Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy characterized by prominent left ventricular (LV) trabeculae, deep intertrabecular recesses, and the thin compacted layer. The disease is potentially associated with sudden cardiac death due to LV dysfunction and ventricular arrhythmias. The presence of accessory pathway and Wolff-Parkinson-White syndrome is particularly rare in adults. Here we describe the rare association of LVNC and ventricular pre-excitation in an 18-year-old female with neonatal hypoxic brain injury. 

Keywords: Wolff-Parkinson-White syndrome; pre-excitation syndromes; isolated noncompaction of the ventricular myocardiu

Diego Chemello

Fernando Pivatto Júnior

Clinical & Biomedical Research

Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy characterized by prominent left ventricular (LV) trabeculae, deep intertrabecular recesses, and the thin compacted layer. The disease is potentially associated with sudden cardiac death due to LV dysfunction and ventricular arrhythmias. The presence of accessory pathway and Wolff-Parkinson-White syndrome is particularly rare in adults. Here we describe the rare association of LVNC and ventricular pre-excitation in an 18-year-old female with neonatal hypoxic brain injury. Keywords: Wolff-Parkinson-White syndrome; pre-excitation syndromes; isolated noncompaction of the ventricular myocardiu

Chemello, Diego

Pivatto Júnior, Fernando

LAReferencia - Red Federada de Repositorios Institucionales de Publicaciones Científicas Latinoamericanas

Left ventricular noncompactation and pre-excitation: an unusual finding in adults

