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noncompaction?
International Journal of Cardiology 184 (2015) 484–485
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Does professional athlete training cause acquired left ventricular hypertrabeculation/noncompaction? C. Stöllberger ⁎, J. Finsterer Krankenanstalt Rudolfstiftung, Juchgasse 25, A-1030 Wien, Austria
a r t i c l e
i n f o
Article history: Received 14 January 2015 Accepted 26 February 2015 Available online 27 February 2015 Keywords: 3-Dimensional Cardiomyopathy Echocardiography Exercise training Noncompaction cardiomyopathy Speckle tracking echocardiography
With interest we read the article by D'Ascenzi et al. about exerciseinduced left ventricular hypertrabeculation/noncompaction (LVHT) in an athlete's heart [1]. They report a case series of four professional basketball players in whom during an intensive training program of 5 months left ventricular trabecular pattern increased. In one athlete who underwent echocardiography after 1 month of detraining, the hypertrabeculation decreased resembling the pattern observed one year before. Additionally, the athletes showed electrocardiographic changes with T wave inversion. These findings, like the recently published findings in pregnant women, challenge the hypothesis that LVHT is due to a disturbed compaction process of the embryonic heart [2]. We have the following questions and concerns: It remains unclear whether LVHT was present already before starting the training. It would be interesting if LVHT was congenital or acquired. Were there any indications from the family history that LVHT in these four athletes was familial and thus congenital? Did any of the four undergo echocardiography before starting with sport activities? Was the family history in any of the four positive for sudden cardiac death, syncope, stroke, embolism, or heart failure? Acquired LVHT, however, has been also reported from non-athletes and non-pregnant patients of whom the majority suffered from a neuromuscular disorder (NMD) [3,4]. If LVHT was already present before study entry without prior exercise, the four athletes should be
investigated for NMDs or chromosomal defects. Did any of the four have elevated creatine-kinase or a family history positive for muscle disease? Furthermore, it would be interesting to know if the athletes were screened for sickle cell anemia, a disorder more prevalent in Africans than Caucasians and also associated with LVHT [5]. Did the athletes have a history or actual intake of any drugs including drugs for “doping” like erythropoietin or somatotropin which are also known to induce muscular growth [6,7]? Did the authors also investigate athletes who did not present with LVHT before onset of the training? In athletes without LVHT before starting the training did LVHT develop during this physical activity? Does LVHT increase only in athletes with pre-existing LVHT or does it also develop in athletes without pre-exercise LVHT? The authors differentiate between noncompaction and hypertrabeculation. Both terms describe the same phenomenon and should be used synonymously. There are different echocardiographic criteria for LVHT in the literature [8–10]. It would be interesting to know according to which echocardiographic criteria was LVHT diagnosed, if interobserver agreement was investigated and if the observers were blinded to the training status of the athletes. It is indicated that in the beginning of the training program, the athletes showed left ventricular trabeculations. Did these trabeculations only increase in thickness during the training or did new trabeculations grow? Was there only an increase in the thickness of the trabeculated layer of the myocardium or also a decrease in thickness of the compacted layer? Was there also an increase in the echogenicity of the endocardium which made the trabeculae better visible — this impression is suggested by Fig. 2. How do the authors explain that left ventricular mass increased from 185 to 288 and 233 g to 376 g in two athletes but only by 13 and 30 g in the two others? Electrocardiographic changes are reported, however the ECGs of only two athletes are shown. Did all four athletes develop negative T waves during training? Did these ECG-changes regress after detraining? In conclusion, these very interesting findings should be supported by studying more extensively a larger group of athletes with various ethnicity in different stages of training to assess the etiology and pathogenesis of LVHT and a group of athletes without LVHT at onset of the training. Conflict of interest
⁎ Corresponding author at: Steingasse 31/18, A-1030 Wien, Austria. E-mail addresses: [email protected], fifi[email protected] (C. Stöllberger).
http://dx.doi.org/10.1016/j.ijcard.2015.02.102 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
The authors report no relationships that could be construed as a conflict of interest.
