scholarly journals Heart transplantation in an adult patient with isolated noncompaction of the left ventricular myocardium

Medicina ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 193 ◽  
Author(s):  
Sigita Glaveckaitė ◽  
Kęstutis Ručinskas ◽  
Jelena Čelutkienė ◽  
Vytė Maneikienė ◽  
Diana Zakarkaitė ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Adult Patient ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Important Process ◽  
Ventricular Noncompaction ◽  
Myocardial Development ◽  
Myocardial Fibers ◽  
Heart Lesions

Isolated noncompaction of the ventricular myocardium is defined as a rare cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibers and meshwork, an important process in myocardial development, in absence of any coexisting congenital heart lesions. A lot of controversies exist about diagnostic criteria, nomenclature, origin, pathogenesis, and prognosis of this disease. Here, we describe an adult patient with isolated left ventricular noncompaction who presented with worsening congestive heart failure and was successfully treated with heart transplantation.

Deloading of the Left Ventricle by Ventricular Assist Device Normalizes Increased Expression of Endothelin ET A Receptors But Not Endothelin-Converting Enzyme-1 in Patients With End-Stage Heart Failure

Circulation ◽  
2000 ◽  
Vol 102 (suppl_3) ◽  
Author(s):  
Henning Morawietz ◽  
Marten Szibor ◽  
Winfried Goettsch ◽  
Babett Bartling ◽  
Matthias Barton ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Transplantation ◽  
Ace Inhibitor ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Converting Enzyme ◽  
Ventricular Assist ◽  
End Stage Heart Failure ◽  
End Stage

Background —Ventricular assist devices (VAD) are implanted in patients with end-stage heart failure for bridging the time until heart transplantation, resulting in hemodynamic unloading of the failing heart, improved cardiac contractile and mitochondrial function, and reversal of cardiac hypertrophy. It is unknown whether VAD unloading may affect the cardiac endothelin (ET) system, which has been proposed as one of the putative pathomechanisms of heart failure. Methods and Results —With the use of standard-calibrated, competitive reverse-transcription–polymerase chain reaction mRNA expression of components of the ET system was analyzed in left ventricular myocardium from nonfailing donor hearts, from failing hearts without and with ACE inhibitor therapy, and from patients with end-stage heart failure at the time of VAD implantation and 103±15 days after VAD implantation during removal with subsequent heart transplantation. ET receptor A (ET A ) was markedly upregulated in failing human myocardium. This increased ET A expression was not affected by ACE inhibitor treatment but was normalized by VAD unloading. ET A expression before or after VAD implantation did not correlate with duration of VAD implantation or suppression of Pro-ANP mRNA. ET B mRNA expression was unaffected by heart failure or VAD. In contrast, increased ET-converting enzyme-1 mRNA and ET-1 peptide levels in failing myocardium were partially normalized by ACE inhibition but not by VAD unloading. Conclusions —We conclude that VAD implantation normalizes ET A expression in failing human left ventricular myocardium, probably as the result of the beneficial effects of VAD unloading.

scholarly journals A Case of Isolated Left Ventricular Noncompaction with Basal ECG-Tracing Strongly Suggestive for Type-2 Brugada Syndrome

2011 ◽  
Vol 2011 ◽  
pp. 1-4
Author(s):  
Maria Banci ◽  
Roberta Martinoli ◽  
Alessandro Dofcaci ◽  
Stefano Piccirilli ◽  
Federica Papetti ◽  
...  
Keyword(s):  
Ventricular Function ◽  
Brugada Syndrome ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Important Process ◽  
Ventricular Noncompaction ◽  
First Report ◽  
Systemic Embolization ◽  
Myocardial Development

Isolated left ventricular noncompaction (ILVNC) is a cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibres and meshwork, an important process in myocardial development. ILVNC is clinically accompanied by depressed ventricular function, arrhythmias, and systemic embolization. We reported a case of ILVNC with basal ECG-tracing strongly suggestive for type-2 Brugada syndrome (BrS). Up to now, this is the first report investigating the association between ILVNC and this particular ECG pattern.