Directory of Open Access Journals

Archives of the Faculty of Veterinary Medicine UFRGS

Case Reporthttp://seer.ufrgs.br/hcpaISSN 2357-9730358Clin Biomed Res. 2017;37(4):358-361http://dx.doi.org/10.4322/2357-9730.76695Left ventricuLar noncompaction and pre-excitation: an unusuaL finding in aduLtsDiego Chemello1, Fernando Pivatto Júnior21 Department of Clinical Medicine, Universidade Federal de Santa Maria (UFSM). Santa Maria, RS, Brazil.2 Internal Medicine Division, Hospital de Clínicas de Porto Alegre (HCPA). Porto Alegre, RS, Brazil. Corresponding author: Fernando Pivatto Júnior fpivatto@gmail.com Hospital de Clínicas de Porto Alegre (HCPA) Rua Ramiro Barcelos, 2350, sala 700. 90035-903, Porto Alegre, RS, Brazil.ABSTRACTLeft ventricular noncompaction (LVNC) is a rare form of cardiomyopathy characterized by prominent left ventricular (LV) trabeculae, deep intertrabecular recesses, and the thin compacted layer. The disease is potentially associated with sudden cardiac death due to LV dysfunction and ventricular arrhythmias. The presence of accessory pathway and Wolff-Parkinson-White syndrome is particularly rare in adults. Here we describe the rare association of LVNC and ventricular pre-excitation in an 18-year-old female with neonatal hypoxic brain injury.Keywords: Wolff-Parkinson-White syndrome; pre-excitation syndromes; isolated noncompaction of the ventricular myocardiumLeft ventricular noncompaction (LVNC) is a rare form of cardiomyopathy characterized by prominent left ventricular (LV) trabeculae, deep intertrabecular recesses, and the thin compacted (C) layer1. The diagnosis is usually performed by echocardiography or magnetic resonance imaging (MRI). The disease is potentially associated with sudden cardiac death (SCD) due to LV dysfunction and ventricular arrhythmias. The presence of accessory pathway and Wolff-Parkinson-White (WPW) syndrome is particularly rare in adults2,3. Here we describe the rare association of LVNC and ventricular pre-excitation in an 18-year-old female with neonatal hypoxic brain injury. There were no arrhythmias or WPW syndrome. Clinical follow-up was performed without complications.CASE PRESENTATIONAn 18-year-old female with severe neonatal hypoxic brain injury and chronic cognitive and motor disabilities was referred for outpatient cardiac consultation for preoperative evaluation. She presented severe scoliosis and motor disabilities requiring orthopedic surgery for spine stabilization. Her cardiac medical history was uneventful. Despite limited functional status, her parents denied any warning symptoms like chest pain, shortness of breath, palpitations, or syncope. Physical examination revealed good peripheral pulses, no peripheral edema, blood pressure 102/60 mmHg, and heart rate of 96 bpm. Cardiac auscultation showed regular rhythm with no murmurs or gallops. There were no signs of cardiomegaly.A 12-lead electrocardiography (ECG) revealed ventricular pre-excitation with right-bundle branch block morphology compatible with a left wall accessory-pathway (Figure 1). A 24-hour Holter did not record arrhythmias. A transthoracic echocardiogram was also performed. Despite limited acoustic window, the left ventricular ejection fraction (LVEF) was normal. However, there were signs of prominent trabeculation and deep recesses that communicate with the left ventricular cavity (Figure 2). These signs were compatible with isolated LVNC.An electrophysiological study (EPS) was considered, but deferred by patient’s family. The patient underwent surgical procedure under cardiac monitoring. No arrhythmias or cardiovascular complications were reported. After 1 year of clinical follow-up, LVEF remained unaltered and the patient http://seer.ufrgs.br/hcpa Clin Biomed Res 2017;37(4) 359Left ventricular noncompaction and pre-excitationFigure 2: Transthoracic echocardiogram obtained in parasternal short axis view showing signs of left ventricular noncompaction, characterized by a relation of noncompacted endocardial to compacted epicardial layer above 2 during end systole (A). The hipertrabeculation is also observed in left ventricular apex (B, red arrow).Figure 1:  The 12-lead electrocardiogram showing ventricular pre-excitation (short PR interval and delta wave). There is a right-bundle branch block pattern, negative delta wave in aVL and isoelectric delta waves in DI and positive delta waves in DII, DIII, aVF and V6.http://seer.ufrgs.br/hcpaClin Biomed Res 2017;37(4)360Chemello, Pivatto Júnior did not develop symptoms or clinical arrhythmias. Family screening (mother and sister) for cardiac abnormalities was negative.DISCUSSIONLVNC or “spongy myocardium” has been recognized as a distinct form of cardiomyopathy. It is thought to result from an arrest of the compaction process during the second month of embryological development, resulting in abnormal left ventricular myocardial architecture4. LVNC occurs in infants (0.81 cases/100,000 per year), children (0.12 cases/100,000 per year) and adults (prevalence 0.014%)1. The disease is defined by three markers: prominent LV trabeculae, deep intertrabecular recesses, and a thin C layer1. The myocardium will have an increased noncompacted (NC) endomyocardial layer depth compared to the C epicardial layer.There is no consensus on diagnostic criteria. Two-dimensional echocardiography is the most common and useful tool for LVNC diagnosis. Jenni et al. proposed criteria based on an end systolic ratio of NC to C layers above 25. More recently, cardiac magnetic resonance (CMR) has been considered a useful resource that may help to accurately describe and diagnose LVNC and distinguish true disease from the prominent hypertrabeculation that can be seen in normal hearts and individuals. A NC/C ratio > 2.3 measured at the end of diastole is considered the cutoff for proper diagnosis1. Three-dimensional echocardiography may play a role in the