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European Journal of Heart Failure 2006 8(8):826-831; doi:10.1016/j.ejheart.2006.02.014
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© 2006 European Society of Cardiology

Familial occurrence of isolated non-compaction cardiomyopathy

Anouk Lorsheyda,*, Maarten-Jan M. Cramera, Birgitta K. Velthuisb, Evert-Jan P. Vonkenb, Jasper van der Smagtc, Peter van Tintelend and Richard N.W. Hauera

a Department of Cardiology, Heart Lung Center Utrecht, University Medical Center Heidelberglaan 100, P.O. Box 85500, 3508 GA Utrecht, The Netherlands
b Department of Radiology, University Medical Center Utrecht, The Netherlands
c Department of Clinical Genetics, University Medical Center Utrecht, The Netherlands
d Department of Clinical Genetics, University Medical Center Groningen, the Netherlands

* Corresponding author. Tel.: +31 30 2506176; fax: +31 30 2505471. E-mail address: A.Lorsheyd{at}hli.azu.nl


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Background and aims: Isolated left ventricular non-compaction cardiomyopathy (LVNC) may have an autosomal dominant or X-linked recessive inheritance. We focus on the familial occurrence of LVNC after misdiagnosing this disorder in symptomatic patients in two families. After identification of the index patient we studied the families more intensively in order to unmask affected family members.

Methods and results: LVNC was defined as an end-systolic non-compacted subendocardial layer of the left ventricular wall of at least twice the thickness of the subepicardial compacted layer (2D echocardiogram and MRI). This was studied in 13 patients in 2 families (A and B). LVNC was found in 3 out of 11 patients in family A. The grandmother was asymptomatic. Her daughter suffered from recurrent syncope and heart failure. Her daughter received a cardiac transplant because of progressive heart failure at the age of 14 years. In family B, LVNC was found in 2 patients, a father and his son and presumed in a brother and a sister of the father who died suddenly at the age of 17 and 21 years, respectively.

Conclusions: In all symptomatic patients, proven LVNC was previously misdiagnosed as hypertrophic or dilated cardiomyopathy. Misdiagnosis may lead to insufficient treatment and will misdirect targeted molecular genetic analysis. LVNC was identified in seven patients in two families. Family screening may unmask affected family members for primary prevention including anti-coagulation and ICD-therapy.

Key Words: Cardiomyopathy • Non-compaction • Familial

Received August 30, 2005; Revised January 13, 2006; Accepted February 28, 2006


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Isolated left ventricular non-compaction cardiomyopathy (LVNC) is a relatively new recognised type of cardiomyopathy with unknown prevalence characterized by an excessive prominent trabecular meshwork and deep intertrabecular recesses. These alterations are due to an intrauterine arrest of compaction of the myocardial fibers in the absence of any coexisting congenital lesions [1-9]. This pattern has been described before as persistent intramyocardial sinusoids in association with congenital heart disease [3,4,10]. The isolated form, however, is not associated with other cardiac anomalies.

The diagnosis can be made by echocardiography or magnetic resonance imaging (MRI) [3,4,6,11,12]. The typical finding is a two-layered structure, with a compacted thin subepicardial layer and a much thicker non-compacted subendocardial layer of trabecularization with deep endomyocardial recesses. On echocardiography, an end-systolic ratio of >2 of the thickness of the non-compacted layer compared to the thickness of the compacted layer (NC/C) is used for the diagnosis of LVNC [4,6]. With Colour Doppler, flow can be visualised in the intertrabecular recesses. Most commonly, the left ventricular mid-lateral, apical and inferior wall segments are involved.

The most common clinical manifestations are heart failure, thrombo-embolic events and ventricular arrhythmias. Mortality and morbidity rates are high. Treatment includes heart failure therapy, anti-coagulation, an implantable cardioverter defibrillator (ICD) or heart transplantation [1-9,13-15].

We focus on the familial occurrence of LVNC after misdiagnosing this disorder in symptomatic patients in two families. After identification of the index patient, we studied the families more extensively in order to unmask affected family members.

