Left Ventricular Noncompaction Cardiomyopathy Research Articles

Non-Compaction Cardiomyopathy Presented with Atrial Fibrillation: A Case Report and Literature Review

Left ventricular non-compaction cardiomyopathy (LVNC) is a rare congenital cardiomyopathy characterized by increased trabeculation in one or more segments of the ventricle. LVNC presented with non-specific symptoms and highly variable clinical presentation ranging from asymptomatic to progressive heart failure and recurrent or life-threatening arrhythmias. 54-year-old Black man with a history of hypertension, diabetes and end-stage renal disease presented with one day palpitations and lightheadedness following a dialysis session. He denied any dyspnea or syncope. On examination, blood pressure was 175/91 mmHg with irregular pulse. No murmur, rubs or gallops were appreciated. Laboratory were unremarkable except increased creatinine and mild anemia with normal thyroid function test. Electrocardiogram (ECG) revealed atrial fibrillation with normal ventricular rate. Transthoracic echocardiogram revealed mildly increased left ventricular (LV) wall thickness with prominent trabeculation and ejection fraction of 55-60 percent, a pseudo-normal LV filling pattern, with concomitant abnormal relaxation and increased filling pressure, suggestive of LVNC. The patient was switched to apixaban. Genetic testing was recommended for family members. LVNC is rare congenital cardiomyopathy with non-specific symptoms and should be considered among the possible diagnosis in patients presenting with arrythmia patients. Echocardiographic and cardiac magnetic resonance imaging can be utilized to establish diagnosis.

Rare association of left ventricular non-compaction and hypertrophic cardiomyopathy.

Rare association of left ventricular non-compaction and hypertrophic cardiomyopathy.

Overlapping Phenotype: Left Ventricular non-Compaction and Hypertrophic Cardiomyopathy

Aim To study the clinical course of the mixed phenotype (hypertrophic cardiomyopathy, HCMP, and left ventricular noncompaction, LVNC); to determine its genetic causes; and to evaluate incidence of cardiovascular complications (CVC) during the follow-up period.Material and methods In screening of 286 patients with HCMP, 8 of them (2.8 %; median age, 41.5 years; 4 men and 4 women) from unrelated families were found to have the mixed phenotype (combination of HCMP and LVNC). For their 10 first-degree relatives, the most frequent phenotype was HCMP without LVNC; however, both isolated LVNC and the mixed phenotype were also observed. Criteria for HCMP and LVNC were confirmed by echocardiography and cardiac magnetic resonance imaging Genotyping was performed by high-throughput sequencing NGT using the TruSight Cardio Sequencing Panel kit.Results Probands with the HCMP+LVNC combination compared to first-degree relatives with isolated HCMP and LVNC were characterized by more pronounced left ventricular dysfunction (ejection fraction, 43.57±7.6 and 53.64±6.51 %, respectively; p<0.001), a higher risk of CVC, and a higher incidence of ventricular tachyarrhythmias (7.9 and 2.2 %, respectively; p<0.01). 11 mutations in 5 genes were found in 8 patients with the mixed phenotype. 72.7 % of mutations were in the MYH7 and MYBPC3 genes that encode the heavy chain of β-myosin and myosin-binding protein C, respectively; however, in some cases, replacements in other genes (DTNA, TGFB2) were also found.Conclusion The mixed phenotype (HCMP and LVNC) is associated with more severe clinical course of the disease and unfavorable CVC.

Left Ventricular Noncompaction: Diagnostic Approach, Prognostic Evaluation, and Management Strategies.

Left ventricular noncompaction cardiomyopathy is a heart disease with relevant potential complications including heart failure, life-threatening arrhythmias, and embolic events. In order to prevent adverse outcomes, it is crucial to appropriately recognize and manage this cardiomyopathy. In this paper, we report the main clinical presentations and imaging modalities used for diagnosis, including echocardiography and magnetic resonance imaging. We highlight the role of a comprehensive functional cardiac evaluation and the possible prognostic implications of both systolic and diastolic dysfunction. Furthermore, we summarize clinical factors and imaging findings which have prognostic significance. Finally, we discuss the main management strategies based on phenotypic expressions which are aimed at treating symptoms and preventing complications.