future, although its role currently remains anecdotal5. Despite advances in imaging technologies, controversies persist and a “gold standard” for the diagnosis of LVNC continues to be lacking as no imaging or pathology signature has yet been agreed6.The association of WPW with LVNC is well recognized. Previous reports include WPW associated with isolated LVNC3,7,8; WPW associated with LVNC and Fabry disease9 or hypertrophic cardiomyopathy10 was also reported. During embryogenesis there is direct continuity of the atrial and ventricular myocardium, which is ultimately disrupted as the annulus fibrosus develops. Defects in the annulus fibrosus are thought to account for the formation of accessory pathways. In ventricular noncompaction, the hypothesized arrest in development characterized by persistence of trabeculations might account for the persistence of myocardial channels between atrium and ventricle, allowing for the development of accessory pathways1.Electrocardiographic changes in LVNC most commonly reported in the literature are left bundle branch block, right bundle branch block, left anterior fascicular block, repolarization abnormalities, atrial fibrillation, and pre-excitation11. Stöllberger and Finsterer2 have analyzed the arrhythmias associated with LVNC and found a different prevalence between children and adults. In adults, the most frequent arrhythmias are ventricular tachycardia, atrial fibrillation, QT prolongation, and atrioventricular block. Ventricular pre-excitation was more frequently reported in children than in adults. In different series, the occurrence of ventricular pre-excitation is estimated in 15% in pediatric series but is rarely observed in adults. Most of ventricular pre-excitation cases associated with LVNC had signs and symptoms that corroborate a clinically relevant accessory pathway (WPW syndrome).In the present case, the diagnosis of LVNC was confirmed by transthoracic echocardiography. Despite limited acoustic window, the NC/C ratio was measured at 2.75 in the inferolateral segment at mid short axis view (Figure 2A). Additional images also showed areas of hypertrabeculation at the apex (Figure 2B). Despite recent concerns about overdiagnosis, LVNC is the main diagnosis12. The ECG also confirmed the presence of ventricular pre-excitation. The main algorithms for accessory pathway location supports a location around the mitral annulus. Despite indication for EPS for precise pathway location and risk stratification, patient´s clinical condition was determinant for a conservative approach.The present case highlights an unusual finding of LVNC and ventricular pre-excitation in an adult patient. Despite the theoretical risks of arrhythmias and even sudden cardiac death, there is no clear warning signs in the present case. Clinical follow-up is important in such cases.REFERENCES1. Arbustini E, Weidemann F, Hall JL. Left ventricular noncompaction: a distinct cardiomyopathy or a trait shared by different cardiac diseases? J Am Coll Cardiol. 2014;64(17):1840-50. PMid:25443708. http://dx.doi.org/10.1016/j.jacc.2014.08.030. 2. Stöllberger C, Finsterer J. Arrhythmias and left ventricular hypertrabeculation /noncompaction. Curr Pharm Des. 2010;16(26):2880-94. PMid:20632950. http://dx.doi.org/10.2174/138161210793176518. 3. Fichet J, Legras A, Bernard A, Babuty D. Aborted sudden cardiac death revealing isolated noncompaction of the left ventricle in a patient with wolff-Parkinson-white syndrome. Pacing Clin Electrophysiol. http://seer.ufrgs.br/hcpa Clin Biomed Res 2017;37(4) 361Left ventricular noncompaction and pre-excitation2007;30(3):444-7. PMid:17367369. http://dx.doi.org/10.1111/j.1540-8159.2007.00690.x. 4. Chin TK, Perloff JK, Williams RG, Jue K, Mohrmann R. Isolated noncompaction of left ventricular myocardium: a study of eight cases. Circulation. 1990;82(2):507-13. PMid:2372897. http://dx.doi.org/10.1161/01.CIR.82.2.507. 5. Gopalamurugan AB, Kapetanakis S, Monaghan MJ, Murgatroyd F. Left ventricular non-compaction diagnosed by real time three dimensional echocardiography. Heart. 2005;91(10):1274. PMid:16162615. http://dx.doi.org/10.1136/hrt.2005.063602. 6. Dawson DK, McLernon DJ, Raj VJ, Maceira AM, Prasad S, Frenneaux MP, et al. Cardiovascular magnetic resonance determinants of left ventricular noncompaction. Am J Cardiol. 2014;114(3):456-62. PMid:24934759. http://dx.doi.org/10.1016/j.amjcard.2014.05.017. 7. Nihei K, Shinomiya N, Kabayama H, Ikeda C, Hosono T, Aoki T, et al. Wolff-Parkinson-White (WPW) syndrome in isolated noncompaction of the ventricular myocardium (INVM). Circ J. 2004;68(1):82-4. PMid:14695471. http://dx.doi.org/10.1253/circj.68.82. 8. Brembilla-Perrot B, Codreanu A, Marie PY, Beurrier D, Husson JL, Hutin O, et al. Association of Wolff-Parkinson-White syndrome with isolated non-compaction of the left ventricle: a case report. Arch Mal Coeur Vaiss. 2006;99(6):626-8. PMid:16878725.9. Alper AT, Kaya A, Tekkesin Aİ, Öz A. Wolff-Parkinson-White and left ventricular noncompaction in a Fabry patient: a case report. Turk Kardiyol Dern Ars. 2016;44(3):248-50. PMid:27138316.10. Alday L, Moreyra E, Bruno E, Rossi N, Maisuls H. Left ventricular noncompaction associated with hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome. Health. 2010;2(3):200-3. http://dx.doi.org/10.4236/health.2010.23029. 11. Jenni R, Oechslin E, Schneider J, Attenhofer Jost C, Kaufmann PA. Echocardiographic and pathoanatomical characteristics of isolated left ventricular non-compaction: a step towards classification as a distinct cardiomyopathy. Heart. 2001;86(6):666-71. PMid:11711464. http://dx.doi.org/10.1136/heart.86.6.666. 12. Niemann M, Störk S, Weidemann F. Left ventricular noncompaction cardiomyopathy: an overdiagnosed disease. Circulation. 2012;126(16):e240-3. PMid:23071178. http://dx.doi.org/10.1161/CIRCULATIONAHA.112.095059. Received: Sept 25, 2017 Accepted: Oct 04, 2017