The familial character of LVNC has been recognized and probably up to 44% of patients do have affected family members [3,14,16]. The pattern of inheritance is generally autosomal dominant. However X-linked recessive inheritance has been recognized. A mutation in the gene encoding P-dystrobrevin (a protein of the dystrophin-associated glycoprotein complex) on chromosome 18q12.1-q12.2 has been described in a single Japanese family [17]. Five out of six affected family members had a congenital heart defect in addition to LVNC. In the X-linked recessive form, mutations in the G4.5 gene encoding tafazzin, on chromosome Xq28 have been identified, but mutations in this gene play only a minor role in the pathogenesis of LVNC as was recently shown by Kenton et al. [18]. Recently, a mutation in the lamin A/C gene has been reported in a patient with LVNC with affected family members having dilated cardiomyopathy. Mutations in Cypher/ZASP have been reported in patients with either dilated cardiomyopathy or LVNC; however, the extent of the contribution of this gene to autosomal dominant LVNC remains to be determined [19]. The transcription factor NKX2.5 has been implicated in LVNC but proof that mutations in this gene can actually cause LVNC in humans is still lacking. In both families, the patients were screened for lamin A/C gene, P-dystrobrevin and G4.5 mutation.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusion
 References
 
After identification of the index patient, a familial screening program was performed after a genetic counselling procedure. Family members underwent assessment of medical history, physical examination, 12-lead electrocardiography and 2D echocardiography. In addition, MRI was performed in 4 patients, in whom the diagnosis LVNC was already obtained by echocardiography. The diagnosis LVNC was established if the end-systolic non-compacted subendocardial layer of the left ventricular wall was at least twice the thickness of the subepicardial compacted layer [3,4,6,11,12]. In total, we studied 11 patients from family A and 3 from family B.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusion
 References
 
The index patient of family A (II-2 Fig. 1) is a 55-year-old woman who was admitted to the Arrhythmia Unit of the University Medical Center Utrecht because of recurrent syncopal episodes. She had a history of paroxysmal atrial fibrillation associated with signs of heart failure. Echocardiography 2 years before had shown findings described as hypertrophic cardiomyopathy with left ventricular (LV) dilatation. For a year, she suffered from frequent syncopal attacks occurring during exercise, without any prodromic signs. She always recovered spontaneously after such events. On admission she appeared to be dyspnoeic on exertion (NYHA functional class III) but denied progression during the last year. Remarkably, there was a family history of dilated cardiomyopathy; her 14-year-old daughter (III-2 Fig. 1.) had a heart transplant because of heart failure.


Figure 1
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  		Fig. 1 Family A. The black symbols indicate the affected family members, and the white symbols indicate the non-affected family members. The arrow indicates the index patient. II:1 has not been screened.

 
The chest X-ray showed an enlarged size of the heart with enlarged left atrium and left ventricle (cor/thorax ratio 17/32cm.).

Echocardiography showed heavy trabecularization and deep invaginations of the left ventricular apex and lateral wall suggesting LVNC. The LV was dilated with an end-diastolic diameter of 66mm. On M-mode, the parasternal long axis of the left atrium measured 64mm. The systolic LV function was severely depressed with signs of augmented left ventricular end-diastolic pressure and a moderate mitral incompetence. The maximal thickness of the non-compacted and compacted myocardium could not be established accurately, and therefore, MRI was carried out. In the LV apex, the non-compacted myocardium measured 28mm vs. 4mm of the compacted myocardial layer. These findings confirmed LVNC (Fig. 2). During exercise testing, no signs of ischaemia were seen. Several premature ventricular complexes occurred. An electrophysiologic study, while on digoxin and amiodarone, revealed severe infranodal conduction disturbance (HV interval 85ms). Ventricular tachyarrhythmias were not inducible during programmed electrical stimulation. Because of the presumed high risk for sudden cardiac death, she received an ICD. She was already on anticoagulant therapy because of paroxysmal atrial fibrillation.


Figure 2
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  		Fig. 2 MRI of the index patient in family A (II-2). In the LV apex, the non-compacted myocardium measures 28mm vs. 4mm of the compacted myocardial layer. The lateral wall is involved as well.

 
The daughter of the index patient (III-2 Fig. 1) was seen annually by the heart transplantation team. She was diagnosed with dilated cardiomyopathy at the age of 7years. At the age of 14, the ECG showed sinus rhythm with an undetermined axis and signs of left and right atrial dilation. Furthermore, there was a prominent R-wave in right precordial leads and left ventricular hypertrophy (LVH). Despite diuretic therapy and ACE inhibition symptoms of congestive heart failure developed. Echocardiography revealed a severely dilated left atrium and left ventricle with wall motion abnormalities. The right ventricle was also dilated. There was severe mitral and tricuspid incompetence. On the age of 14years, she received a heart transplant. Revision of the echocardiogram before the heart transplantation meets the criteria for LVNC.

The mother of the index patient (I-2 Fig. 1), a 79-year-old lady, had a history of angina pectoris. She had episodes of dizziness and sudden acceleration of the heart rate.