C. Stöllberger, J. Finsterer / International Journal of Cardiology 184 (2015) 484–485
References [1] F. D'Ascenzi, A. Pelliccia, B.M. Natali, M. Bonifazi, S. Mondillo, Exercise-induced leftventricular hypertrabeculation in athlete's heart, Int. J. Cardiol. 181C (2014) 320–322. [2] S. Gati, M. Papadakis, N.D. Papamichael, A. Zaidi, N. Sheikh, M. Reed, R. Sharma, B. Thilaganathan, S. Sharma, Reversible de novo left ventricular trabeculations in pregnant women: implications for the diagnosis of left ventricular non-compaction in low risk populations, Circulation 130 (2014) 475–483. [3] J. Finsterer, C. Stöllberger, B. Schubert, Acquired left ventricular noncompaction as a cardiac manifestation of neuromuscular disorders, Scand. Cardiovasc. J. 42 (2008) 25–30. [4] L. García-Díaz, F. Coserria, G. Antiñolo, Hypertrophic cardiomyopathy due to mitochondrial disease: prenatal diagnosis, management, and outcome, Case Rep. Obstet. Gynecol. 472356 (2013)http://dx.doi.org/10.1155/2013/472356. [5] S. Gati, M. Papadakis, N. Van Niekerk, M. Reed, T. Yeghen, S. Sharma, Increased left ventricular trabeculation in individuals with sickle cell anaemia: physiology or pathology? Int. J. Cardiol. 168 (2013) 1658–1660.
485
[6] I. Ahmet, H.J. Tae, M. Brines, A. Cerami, E.G. Lakatta, M.I. Talan, Chronic administration of small nonerythropoietic peptide sequence of erythropoietin effectively ameliorates the progression of postmyocardial infarction-dilated cardiomyopathy, J. Pharmacol. Exp. Ther. 345 (2013) 446–456. [7] I. Esen, I. Cetin, F. Demirel, F. Ekici, The effect of recombinant human growth hormone therapy on left-ventricular chamber size and function in children with growth hormone deficiency, Pediatr. Cardiol. 34 (2013) 1854–1859. [8] T.K. Chin, J.K. Perloff, R.G. Williams, K. Jue, R. Mohrmann, Isolated noncompaction of left ventricular myocardium. A study of eight cases, Circulation 82 (1990) 507–513. [9] R. Jenni, E. Oechslin, J. Schneider, C. Attenhofer Jost, P.A. Kaufmann, Echocardiographic and pathoanatomical characteristics of isolated left ventricular noncompaction: a step towards classification as a distinct cardiomyopathy, Heart 2001 (2001) 666–671. [10] C. Stöllberger, J. Finsterer, G. Blazek, Left ventricular hypertrabeculation/ noncompaction and association with additional cardiac abnormalities and neuromuscular disorders, Am. J. Cardiol. 90 (2002) 899–902.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Does professional athlete training cause acquired left ventricular hypertrabeculation/noncompaction? C. Stöllberger ⁎, J. Finsterer Krankenanstalt Rudolfstiftung, Juchgasse 25, A-1030 Wien, Austria
a r t i c l e
i n f o
Article history: Received 14 January 2015 Accepted 26 February 2015 Available online 27 February 2015 Keywords: 3-Dimensional Cardiomyopathy Echocardiography Exercise training Noncompaction cardiomyopathy Speckle tracking echocardiography
With interest we read the article by D'Ascenzi et al. about exerciseinduced left ventricular hypertrabeculation/noncompaction (LVHT) in an athlete's heart [1]. They report a case series of four professional basketball players in whom during an intensive training program of 5 months left ventricular trabecular pattern increased. In one athlete who underwent echocardiography after 1 month of detraining, the hypertrabeculation decreased resembling the pattern observed one year before. Additionally, the athletes showed electrocardiographic changes with T wave inversion. These findings, like the recently published findings in pregnant women, challenge the hypothesis that LVHT is due to a disturbed compaction process of the embryonic heart [2]. We have the following questions and concerns: It remains unclear whether LVHT was present already before starting the training. It would be interesting if LVHT was congenital or acquired. Were there any indications from the family history that LVHT in these four athletes was familial and thus congenital? Did any of the four undergo echocardiography before starting with sport activities? Was the family history in any of the four positive for sudden cardiac death, syncope, stroke, embolism, or heart failure? Acquired LVHT, however, has been also reported from non-athletes and non-pregnant patients of whom the majority suffered from a neuromuscular disorder (NMD) [3,4]. If LVHT was already present before study entry without prior exercise, the four athletes should be