English

Em Questao

Case Report
http://seer.ufrgs.br/hcpaISSN 2357-9730358
Clin Biomed Res. 2017;37(4):358-361
http://dx.doi.org/10.4322/2357-9730.76695
Left ventricuLar noncompaction and pre-excitation: 
an unusuaL finding in aduLts
Diego Chemello1, Fernando Pivatto Júnior2
1 Department of Clinical Medicine, 
Universidade Federal de Santa Maria 
(UFSM). Santa Maria, RS, Brazil.
2 Internal Medicine Division, Hospital de 
Clínicas de Porto Alegre (HCPA). Porto 
Alegre, RS, Brazil.
 Corresponding author: 
Fernando Pivatto Júnior 
fpivatto@gmail.com 
Hospital de Clínicas de Porto Alegre 
(HCPA) 
Rua Ramiro Barcelos, 2350, sala 700. 
90035-903, Porto Alegre, RS, Brazil.
ABSTRACT
Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy characterized 
by prominent left ventricular (LV) trabeculae, deep intertrabecular recesses, and the 
thin compacted layer. The disease is potentially associated with sudden cardiac death 
due to LV dysfunction and ventricular arrhythmias. The presence of accessory pathway 
and Wolff-Parkinson-White syndrome is particularly rare in adults. Here we describe 
the rare association of LVNC and ventricular pre-excitation in an 18-year-old female 
with neonatal hypoxic brain injury.
Keywords: Wolff-Parkinson-White syndrome; pre-excitation syndromes; isolated 
noncompaction of the ventricular myocardium
Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy 
characterized by prominent left ventricular (LV) trabeculae, deep intertrabecular 
recesses, and the thin compacted (C) layer1. The diagnosis is usually 
performed by echocardiography or magnetic resonance imaging (MRI). 
The disease is potentially associated with sudden cardiac death (SCD) due 
to LV dysfunction and ventricular arrhythmias. The presence of accessory 
pathway and Wolff-Parkinson-White (WPW) syndrome is particularly rare 
in adults2,3. Here we describe the rare association of LVNC and ventricular 
pre-excitation in an 18-year-old female with neonatal hypoxic brain injury. 
There were no arrhythmias or WPW syndrome. Clinical follow-up was 
performed without complications.
CASE PRESENTATION
An 18-year-old female with severe neonatal hypoxic brain injury and 
chronic cognitive and motor disabilities was referred for outpatient cardiac 
consultation for preoperative evaluation. She presented severe scoliosis 
and motor disabilities requiring orthopedic surgery for spine stabilization. 
Her cardiac medical history was uneventful. Despite limited functional status, 
her parents denied any warning symptoms like chest pain, shortness of breath, 
palpitations, or syncope. Physical examination revealed good peripheral 
pulses, no peripheral edema, blood pressure 102/60 mmHg, and heart rate 
of 96 bpm. Cardiac auscultation showed regular rhythm with no murmurs or 
gallops. There were no signs of cardiomegaly.
A 12-lead electrocardiography (ECG) revealed ventricular pre-excitation 
with right-bundle branch block morphology compatible with a left wall 
accessory-pathway (Figure 1). A 24-hour Holter did not record arrhythmias. 
A transthoracic echocardiogram was also performed. Despite limited acoustic 
window, the left ventricular ejection fraction (LVEF) was normal. However, there 
were signs of prominent trabeculation and deep recesses that communicate 
with the left ventricular cavity (Figure 2). These signs were compatible with 
isolated LVNC.
An electrophysiological study (EPS) was considered, but deferred by 
patient’s family. The patient underwent surgical procedure under cardiac 
monitoring. No arrhythmias or cardiovascular complications were reported. 
After 1 year of clinical follow-up, LVEF remained unaltered and the patient 
http://seer.ufrgs.br/hcpa Clin Biomed Res 2017;37(4) 359
Left ventricular noncompaction and pre-excitation
Figure 2: Transthoracic echocardiogram obtained in parasternal short axis view showing signs of left ventricular 
noncompaction, characterized by a relation of noncompacted endocardial to compacted epicardial layer above 2 during 
end systole (A). The hipertrabeculation is also observed in left ventricular apex (B, red arrow).
