Clinical Characterization of Left Ventricular Noncompaction in Children

Pignatelli, Ricardo H.; McMahon, Colin J.; Dreyer, William J.; Denfield, Susan W.; Price, Jack F.; Belmont, John W.; Craigen, William J.; Wu, Jen Huang; Said, Howaida El; Bezold, Louis I.; Clunie, Sarah K.; Fernbach, Susan; Bowles, Neil E.; Towbin, Jeffrey A.

doi:10.1161/01.cir.0000100664.10777.b8

Cited by 586 publications

(240 citation statements)

References 22 publications

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“…4 Isolated left ventricular noncompaction has been described in children as well as adults, including the elderly. 5 The prevalence is low, probably 0.05%, but may actually be higher because of underdiagnosing or misdiagnosing as hypertrophic cardiomyopathy. 6 Men appear to be affected more often (about 70%) than women.…”

mentioning

confidence: 99%

Isolated left ventricular noncompaction in a patient presenting with a subacute myocardial infarction

Swinkels¹,

Boersma²,

Rensing³

et al. 2007

NHJL

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Isolated left ventricular noncompaction in a patient presenting with a subacute myocardial infarctionIsolated left ventricular noncompaction is a rare cardiomyopathy that is often not recognised. So far, it is not well established how best to manage this abnormality. We describe a patient in whom the diagnosis of isolated left ventricular noncompaction was made after presentation with a subacute myocardial infarction. Because of nonsustained ventricular tachycardias during hospitalisation, which were inducible and deteriorated into ventricular fibrillation on electrophysiological examination after coronary artery bypass grafting, he received an implantable defibrillator. Whether the ventricular tachycardias were due to the myocardial infarction or to the noncompacted myocardium remains uncertain. (Neth Heart J 2007; 15:109-11.) Keywords: noncompaction (isolated), cardiomyopathy, echocardiographyA 73-year-old man without a cardiac history presented to the Emergency Department because of chest pain radiating to the throat for two days. On physical examination he measured 1.70 m and weighed 58 kg. His blood pressure was 110/60 mmHg and the pulse regular at a rate of 70 beats/min. The jugular venous pressure appeared normal. Cardiac auscultation revealed normal heart sounds without murmurs. The lungs were clear to auscultation. The electrocardiogram showed sinus rhythm with right bundle branch block, 1 mm ST-segment elevation in leads I, II, aVL and V 3 to V 6 , and slightly terminally negative T waves in leads V 3 to V 6 . The chest X-ray was normal with a cardiothoracic ratio of 43%. Creatine kinase (CK) and CK-MB were increased at presentation (2263 and 356 U/l, respectively). The diagnosis of subacute anterolateral myocardial infarction was made and the patient received aspirin, clopidogrel, lowmolecular-weight heparins, nitrates, β-blockers and a statin. The next day, the CK and CK-MB had fallen and transthoracic echocardiography revealed akinetic anterolateral wall segments, a left ventricular ejection fraction of 35 to 40%, no significant valve disease, and prominent trabeculation of the apex of the left ventricular myocardium consistent with noncompaction. The presence of noncompaction was confirmed by contrast echocardiography (1.5 ml SonoVue intravenously), showing direct communication between the left ventricular cavity and the deep intertrabecular recesses (figure 1). The patient's convalescence was complicated by the occurrence of recurrent nonsustained ventricular tachycardia from the fourth day after admission, and ST depression (without chest pain) during bicycle ergometry on the fifth day after admission. Coronary angiography showed significant two-vessel disease of the left anterior descending (LAD) and left circumflex (LCX) coronary artery. Three weeks after admission, the patient underwent coronary artery bypass grafting (CABG). The left internal mammary artery was anastomosed with the LAD, and a venous jump graft was anastomosed with the obtuse marginal branch of the LCX via the anterolateral br...

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mentioning

confidence: 99%

Isolated left ventricular noncompaction in a patient presenting with a subacute myocardial infarction

Swinkels¹,

Boersma²,

Rensing³

et al. 2007

NHJL

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“…Left Ventricular Non-Compaction Cardiomyopathy is caused by an arrest in the normal process of endomyocardial morphogenesis and characterized with multiple prominent trabeculations and deep inter-trabecular recesses communicating with the ventricular cavity [2,3]. Patient with LVNC may be present with heart failure, thrombus embolism, and ventricular arrhythmias [4].…”

Section: Discussionmentioning

confidence: 99%

“…Familial occurrence of LVNC has been reported with an incidence as high as 44% [2]. Echocardiography and Magnetic resonance imaging (MRI) usually use for diagnosis [3].…”

Section: Introductionmentioning

confidence: 99%

Peripartum noncompaction cardiomyopaty:new diagnosed after pregnancy

Asoğlu¹,

Türkmen²,

Aktürk³

et al. 2018

Med-Science

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Left-ventricular non-compaction (LVNC) cardiomyopathy is an arrest in the normal process of myocardial compaction and few cases have been reported just after pregnancy. In this case report, we present a patient who had heart failure symptoms at first month of after 38 weeks pregnancy. Echocardiography revealed prominent trabeculation and deep intertrabecular recesses at the left ventricular with an impaired ejection fraction. There is no specific treatment for LVNC just after pregnancy besides the usual management of dilated cardiomyopathy.

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“…LVHT may also develop as a compensatory mechanism of an impaired myocardium (1,13). LBB is a rare finding in children with LVHT, but occurs more frequently in adults (14)(15)(16)(17)(18)(19).…”

Section: Discussionmentioning

confidence: 99%