investigated for NMDs or chromosomal defects. Did any of the four have elevated creatine-kinase or a family history positive for muscle disease? Furthermore, it would be interesting to know if the athletes were screened for sickle cell anemia, a disorder more prevalent in Africans than Caucasians and also associated with LVHT [5]. Did the athletes have a history or actual intake of any drugs including drugs for “doping” like erythropoietin or somatotropin which are also known to induce muscular growth [6,7]? Did the authors also investigate athletes who did not present with LVHT before onset of the training? In athletes without LVHT before starting the training did LVHT develop during this physical activity? Does LVHT increase only in athletes with pre-existing LVHT or does it also develop in athletes without pre-exercise LVHT? The authors differentiate between noncompaction and hypertrabeculation. Both terms describe the same phenomenon and should be used synonymously. There are different echocardiographic criteria for LVHT in the literature [8–10]. It would be interesting to know according to which echocardiographic criteria was LVHT diagnosed, if interobserver agreement was investigated and if the observers were blinded to the training status of the athletes. It is indicated that in the beginning of the training program, the athletes showed left ventricular trabeculations. Did these trabeculations only increase in thickness during the training or did new trabeculations grow? Was there only an increase in the thickness of the trabeculated layer of the myocardium or also a decrease in thickness of the compacted layer? Was there also an increase in the echogenicity of the endocardium which made the trabeculae better visible — this impression is suggested by Fig. 2. How do the authors explain that left ventricular mass increased from 185 to 288 and 233 g to 376 g in two athletes but only by 13 and 30 g in the two others? Electrocardiographic changes are reported, however the ECGs of only two athletes are shown. Did all four athletes develop negative T waves during training? Did these ECG-changes regress after detraining? In conclusion, these very interesting findings should be supported by studying more extensively a larger group of athletes with various ethnicity in different stages of training to assess the etiology and pathogenesis of LVHT and a group of athletes without LVHT at onset of the training. Conflict of interest
⁎ Corresponding author at: Steingasse 31/18, A-1030 Wien, Austria. E-mail addresses: [email protected], fifi[email protected] (C. Stöllberger).
http://dx.doi.org/10.1016/j.ijcard.2015.02.102 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
The authors report no relationships that could be construed as a conflict of interest.
C. Stöllberger, J. Finsterer / International Journal of Cardiology 184 (2015) 484–485
References [1] F. D'Ascenzi, A. Pelliccia, B.M. Natali, M. Bonifazi, S. Mondillo, Exercise-induced leftventricular hypertrabeculation in athlete's heart, Int. J. Cardiol. 181C (2014) 320–322. [2] S. Gati, M. Papadakis, N.D. Papamichael, A. Zaidi, N. Sheikh, M. Reed, R. Sharma, B. Thilaganathan, S. Sharma, Reversible de novo left ventricular trabeculations in pregnant women: implications for the diagnosis of left ventricular non-compaction in low risk populations, Circulation 130 (2014) 475–483. [3] J. Finsterer, C. Stöllberger, B. Schubert, Acquired left ventricular noncompaction as a cardiac manifestation of neuromuscular disorders, Scand. Cardiovasc. J. 42 (2008) 25–30. [4] L. García-Díaz, F. Coserria, G. Antiñolo, Hypertrophic cardiomyopathy due to mitochondrial disease: prenatal diagnosis, management, and outcome, Case Rep. Obstet. Gynecol. 472356 (2013)http://dx.doi.org/10.1155/2013/472356. [5] S. Gati, M. Papadakis, N. Van Niekerk, M. Reed, T. Yeghen, S. Sharma, Increased left ventricular trabeculation in individuals with sickle cell anaemia: physiology or pathology? Int. J. Cardiol. 168 (2013) 1658–1660.
485
[6] I. Ahmet, H.J. Tae, M. Brines, A. Cerami, E.G. Lakatta, M.I. Talan, Chronic administration of small nonerythropoietic peptide sequence of erythropoietin effectively ameliorates the progression of postmyocardial infarction-dilated cardiomyopathy, J. Pharmacol. Exp. Ther. 345 (2013) 446–456. [7] I. Esen, I. Cetin, F. Demirel, F. Ekici, The effect of recombinant human growth hormone therapy on left-ventricular chamber size and function in children with growth hormone deficiency, Pediatr. Cardiol. 34 (2013) 1854–1859. [8] T.K. Chin, J.K. Perloff, R.G. Williams, K. Jue, R. Mohrmann, Isolated noncompaction of left ventricular myocardium. A study of eight cases, Circulation 82 (1990) 507–513. [9] R. Jenni, E. Oechslin, J. Schneider, C. Attenhofer Jost, P.A. Kaufmann, Echocardiographic and pathoanatomical characteristics of isolated left ventricular noncompaction: a step towards classification as a distinct cardiomyopathy, Heart 2001 (2001) 666–671. [10] C. Stöllberger, J. Finsterer, G. Blazek, Left ventricular hypertrabeculation/ noncompaction and association with additional cardiac abnormalities and neuromuscular disorders, Am. J. Cardiol. 90 (2002) 899–902.