Recreational marathon running does not cause exercise-induced left ventricular hypertrabeculation

BackgroundMarathon running in novices represents a natural experiment of short-term cardiovascular remodeling in response to running training. We examine whether this stimulus can produce exercise-induced left ventricular (LV) trabeculation. MethodsSixty-eight novice marathon runners aged 29.5 ± 3.2 years had indices of LV trabeculation measured by echocardiography and cardiac magnetic resonance imaging 6 months before and 2 weeks after the 2016 London Marathon race, in a prospective longitudinal study. ResultsAfter 17 weeks unsupervised marathon training, indices of LV trabeculation were essentially unchanged. Despite satisfactory inter-observer agreement in most methods of trabeculation measurement, criteria defining abnormally hypertrabeculated cases were discordant with each other. LV hypertrabeculation was a frequent finding in young, healthy individuals with no subject demonstrating clear evidence of a cardiomyopathy. ConclusionTraining for a first marathon does not induce LV trabeculation. It remains unclear whether prolonged, high-dose exercise can create de novo trabeculation or expose concealed trabeculation. Applying cut off values from published LV noncompaction cardiomyopathy criteria to young, healthy individuals risks over-diagnosis.

Desminopathy: Novel Desmin Variants, a New Cardiac Phenotype, and Further Evidence for Secondary Mitochondrial Dysfunction.

Background: The pleomorphic clinical presentation makes the diagnosis of desminopathy difficult. We aimed to describe the prevalence, phenotypic expression, and mitochondrial function of individuals with putative disease-causing desmin (DES) variants identified in patients with an unexplained etiology of cardiomyopathy. Methods: A total of 327 Czech patients underwent whole exome sequencing and detailed phenotyping in probands harboring DES variants. Results: Rare, conserved, and possibly pathogenic DES variants were identified in six (1.8%) probands. Two DES variants previously classified as variants of uncertain significance (p.(K43E), p.(S57L)), one novel DES variant (p.(A210D)), and two known pathogenic DES variants (p.(R406W), p.(R454W)) were associated with characteristic desmin-immunoreactive aggregates in myocardial and/or skeletal biopsy samples. The individual with the novel DES variant p.(Q364H) had a decreased myocardial expression of desmin with absent desmin aggregates in myocardial/skeletal muscle biopsy and presented with familial left ventricular non-compaction cardiomyopathy (LVNC), a relatively novel phenotype associated with desminopathy. An assessment of the mitochondrial function in four probands heterozygous for a disease-causing DES variant confirmed a decreased metabolic capacity of mitochondrial respiratory chain complexes in myocardial/skeletal muscle specimens, which was in case of myocardial succinate respiration more profound than in other cardiomyopathies. Conclusions: The presence of desminopathy should also be considered in individuals with LVNC, and in the differential diagnosis of mitochondrial diseases.

Pediatric Mixed Left Ventricular Non-Compaction and Restrictive Cardiomyopathy Bridged to Heart Transplant with Ventricular Assist

Left ventricular noncompaction cardiomyopathy (LVNC) is a rare form of heritable cardiomyopathy with wide genotypic variability, numerous phenotypic variations, and a wide spectrum of clinical disease from asymptomatic to end stage heart failure. Here, we present a case of a 2-year-old boy who presented to their pediatrician with a cough as a first clinical sign of heart failure, rapidly progressing to severe heart failure. He was found to have mixed LVNC with a restrictive phenotype, a rare phenotype of this form of cardiomyopathy. Eventually, the patient was supported via mechanical circulation with a Berlin Heart EXCOR® ventricular assist device as bridge to successful cardiac transplantation. Genetic testing for inherited cardiomyopathies found a mutation in MYH7 (Arg369Gln), known to be associated with various forms of cardiomyopathy, but has not been reported in restrictive LVNC.

Whole-exome sequencing reveals two de novo variants in the RBM20 gene in two Chinese patients with left ventricular non-compaction cardiomyopathy.