On echocardiography, LV systolic function was depressed with dilation of the left atrium. The LV apex showed crypts with augmentation of the wall thickness. MRI of the heart confirmed the suspicion on LVNC; the non-compacted myocardium of the apex measured 20 mm to 3.5 mm of the compacted layer. The LV wall showed remarkable trabecularization from apex to basolateral (Fig. 3). Patient was diagnosed to have LVNC and started with aspirin and diuretic therapy. Holter monitoring showed non-sustained atrial tachycardia. No ventricular arrhythmias were recorded.


Figure 3
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  		Fig. 3 MRI of the mother of the index patient (I-2) in family A. The non-compacted myocardium of the apex measures 20-3.5mm of the compacted layer. The LV wall showed remarkable trabecularization from apex to basolateral.

 
The father, four sisters, two brothers and the first-born daughter of the index patient were screened but they showed no evidence of LVNC.

In family B, the index patient (III-1 Fig. 4) was a 34-year-old male. Because his father was known to have hypertrophic cardiomyopathy and a positive family history for sudden cardiac death at young age, he had been screened 15 years before. Since his ECG showed criteria for left ventricular hypertrophy the diagnosis of hypertrophic cardiomyopathy seemed likely as well. The echocardiogram at that time was considered normal. At the age of 21years, a syncopal attack occurred followed by treatment with amiodarone. Echocardiography at the age of 26 revealed a dilated left ventricle and a slightly depressed LV systolic function but no ventricular hypertrophy. Echocardiography was repeated at the age of 34years. Trabecularization was remarkable in the LV apex. MRI showed a non-compacted layer of 17.4mm in contrast to 4.1mm of the compacted layer. The diagnosis of hypertrophic cardiomyopathy was rejected in favour of LVNC (Fig. 5). Because of the risk for thrombo-embolic complications, he was put on anticoagulant therapy. Amiodarone was continued.


Figure 4
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  		Fig. 4 Family B. Black symbols indicate proven isolated left ventricular non-compaction cardiomyopathy, white symbols indicate non-affected family members. The arrow indicates the index patient. I:1, I:2, II:1 and II:5 have not been screened. White symbols with a diagonal line indicate deceased family members. SCD=sudden cardiac death.

 


Figure 5
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  		Fig. 5 MRI of the index patient in family B (III-1) shows in the apical area a non-compacted layer of 17.4mm in contrast to 4.1mm of the compacted layer.

 
The father of this patient (II-2 Fig. 4) was diagnosed as having hypertrophic cardiomyopathy at the age of 17years after being assessed because of recurrent syncope during exercise. The first episode was at the age of 15years during a running contest. The second and third syncope also occurred during exercise, after a short run. His brother died suddenly at the age of 17years during cycling, and a sister died at the age of 21years during a running contest. Echocardiography showed an asymmetrical septal hypertrophy without obstruction. He had been on beta blockers since the age of 37years. He suffered a fourth syncope at the age of 42years again during jogging. Electrocardiography showed criteria for left ventricular hypertrophy. Echocardiography revealed asymmetrical septal hypertrophy without obstruction. Holter monitoring showed no ventricular arrhythmias. During electrophysiologic study, a sustained monomorphic ventricular tachycardia with right bundle branch block morphology could be induced by programmed electrical stimulation in the right ventricular apex, which deteriorated into ventricular fibrillation. Therapy with amiodarone was started. No syncopal attacks have occurred since. At the age of 58years, he presented with a decline in exercise tolerance. He had recurrent atrial flutter treated by electrical cardioversion. Echocardiography showed a non-obstructive hypertrophic cardiomyopathy with an increased left ventricular diastolic diameter (65mm) and enlarged left atrium (66mm). The left ventricular ejection fraction was severely reduced to 25%. After establishing LVNC in his son, all echocardiographic studies were revised. Again, LVNC was found. MRI confirmed this by measuring a 4.5-mm-thick compact myocardium vs. a 10-mm-thick non-compacted apicolateral layer (Fig. 6). The patient started oral anticoagulant therapy. Screening of the sister of the index patient showed no evidence of LVNC. The diagnosis of LVNC was presumed in the brother and sister of the father since they died suddenly at the age of 17 and 21years, respectively. The results are summarized in Table 1.


Figure 6
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  		Fig. 6 MRI confirms the diagnosis LVNC in the father of the index patient (II-2) by measuring a 4.5-mm-thick compact myocardium vs. a 10-mm-thick non-compacted apicolateral layer.