Figure 1:  The 12-lead electrocardiogram showing ventricular pre-excitation (short PR interval and delta wave). There 
is a right-bundle branch block pattern, negative delta wave in aVL and isoelectric delta waves in DI and positive delta 
waves in DII, DIII, aVF and V6.
http://seer.ufrgs.br/hcpaClin Biomed Res 2017;37(4)360
Chemello, Pivatto Júnior 
did not develop symptoms or clinical arrhythmias. 
Family screening (mother and sister) for cardiac 
abnormalities was negative.
DISCUSSION
LVNC or “spongy myocardium” has been recognized 
as a distinct form of cardiomyopathy. It is thought to result 
from an arrest of the compaction process during the 
second month of embryological development, resulting 
in abnormal left ventricular myocardial architecture4. 
LVNC occurs in infants (0.81 cases/100,000 per year), 
children (0.12 cases/100,000 per year) and adults 
(prevalence 0.014%)1. The disease is defined by three 
markers: prominent LV trabeculae, deep intertrabecular 
recesses, and a thin C layer1. The myocardium will 
have an increased noncompacted (NC) endomyocardial 
layer depth compared to the C epicardial layer.
There is no consensus on diagnostic criteria. 
Two-dimensional echocardiography is the most common 
and useful tool for LVNC diagnosis. Jenni et al. proposed 
criteria based on an end systolic ratio of NC to C layers 
above 25. More recently, cardiac magnetic resonance 
(CMR) has been considered a useful resource that 
may help to accurately describe and diagnose LVNC 
and distinguish true disease from the prominent 
hypertrabeculation that can be seen in normal hearts 
and individuals. A NC/C ratio > 2.3 measured at the 
end of diastole is considered the cutoff for proper 
diagnosis1. Three-dimensional echocardiography may 
play a role in the future, although its role currently 
remains anecdotal5. Despite advances in imaging 
technologies, controversies persist and a “gold 
standard” for the diagnosis of LVNC continues to 
be lacking as no imaging or pathology signature has 
yet been agreed6.
The association of WPW with LVNC is well 
recognized. Previous reports include WPW associated 
with isolated LVNC3,7,8; WPW associated with LVNC 
and Fabry disease9 or hypertrophic cardiomyopathy10 
was also reported. During embryogenesis there 
is direct continuity of the atrial and ventricular 
myocardium, which is ultimately disrupted as the 
annulus fibrosus develops. Defects in the annulus 
fibrosus are thought to account for the formation of 
accessory pathways. In ventricular noncompaction, 
the hypothesized arrest in development characterized 
by persistence of trabeculations might account for 
the persistence of myocardial channels between 
atrium and ventricle, allowing for the development 
of accessory pathways1.
Electrocardiographic changes in LVNC most 
commonly reported in the literature are left bundle 
branch block, right bundle branch block, left anterior 
fascicular block, repolarization abnormalities, atrial 
fibrillation, and pre-excitation11. Stöllberger and Finsterer2 
have analyzed the arrhythmias associated with LVNC 
and found a different prevalence between children 
and adults. In adults, the most frequent arrhythmias 
are ventricular tachycardia, atrial fibrillation, QT 
prolongation, and atrioventricular block. Ventricular 
pre-excitation was more frequently reported in children 
than in adults. In different series, the occurrence 
of ventricular pre-excitation is estimated in 15% in 
pediatric series but is rarely observed in adults. Most 
of ventricular pre-excitation cases associated with 
LVNC had signs and symptoms that corroborate a 
clinically relevant accessory pathway (WPW syndrome).
In the present case, the diagnosis of LVNC was 
confirmed by transthoracic echocardiography. Despite 
limited acoustic window, the NC/C ratio was measured 
at 2.75 in the inferolateral segment at mid short axis 
view (Figure 2A). Additional images also showed 
areas of hypertrabeculation at the apex (Figure 2B). 
Despite recent concerns about overdiagnosis, LVNC 
is the main diagnosis12. The ECG also confirmed 
the presence of ventricular pre-excitation. The main 