ImportancePathogenic variants in the RBM20 gene are associated with aggressive dilated cardiomyopathy (DCM). Recently, RBM20 was found to be associated with left ventricular non‐compaction cardiomyopathy (LVNC). Thus far, only five families with LVNC have been reported to carry variants in RBM20. It remains unknown whether the variants in RBM20 associated with DCM can also cause LVNC.ObjectiveTo elucidate the causative RBM20 variant in two unrelated patients with both LVNC and DCM, and to identify the clinical characteristics associated with variants in RBM20.MethodsTrio whole‐exome sequencing (WES) was performed. Variants were filtered and classified in accordance with the guidelines of the American College of Medical Genetics and Genomics (ACMG).ResultsWe identified two distinct de novo variants in RBM20 (one per patient) in these two patients with LVNC. Both variants have been reported in patients with DCM, without the LVNC phenotype. Patient 1 was an 11‐year‐old girl who had DCM, LVNC, and heart failure; the ratio of noncompacted‐to‐compacted myocardium was 2.7:1. A de novo heterozygous variant c.1907G>A (p.Arg636His) in exon 9 was identified in this patient. Patient 2 was a 13‐year‐old boy who had clinical phenotypes identical to those of Patient 1; the ratio of noncompacted‐to‐compacted myocardium was 3.2:1 in this patient. WES revealed a de novo heterozygous variant c.1909A>G (p.Ser637Gly) in exon 9. Both variants were previously characterized as pathogenic, and our study classified them as pathogenic variants based on the ACMG guidelines.InterpretationWe found that two patients with LVNC had variants in RBM20. Our results extended the clinical spectrum of the two RBM20 variants and illustrated that the same variant in RBM20 can cause DCM, with or without the LVNC phenotype.

ISOLATED LEFT VENTRICULAR NON COMPACTION CARDIOMYOPATHY ASSOCIATED WITH ACUTE STROKE IN YOUNG ADULT: CHALLENGING DIAGNOSIS AND TREATMENT

Left Ventricular Non compaction cardiomyopathy (LVNC) is a rare cardiomyopathy with prevalence of 0.05 %. It is characterized by prominent myocardial trabeculations and deep intertrabecular recesses in LV cavity. It has been associated with systemic thromboembolism, heart failure and sudden cardiac

Bridging the gap between hypertrabeculation phenotype, noncompaction phenotype and left ventricular noncompaction cardiomyopathy.

Left ventricular noncompaction (LVNC) is an increasingly recognised cardiomyopathy characterised by excessive trabeculation and deep intertrabecular recesses in direct communication with the left ventricular cavity. In LVNC, hypertrabeculation has been associated with heart failure, ventricular arrhythmia, and systemic thromboembolism. However, hypertrabeculation alone is not sufficient to define a subject as at risk for such complications and thus should not be sufficient to diagnose LVNC. Despite several studies having investigated parameters to predict adverse cardiovascular events, physicians have no effective tools to differentiate between clinically silent hypertrabeculation and LVNC. The aim of this paper was to review literature on LVNC diagnostic criteria and to provide an easy and accessible diagnostic algorithm to distinguish between hypertrabeculation phenotype, non-compaction phenotype and LVNC cardiomyopathy.

Elevated myocardial SORBS2 and the underlying implications in left ventricular noncompaction cardiomyopathy.

BackgroundLeft ventricular noncompaction cardiomyopathy (LVNC) is a hereditary heart disease characterized by an excessive trabecular meshwork of deep intertrabecular recesses within the ventricular myocardium. The guidelines for management of LVNC patients aim to improve quality of life by preventing cardiac heart failure. However, the mechanism underlying LVNC-associated heart failure remains poorly understood.MethodsUsing protein mass spectrometry analysis, we established that Sorbin And SH3 Domain Containing 2 (SORBS2) is up-regulated in LVNC hearts without changes to structure proteins. We conducted in vivo experiments wherein the heart tissues of wild-type mice were injected with an AAV9 vector to overexpress SORBS2, followed by analysis using echocardiography, T-tubule analysis and Ca2+ imaging to identify functional and morphological changes. In addition, we analyzed the function and structure of SORBS2 overexpressing human embryonic stem cell (hESC) derived cardiomyocytes (hESC-CM) via immunoblotting, immunohistochemistry, immunofluorescence, and confocal Ca2+ imaging.FindingsLVNC myocardial tissues feature strongly elevated expression of SORBS2, microtubule densification and redistribution of Junctophilin 2 (JP2). SORBS2 interacts with β-tubulin, promoting its polymerization in 293T cells and hESC-derived CMs. In vivo, cardiac dysfunction, β-tubulin densification, JP2 translocation, T-tubule disorganization and Ca2+ handling dysfunction were observed in mice overexpressing SORBS2.InterpretationWe identified a novel mechanism through which SORBS2 interacts with β-tubulin and promotes microtubule densification, eventually effecting JP2 distribution and T-tubule, potentially contributing to heart failure in LVNC disease.FundThis work was supported by a CAMS Initiative for Innovative Medicine grant (CAMS-I2M, 2016-I2M-1-015 to Y.J.Wei)