Absence of the left ventricular myocardium in a newborn

1996 ◽  
Vol 6 (4) ◽  
pp. 344-347 ◽  
Author(s):  
Angelika Lindinger ◽  
Yvonne Masur ◽  
Hans-Gerhard Limbach
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Ventricular Myocardium ◽  
Arrhythmogenic Right Ventricular Dysplasia ◽  
Left Ventricular ◽  
Adolescent And Young Adult ◽  
Left Ventricular Myocardium ◽  
Fatty Replacement ◽  
Myocardial Fibers ◽  
The Right

SummaryAbsence of myocardial fibers in the right ventricle is the essence of so-called Uhl's anomaly, which should be distinguished from the fatty replacement producing arrhythmogenic right ventricular dysplasia of the adolescent and young adult. In this report, we describe a newborn with nearly complete absence of the myocardium of the left ventricle. The infant died on the seventh day because of myocardial incompetence of the left ventricle, which was unable to open the aortic valve.

scholarly journals Noncompaction of the Left Ventricular Myocardium: A Cause of Syncope in a Young Patient

2013 ◽  
Vol 1 (3) ◽  
pp. 32
Author(s):  
Deephak Swaminath ◽  
Ragesh Panikkath ◽  
Roshni Narayanan ◽  
Sam Copeland
Keyword(s):  
High Risk ◽  
Young Patient ◽  
Ventricular Arrhythmias ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Clinical Presentations ◽  
Embryonic Life

Noncompaction of the left ventricular myocardium (LVNC) is a rare cardiomyopathywith a spectrum of clinical presentations. The pathogenesis of this type of cardiomyopathyinvolves an arrest in the process of compaction during embryonic life. Identificationof high risk individuals with this syndrome is challenging; it can cause presentationsranging from an asymptomatic state to malignant ventricular arrhythmias and suddendeath. We present a 19-year-old man who presented with syncope and was later diagnosedwith left ventricular noncompaction.

Heart transplantation in a patient with isolated noncompaction of the left ventricular myocardium

2004 ◽  
Vol 77 (5) ◽  
pp. 1806-1808 ◽  
Author(s):  
Sotiris C Stamou ◽  
Edward A Lefrak ◽  
Freydoon C Athari ◽  
Nelson A Burton ◽  
Paul S Massimiano
Keyword(s):  
Heart Transplantation ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium

Isolated non-compaction of the left ventricular myocardium in an adult treated with heart transplantation

2006 ◽  
Vol 56 (1) ◽  
pp. 35-39 ◽  
Author(s):  
J. Fernando Val-Bernal ◽  
J. Francisco Nistal ◽  
María Martino ◽  
M. Francisca Garijo
Keyword(s):  
Heart Transplantation ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium

scholarly journals The results of surgical treatment of a patient with isolated left ventricular apical hypoplasia and left ventricular noncompaction

2019 ◽  
pp. 97-103
Author(s):  
V. I. Skidan ◽  
Kh. A. Bsharat ◽  
Yu. I. Aseeva ◽  
G. P. Nartsissova ◽  
E. N. Pavlyukova
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Surgical Treatment ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Permanent Form

There is a presentation of the results of a two-year follow-up after surgical treatment of a patient with chronic heart failure and a permanent form of atrial fibrillation, in which isolated apex hypoplasia and non-compaction of left ventricular myocardium were revealed.

scholarly journals Effects of Telmisartan on Myocardial Protein Profiles in Hypertensive Rats

2021 ◽  
Vol 34 (3) ◽  
pp. 299-299
Author(s):  
Yu Feng ◽  
Man-li Zhou ◽  
Jian-zhang Wang ◽  
Jia-qi Zhang ◽  
Shu-le Qian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Sterile Water ◽  
Protein Profiles ◽  
Related Protein ◽  
Hypertensive Rats ◽  
Treatment Groups ◽  
Proteasome 26S

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

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