algorithms for accessory pathway location supports 
a location around the mitral annulus. Despite 
indication for EPS for precise pathway location and 
risk stratification, patient´s clinical condition was 
determinant for a conservative approach.
The present case highlights an unusual finding 
of LVNC and ventricular pre-excitation in an adult 
patient. Despite the theoretical risks of arrhythmias 
and even sudden cardiac death, there is no clear 
warning signs in the present case. Clinical follow-up 
is important in such cases.
REFERENCES
1. Arbustini E, Weidemann F, Hall JL. 
Left ventricular noncompaction: a 
distinct cardiomyopathy or a trait 
shared by different cardiac diseases? 
J Am Coll Cardiol. 2014;64(17):1840-
50. PMid:25443708. http://dx.doi.
org/10.1016/j.jacc.2014.08.030. 
2. Stöllberger C, Finsterer J. Arrhythmias 
and left ventricular hypertrabeculation 
/noncompaction. Curr Pharm 
Des. 2010;16(26):2880-94. 
PMid:20632950. http://dx.doi.org/10.2
174/138161210793176518. 
3. Fichet J, Legras A, Bernard A, Babuty 
D. Aborted sudden cardiac death 
revealing isolated noncompaction 
of the left ventricle in a patient with 
wolff-Parkinson-white syndrome. 
Pacing Clin Electrophysiol. 
http://seer.ufrgs.br/hcpa Clin Biomed Res 2017;37(4) 361
Left ventricular noncompaction and pre-excitation
2007;30(3):444-7. PMid:17367369. 
http://dx.doi.org/10.1111/j.1540-
8159.2007.00690.x. 
4. Chin TK, Perloff JK, Williams RG, 
Jue K, Mohrmann R. Isolated 
noncompaction of left ventricular 
myocardium: a study of eight 
cases. Circulation. 1990;82(2):507-
13. PMid:2372897. http://dx.doi.
org/10.1161/01.CIR.82.2.507. 
5. Gopalamurugan AB, Kapetanakis 
S, Monaghan MJ, Murgatroyd F. 
Left ventricular non-compaction 
diagnosed by real time three 
dimensional echocardiography. Heart. 
2005;91(10):1274. PMid:16162615. 
http://dx.doi.org/10.1136/
hrt.2005.063602. 
6. Dawson DK, McLernon DJ, Raj VJ, 
Maceira AM, Prasad S, Frenneaux 
MP, et al. Cardiovascular magnetic 
resonance determinants of left 
ventricular noncompaction. Am 
J Cardiol. 2014;114(3):456-62. 
PMid:24934759. http://dx.doi.
org/10.1016/j.amjcard.2014.05.017. 
7. Nihei K, Shinomiya N, Kabayama H, 
Ikeda C, Hosono T, Aoki T, et al. Wolff-
Parkinson-White (WPW) syndrome 
in isolated noncompaction of the 
ventricular myocardium (INVM). Circ 
J. 2004;68(1):82-4. PMid:14695471. 
http://dx.doi.org/10.1253/circj.68.82. 
8. Brembilla-Perrot B, Codreanu A, 
Marie PY, Beurrier D, Husson JL, 
Hutin O, et al. Association of Wolff-
Parkinson-White syndrome with 
isolated non-compaction of the left 
ventricle: a case report. Arch Mal 
Coeur Vaiss. 2006;99(6):626-8. 
PMid:16878725.
9. Alper AT, Kaya A, Tekkesin Aİ, Öz 
A. Wolff-Parkinson-White and left 
ventricular noncompaction in a 
Fabry patient: a case report. Turk 
Kardiyol Dern Ars. 2016;44(3):248-50. 
PMid:27138316.
10. Alday L, Moreyra E, Bruno E, 
Rossi N, Maisuls H. Left ventricular 
noncompaction associated with 
hypertrophic cardiomyopathy and 
Wolff-Parkinson-White syndrome. 
Health. 2010;2(3):200-3. http://dx.doi.
org/10.4236/health.2010.23029. 
11. Jenni R, Oechslin E, Schneider 
J, Attenhofer Jost C, Kaufmann 
PA. Echocardiographic and 
pathoanatomical characteristics 
of isolated left ventricular non-
compaction: a step towards 
classification as a distinct 
cardiomyopathy. Heart. 
2001;86(6):666-71. PMid:11711464. 
http://dx.doi.org/10.1136/
heart.86.6.666. 
12. Niemann M, Störk S, Weidemann 
F. Left ventricular noncompaction 
cardiomyopathy: an overdiagnosed 
disease. Circulation. 
2012;126(16):e240-3. PMid:23071178. 
http://dx.doi.org/10.1161/
CIRCULATIONAHA.112.095059. 
Received: Sept 25, 2017 
Accepted: Oct 04, 2017


https://seer.ufrgs.br/hcpa/article/download/76695/pdf

Left ventricular noncompactation and pre-excitation: an unusual finding in adults

Abstract

Similar works

Full text

Available Versions

LAReferencia - Red Federada de Repositorios Institucionales de Publicaciones Científicas Latinoamericanas

Directory of Open Access Journals

Archives of the Faculty of Veterinary Medicine UFRGS

Em Questao

Directory of Open Access Journals