The Fabry cardiovascular phenotype: Aortic stiffness in Fabry disease is linked to left ventricular hypertrophy and myocardial inflammation but not storage or fibrosis

Marathon running in novices represents a natural experiment of short-term cardiovascular remodeling in response to running training. We examine whether this stimulus can produce exercise-induced left ventricular (LV) trabeculation.Sixty-eight novice marathon runners aged 29.5 ± 3.2 years had indices of LV trabeculation measured by echocardiography and cardiac magnetic resonance imaging 6 months before and 2 weeks after the 2016 London Marathon race, in a prospective longitudinal study.After 17 weeks unsupervised marathon training, indices of LV trabeculation were essentially unchanged. Despite satisfactory inter-observer agreement in most methods of trabeculation measurement, criteria defining abnormally hypertrabeculated cases were discordant with each other. LV hypertrabeculation was a frequent finding in young, healthy individuals with no subject demonstrating clear evidence of a cardiomyopathy.Training for a first marathon does not induce LV trabeculation. It remains unclear whether prolonged, high-dose exercise can create de novo trabeculation or expose concealed trabeculation. Applying cut off values from published LV noncompaction cardiomyopathy criteria to young, healthy individuals risks over-diagnosis.

Co-Phenotype of Left Ventricular Non-Compaction Cardiomyopathy and Atypical Catecholaminergic Polymorphic Ventricular Tachycardia in Association With R169Q, a Ryanodine Receptor Type 2 Missense Mutation.

Left ventricular non-compaction (LVNC) is a cardiomyopathy characterized by prominent trabeculae and intertrabecular recesses. We present the cases of 3 girls with the sameryanodine receptor type 2(RYR2) mutation who had phenotypes of both catecholaminergic polymorphic ventricular tachycardia (CPVT) and LVNC .Methods and Results:Clinical characteristics and genetic background of the 3 patients were analyzed retrospectively. Age at onset was 5, 6, and 7 years, respectively. Clinical presentation included syncope during exercise in all 3 patients and cardiac arrest in 2 patients. LVNC diagnosis was confirmed on echocardiography according to previously defined criteria. Exercise stress testing provoked ventricular arrhythmia in two of the patients. Beta-blockers (n=3) and flecainide (n=2) were given, and an implantable cardioverter defibrillator was used in 1 patient. Genotyping identified the sameRYR2-R169Q missense mutation and no other CPVT- or LVNC-related gene mutations. Functional analysis of the mutation using HEK293 cells with single-cell Ca2+imaging and [3H]ryanodine binding analysis, indicated a gain of function: a reduced threshold for overload-induced Ca2+release from the sarcoplasmic reticulum and increased fractional Ca2+release. The rare association of LVNC and CPVT phenotypes withRYR2mutations is less likely to be coincidental. Screening for life-threatening arrhythmias using exercise or pharmacologic stress tests is recommended in LVNC patients to prevent sudden cardiac death in those with preserved LV function.

Role of deformation imaging in left ventricular non-compaction and hypertrophic cardiomyopathy: an Indian perspective

BackgroundSpeckle tracking echocardiography (STE) has emerged as a novel feasible tool for the assessment of left ventricular rotational parameters. Since hypertrophic cardiomyopathy(HCM) shares morphologic features with left ventricular non-compaction (LVNC), we used this imaging modality to compare rotational mechanics between these two entities.ResultsWe compared global and regional LV function and rotational mechanics between LVNC, HCM, and healthy subjects using STE. Longitudinal strain and torsion were obtained from echocardiographic images from parasternal short axis as well as standard LV apical views. Twelve patients with LVNC [mean age 46.12 ± 14.66 years; median 47.5 IQR (39.25–58.5) years] were compared with 18 HCM patients [mean age 49.48± 17.22 years; median 56 IQR (33–65) years] and 18 healthy subjects [mean age: 51.50± 12.51 years; median 51(45.75-58) years]. LVNC group showed a significantly reduced longitudinal strain at the apical region compared to HCM group (− 12.18 ± 6.25 vs − 18.37 ± 3.67; P < 0.05). Rigid body rotation(RBR) was found in 50% of patients whereas the other half had a normal rotation at the apex and the base. Among the patients with RBR, all patients had a uniform counterclockwise rotation.ConclusionLongitudinal strain was impaired in both the forms of cardiomyopathy; however, LVNC showed a more significant reduction in the apical region compared to patients with HCM suggesting a development abnormality in these regions. A reduction in left ventricular torsion was specifically noted among patients with LVNC with a uniform anticlockwise rotation of LV base and apex.

