. The fact that FFR value had an inverse relationship with future adverse events is an in- direct evidence that FFR value is still valid even in culprit vessel in patients with NSTEMI.

    References: 1) Clinical and prognostic value of poststenting fractional flow reserve in acute coronary syndromes

    2) Pijls NH, De Bruyne B, Peels K, Van Der Voort PH, Bonnier HJ, Bartunek J, Koolen JJ, Koolen JJ. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. N Engl J Med 1996;334:1703-1708.

    3) Tonino P.A., De Bruyne B., Pijls N.H., et al; Fractional flow reserve versus angiography for guiding percutaneous coronary intervention. N Engl J Med. 2009;360:213-224

    4) Fearon W.F., Low A.F., Yong A.S., et al; Prognostic value of the Index of Microcirculatory Resistance measured after primary percutaneous coronary intervention. Circulation. 2013;127:2436-2441.

    Conflict of Interest:

    None declared

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  7. Inverse Prognostic Value of Post-PCI FFR in Patients with NSTEMI

    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

    Conflict of Interest:

    None declared

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  8. Expediating the pathway to SVT ablation

    Honarbakhsh et al should be congratulated upon their innovative research in improving the care for patients with arrhythmias. Their paper not only demonstrates an effective community treatment strategy but importantly is cost effective during the current austerity. Potential further cost savings and enhanced patient experiences could be anticipated by encouraging General Practitioners to subsequently refer patients wishing for a curative strategy directly to Electrophysiologists for consideration of an ablation.

    Patients affected by SVTs usually experience frustrating recurrent attendances at Accident and Emergency departments prior to referral to Electrophysiologists, despite our knowledge that ablations are successful in 95% at the first procedure. Similarly, many journeys to the AED are aborted as the symptoms self terminate prior to arrival or have abated by the time of medical review. Thus frequently ECGs fail to capture their arrhythmia and clinch the diagnosis, protracting the time to effective treatment. The PARA group had a statistically significant greater chance of receiving a copy of their ECG (85% v 63%, p-value 0.035) and therefore this often illusive information would have a greater chance of being available for inclusion in the onward referral to the Cardiologist or Electrophysiologist.

    Partnerships between community and tertiary care services can expedite and improve arrhythmia care, reducing some of the burden on over stretched Emergency Departments.

    Conflict of Interest:

    None declared

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  9. Multilevel analysis of variance and hospital performance in heart failure management

    Dear Editor,

    We have read with interest the article written by Emdin et al (1) using multilevel regression analysis of variance to investigate hospital performance for heart failure management. We were pleased to note that the authors apply and refer to our previous methodological work concerning the use of the Intraclass Correlation (ICC) and Median Odds Ratio (MOR).(2) However, the authors did not consider a recent paper of ours investigating survival after heart failure hospitalization and applying a modern multilevel analytical framework.(3)

    Nevertheless, the article by Emdin et al (1) actually applies a similar way of reasoning that we presented in our previous article.(3) In this respect, we would like to take this opportunity to comment on their study.(1)

    First, much of variation in performance identified by the authors could be attributed to the ward rather than to the hospital level since the ward-level is where the genuine organisational effect could take place. In our recent study we found that the ward ICC (around 5.3%) was much larger than the hospital ICC (0.04%).(3)

    Second, while the issue of confounding, and hence the need to adjust for patient case-mix, is a cause of concern in the case of outcome indicator, it is normally not a concern when it comes to process indicators (4) and the authors should have discussed this aspect.

    Third, the authors used backward stepwise single-level regression to identify the hospital characteristics that "were significantly associated with a better performance score". We think this identification should be based on a priori theory rather than on a posteriori finding of statistical significance. Besides, the use of single level regression analysis for this task is unsuitable as it does not consider the intra- hospital correlation and provides spurious "significant" associations.(2)

    Otherwise we agree with Emdin et al(1) methodological approach and interpretation of the results. However, a reference to our previous article (3) should have been made.

    Kind Regards,

    Nermin Ghith, PHD candidate, Research Unit of Chronic Conditions, Bispebjerg Hospital, Copenhagen.

    Prof. Juan Merlo MD, PhD, Head of the Research Unit for Social Epidemiology, Dept. Clin. Sci.(Malmo), Faculty of Medicine, Lund University, Sweden

    -References

    1. Emdin CA, Conrad N, Kiran A, Salimi-Khorshidi G, Woodward M, Anderson SG, et al. Variation in hospital performance for heart failure management in the National Heart Failure Audit for England and Wales. Heart. 2016.

    2. Merlo J, Chaix B, Ohlsson H, Beckman A, Johnell K, Hjerpe P, et al. A brief conceptual tutorial of multilevel analysis in social epidemiology: using measures of clustering in multilevel logistic regression to investigate contextual phenomena. Journal of Epidemiology and Community Health. 2006;60(4):290-7.

    3. Ghith N, Wagner P, Fr?lich A, Merlo J. Short Term Survival after Admission for Heart Failure in Sweden: Applying Multilevel Analyses of Discriminatory Accuracy to Evaluate Institutional Performance. PLoS ONE. 2016;11(2):e0148187.

    4. Rubin HR, Pronovost P, Diette GB. The advantages and disadvantages of process?based measures of health care quality. International Journal for Quality in Health Care. 2001;13(6):469-74.

    Conflict of Interest:

    None declared

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  10. 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.

    Conflict of Interest:

    None declared

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