Isolated Left Ventricular Noncompaction as a Cause for Heart Failure and Heart Transplantation: A Single Center Experience

Kovačevic-Preradović, Tamara; Jenni, Rolf; Oechslin, Erwin; Noll, Georg; Seifert, Burkhardt; Jost, Christine H. Attenhofer

doi:10.1159/000147899

Cited by 93 publications

(59 citation statements)

References 53 publications

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“…In a study on 42 patients, 50% presented with dyspnoea, 19% with chest pain, and 14% with palpitations [68]. Among patients with heart failure, LVHT is the cause in 3% of the adult cases [70] and in 2.9% of the paediatric cases [71]. Indications to carry out TTE in LVHT patients include heart failure, chest pain, syncope, NMDs, stroke/ embolism, hypertension, or family screening.…”

Section: Clinical Presentationmentioning

confidence: 99%

Left ventricular non-compaction and its cardiac and neurologic implications

Finsterer

2010

Heart Fail Rev

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Left ventricular non-compaction, also known as left ventricular hypertrabeculation (LVHT), is a morphological abnormality of the left ventricular myocardium, characterised by a meshwork of myocardial strings, interlacing, and orderless in arrangement. LVHT is most frequently located in the apex and the lateral wall and may occur with or without other congenital or acquired cardiac abnormalities. LVHT is believed to be congenital in the majority of the cases but may develop during life in single cases (acquired LVHT). Congenital LVHT is believed to result from defective late-stage embryonic development of the myocardial architecture. The pathogenesis of acquired LVHT remains speculative. LVHT is most frequently found on transthoracic echocardiography and cardiac MRI but may be visualised also with other imaging techniques. In the majority of the cases, LVHT is associated with hereditary cardiac, neuromuscular, non-cardiac/non-muscle disease, or chromosomal aberrations. In the majority of the cases, LVHT is complicated by ventricular arrhythmias, systolic dysfunction, cardiac embolism, or sudden cardiac death. LVHT per se does not require a specific treatment. Only in case of complications, such as ventricular arrhythmias, cardioembolism, or systolic dysfunction, adequate therapy is indicated. Though initially assessed as poor, the prognosis of LVHT has meanwhile improved, most likely due to the increased awareness for the abnormality and the timely administration of adequate therapy.

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Section: Clinical Presentationmentioning

confidence: 99%

Left ventricular non-compaction and its cardiac and neurologic implications

Finsterer

2010

Heart Fail Rev

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“…По данным нескольких ЭхоКГ-иссле-дований взрослой популяции, частота СНМЛЖ коле-блется в пределах 0,014-1,3% [7]. Среди пациентов с сердечной недостаточностью частота СНМЛЖ выше и составляет около 3% [8]. Такие разные оценки частоты СНМЛЖ связаны, скорее всего, с различ-ными подходами к диагностике и разными методами визуализации.…”

Section: некомпактный миокард левого желудочка: симптом синдром или unclassified

Non-Compaction Left Ventricle Myocardium: A Symptom, Syndrome or Development Variation?

Поляк¹,

Мершина²,

Заклязьминская³

2017

Russ J Cardiol

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“…This figure is probably an underestimate and with increasing awareness the diagnosis of LVNC is more frequent. In the contemporary registry of systolic heart failure (HF), LVNC was confirmed in 3% of 960 consecutive HF patients [7]. …”

Section: Epidemiologymentioning

confidence: 99%

Left ventricular non-compaction with congenital diaphragmatic hernia causing cardiac dextroposition

Rubiś

Miszalski−Jamka

Cleland

et al. 2012

Journal of Rare Cardiovascular Diseases

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A 45-year-old man with a 2-month history of breathlessness, fatigue and irregular heart rate was referred to our centre after first-ever cardio-pulmonary decompensation. At presentation he was stable with heart rate of 120/min, blood pressure of 140/90 mmHg, in NYHA class II. 12-lead ECG showed atrial fibrillation, low R-waves voltage and deep S-waves with non specific ST changes in V1-V6. A posterior-anterior chest X-ray showed an enlarged cardiac silhouette, whereas on lateral picture an unusual structure was identified in the thorax cavity. An echocardiogram showed an enlarged, hypertrophied left ventricle (LV) with severe global systolic impairment. A computed tomography revealed an intestinal loop, characterized as the anterior Morgagni type congenital diaphragm hernia, in the anterior mediastinum resulting in the heart dislocation to the right side. Cardiac magnetic resonance revealed a thinned apex coupled with increased trabeculation at the apex, posterior, lateral and anterior wall. The measurements of double-layered LV wall, confirmed the diagnosis of LV non-compaction (LVNC). This case is an illustrate of a constellation of rare anomalies of LVNC, persistent left superior vena cava with a congenital anterior Morgagni-type diaphragm hernia, causing heart dextroposition. On multidisciplinary team meeting the general decision of conservative treatment was made with typical systolic heart failure pharmacotherapy, restoration of sinus rhythm, considering referral to ICD and/or CRT-D, and regular clinical and echocardiographic follow-up of both patient and patient's pedigree. JRCD 2012; 1: 18-23 Case presentationPreviously fit and well 45-year-old man with 2-month history of gradually increasing breathlessness, fatigue and irregular heart rate was referred from the district hospital after cardio-pulmonary decompensation for the exhaustive cardiological work-up. The patient had typical risk factors of cardiovascular diseases such as hypertension, hyperlipidemia and nicotine abuse, otherwise the medical and family history was unremarkable. At presentation he was stable with an irregular heart rate of 120 beats per minute (bpm), arterial blood pressure of 140/90 mm Hg, oxygen saturation of 98%, in New York Heart Association (NYHA) class II. On physical examination he was euvolemic, with normal jugular venous pressure and clear lung fields. Interestingly, heart sounds were more audible at the right side of the chest. Standard 12-lead ECG showed atrial fibrillation, low R-waves voltage and deep S-waves with non specific ST changes in V 1 -V 6 (Figure 1). However, after electrodes were replaced to the right side of the thorax, ECG revealed prominent R waves in precordial leads (Figure 2). A posterior-anterior chest X-ray showed an enlarged cardiac silhouette, whereas on lateral X-ray an unusual structure was identified in the thorax cavity (Figure 3 and 4, arrows). A transthoracic echocardiogram was of poor quality, nevertheless, revealed enlarged and hypertrophied left ventricle (LV) with severe global ...

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Isolated Left Ventricular Noncompaction as a Cause for Heart Failure and Heart Transplantation: A Single Center Experience

Cited by 93 publications

References 53 publications

Left ventricular non-compaction and its cardiac and neurologic implications

Left ventricular non-compaction and its cardiac and neurologic implications

Non-Compaction Left Ventricle Myocardium: A Symptom, Syndrome or Development Variation?

Left ventricular non-compaction with congenital diaphragmatic hernia causing cardiac dextroposition

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