A common pediatric presentation of an unusual disease: non-compaction cardiomyopathy

Background: Shortness of breath is a very common presentation at the pediatric emergency department, but making a diagnosis based on it is very challenging for physicians because of the numerous differential diagnoses, including respiratory and cardiac causes. Case Presentation: Herein, we describe the case of a 2-month-old patient who presented to our emergency department in October 2017 with shortness of breath for 3 weeks duration. She was diagnosed as having lower respiratory tract infection; a cardiac murmur was incidentally found, which turned out to be a very rare congenital cardiac disease: left ventricular non-compaction cardiomyopathy (LVNC). She was treated with anti-failure medications but unfortunately died before cardiac transplant. Conclusion: As demonstrated by this case, non-compaction cardiomyopathy can be easily missed and misdiagnosed because of its rarity and diverse symptoms on presentation. Since corresponding treatment modalities are lacking, the prevention of associated complications is the primary goal of LVNC management.

Некомпактная кардиомиопатия: дополнительные предикторы жизнеугрожающих событий для отбора пациентов на имплантацию кардиовертера-дефибриллятора

Некомпактная кардиомиопатия: дополнительные предикторы жизнеугрожающих событий для отбора пациентов на имплантацию кардиовертера-дефибриллятора

136 Long Term Clinical Outcomes in CMR Quantified Left Ventricular Noncompaction

There is currently no diagnostic gold standard for Left Ventricular Noncompaction cardiomyopathy (LVNC) and no definitive method to accurately delineate noncompacted myocardium. We developed a novel tool based on signal intensity to quantify noncompacted myocardial mass in 97 patients with isolated Petersen criteria LVNC and assess the association with major adverse cardiovascular and cerebrovascular events (MACCE) including cardiac death, cardiac transplantation, cardiac re-synchronization device, ventricular tachycardia and ischemic stroke. 81(83.5%) patients had preserved and 16 (16.5%) had reduced LV systolic function. In addition, five (5.2%) patients had late gadolinium enhancement (LGE); all patients had reduced LV function. Patients with reduced function had more end-systolic noncompacted mass (61.9g+/-22.4 vs 38.1g+/-15.8, p<0.001) and larger end-systolic noncompacted to total myocardial mass (44%+/-9 vs 36%+/-12, p=0.003). MACCE occurred in 12(12.3%) patients; 10(10.3%) with impaired LV function and 2(2.5%) with preserved LV function; p<0.001. Cardiac death only occurred in patients with reduced function (3/16; 18.8% and LGE (2/5; 40%); p=0.038 and 0.063. Signal intensity can accurately define noncompacted myocardium and quantify myocardial mass. In patients with isolated Petersen criteria LVNC, reduced LV function and LGE were predictors of MACCE (p<0.001) but the amount of noncompaction was not. Moving forward, future diagnostic criteria cannot be limited to the presence of noncompaction and must include LV parameters.

45 Severe secondary mitral regurgitation due to left ventricular non- compactation cardiomyopathy- a rare cause of heart failure