 


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  		Table 1 Characteristics and complications in patients with LVNC

 
In the index of family A, the lamin A/C gene was evaluated with denaturating gradient gel electrophoresis. In both families, the patients were screened for P-dystrobrevin and G4.5 mutation. No mutations were found. In both families, inheritance was most compatible with an autosomal dominant pattern. No evidence of neuromuscular disease or facial dysmorphism have been observed.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusion
 References
 
LVNC is a relatively recently recognised type of cardiomyopathy with potential life-threatening complications such as heart failure, ventricular arrhythmias and thrombo-embolic events. As demonstrated in this report, there is a danger of initial misdiagnosis, which could lead to insufficient treatment, hamper early diagnosis in relatives and misdirect targeted molecular genetic analysis [20,21].

In 3 out of 11 examined persons in family A and in two out of three examined members of family B, the diagnosis of LVNC was established. LVNC was presumed in two first-degree relatives of family B with sudden death at young age.

Our study shows that screening of family members of patients with LVNC is important. After identification of both index patients, the diagnosis was established in three other family members with important clinical consequences. Screening may unmask affected family members for primary prevention including anti-coagulation and ICD-therapy.

The diagnosis LVNC can be established by echocardiography. An end-systolic non-compacted endocardial layer of at least twice the thickness of the compacted epicardial layer is considered for proper diagnosis of LVNC [4,6]. Echocardiography, however, poses inherent problems in determining the non-compacted layer, especially in the LV apex, the most commonly non-compacted area. In our study, the diagnosis of LVNC was confirmed after additional MRI was performed. Recently, Petersen et al. published a study to test the diagnostic accuracy of cardiovascular magnetic imaging (CMR) in LVNC. In contrast to echocardiography, a ratio of non-compacted to compacted layer (NC/C) of >2.3 in diastole was considered to distinguish for pathological non-compaction. In diastole, the pattern of trabecularization can be measured more easily [22].

The clinical characteristics of LVNC have been extensively described by Oechslin et al. [4] in a report of 34 patients with a heterogenic phenotype and by Ichida et al., who conducted a nation wide survey of Japanese children in order to clarify the clinical features of LVNC [3]. In contrast to earlier reports, most patients in Ichida's study were asymptomatic at initial presentation and had a protracted clinical course with gradual depression of left ventricular function, no systemic embolism and rarely, episodes of ventricular tachycardia.

In our study population, the clinical manifestations of LVNC also varied. In family A, most patients presented themselves with signs and symptoms of heart failure (II-2 and III-2), which led to heart transplantation in the 14-year-old daughter because of progression of her disease. In family B, both patients presented with syncope probably as a result of ventricular arrhythmias, which was presumably also the cause of death in the two relatives who died at a young age. Thrombo-embolic events did not occur. During a mean follow-up of 35months, no deaths occurred.

A remarkable finding was the degree of trabecularization in both families. In family A, there was a fine network of non-compacted myocardium vs. a coarser network of non-compacted myocardium in family B. To our knowledge, this difference in aspect of trabecularization of the LV in LVNC has not been described before. It probably reflects the heterogeneous nature of this condition.

Recently, results of family screening were published by Ross et al. [23]. They found in 8 of 32 asymptomatic relatives, echocardiographic abnormalities including LVNC, LVNC with impaired LV systolic function and LV enlargement without LVNC. In contrast to our study, they conclude that LVNC has a better prognosis than previously thought and suggest that LVNC could be classified as a sub-type or variant of idiopathic DCM rather than a distinct cardiomyopathy. We believe, however, that LVNC is a cardiomyopathy in which sudden cardiac death and heart failure can occur at a young age. The impaired left ventricular function and dilation of the left ventricle can be seen as the preliminary stage of heart failure. Awareness of this condition is important because a fulminant course is possible.

Familial forms of LVNC have been described before [2-4,6], which has led to extensive genetic analysis [3,16-19,22-24]. The families in this report are consistent with autosomal dominant inheritance with variable expression. Many different genes have been implicated in this disorder, but their role is either limited or remains to be evaluated.

Unfortunately, in our study, no mutations were found in the P-dystrobrevin and lamin A/C genes. Given the limited contribution of molecular genetic diagnosis in LVNC, at this point, family studies will have to rely heavily on cardiologic evaluation.


   5. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusion
References
 
LVNC is often misdiagnosed as hypertrophic or dilated cardiomyopathy probably because of a lack of knowledge of this uncommon disease. LVNC was identified in 7 patients in 2 families, of which 5 were proven and 2 presumed. Misdiagnosis may lead to insufficient treatment and will misdirect targeted molecular genetic analysis. Life-threatening complications and sudden death can occur at young age, but asymptomatic survival to old age is possible. Family screening may identify affected family members for primary prevention including anti-coagulation and ICD-therapy.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 

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