Abstract Introduction Left ventricular non-compaction is a rare form of cardiomyopathy charactherized by the presence of a two layered ventricular wall- a thinner epicardial layer and an inner, non-compacted layer with prominent trabeculations associated with deep, intratrabecular recesses that communicate with left ventricle cavity. Clinical manifestations vary in severity, including symptoms of heart failure, thromboembolic events or arrhythmias. Left ventricular (LV) dysfunction leads to tethering of the mitral apparatus and is a cause for secondary significant mitral regurgitation. Case presentation We report the case of a 57 year-old female patient, diagnosed with severe mitral regurgitation one year before presentation, with severe heart failure (HF) symptoms, referred to our clinic for the surgical replacement of the mitral valve. Clinical examination revealed no signs of pulmonary or systemic congestion and systolic apical murmur. Blood tests were normal, except for the elevated BNP (552 pg/ml). Electrocardiogram showed sinus rhythm and left ventricular hypertrophy. Coronary angiogram did not identify any coronary artery lesions. Echocardiography revealed mildly dilated left ventricle, but wih proeminent trabeculations and two distinct myocardial layers with a non-compacted/compacted ratio of 2:1 in the anterior and lateral walls, diagnostic for left ventricular non-compaction cardiomyopathy. LV ejection fraction was 40% , with severe secondary mitral regurgitation due to significant antero-posterior dilation of the mitral ring, with intact mitral leaflets; mild pulmonary hypertension was present. Magnetic resonance imaging (MRI) identified a two layer antero-lateral myocardium and confirmed the echo diagnosis; there was no evidence of scarring as there was absent late gadolinium enhacement. In the absence of fibrosis on MRI or any arrhythmic events on repeated Holter ECG monitoring, the implantation of a cardiac defibrillator was deferred. Given the secondary cause for mitral regurgitation (LV dysfunction), specific HF medication with beta blocker and renin-angiotensin-aldosterone blockade was initiated and titrated to optimal doses. With medical treatment the evolution was favourable. Currently, 3 years after the initial diagnosis, 6 minutes walk test revealed good functional capacity (510 m), a BNP value of 104 pg/l, without any worsening of LV systolic function nor progression of pulmonary hypertension. Conclusion Left ventricular non-compaction cardiomyopathy is a rare cause of heart failure, but due to advances in imaging modalities and increasing awareness, its prevalence is growing. Its pathogenesis and prognosis largely remain unknown, but early and adequate initiation of neurohormonal medication may be just as essential in order to prevent complications and improve long term prognosis, as for other forms of cardiomiopathy, even in the presence of severe secondary mitral regurgitation.

Cardiovascular magnetic resonance based diagnosis of left ventricular non-compaction cardiomyopathy: impact of cine bSSFP strain analysis

BackgroundInvestigation of the myocardial strain characteristics of the left ventricular non-compaction (LVNC) phenotype with cardiovascular magnetic resonance (CMR) feature tracking.MethodsCMR cine balanced steady-state free precession data sets of 59 retrospectively identified LVNC phenotype patients (40 years, IQR: 28–50 years; 51% male) and 36 healthy subjects (39 years, IQR: 30–47 years; 44% male) were evaluated for LV volumes, systolic function and mass. Hypertrabeculation in patients and healthy subjects was evaluated against established CMR diagnostic criteria. Global circumferential strain (GCS), global radial strain (GRS) and global longitudinal strain (GLS) were evaluated with feature-tracking software. Subgroup analyses were performed in patients (n = 25) and healthy subjects (n = 34) with normal LV volumetrics, and with healthy subjects (n = 18) meeting at least one LVNC diagnostic criteria.ResultsAll LVNC phenotype patients, as well as a significant proportion of healthy subjects, met morphology-based CMR diagnostic criteria: non-compacted (NC): compacted myocardial diameter ratio > 2.3 (100% vs. 19.4%), NC mass > 20% (100% vs. 44.4%) and > 25% (100% vs. 13.9%), and NC mass indexed to body surface area > 15 g/m2 (100% vs. 41.7%). LVNC phenotype patients demonstrated reduced GRS (26.4% vs. 37.1%; p < 0.001), GCS (− 16.5% vs. -20.5%; p < 0.001) and GLS (− 14.6% vs. -17.1%; p < 0.001) compared to healthy subjects, with statistically significant differences persisting on subgroup comparisons of LVNC phenotype patients with healthy subjects meeting diagnostic criteria. GCS also demonstrated independent and incremental diagnostic value beyond each of the morphology-based CMR diagnostic criteria.ConclusionsLVNC phenotype patients demonstrate impaired strain by CMR feature tracking, also present on comparison of subjects with normal LV volumetrics meeting diagnostic criteria. The high proportion of healthy subjects meeting morphology-based CMR diagnostic criteria emphasizes the important potential complementary diagnostic value of strain in differentiating LVNC from physiologic hypertrabeculation.

Single Centre Experience of Adult Left Ventricular Non-Compaction Cardiomyopathy in South-East Asian Population

Single Centre Experience of Adult Left Ventricular Non-Compaction Cardiomyopathy in South-East Asian Population