tal1 Regulates the formation of intercellular junctions and the maintenance of identity in the endocardium.

The endocardium forms the inner lining of the heart tube, where it enables blood flow and also interacts with the myocardium during the formation of valves and trabeculae. Although a number of studies have identified regulators in the morphogenesis of the myocardium, relatively little is known about the molecules that control endocardial morphogenesis. Prior work has implicated the bHLH transcription factor Tal1 in endocardial tube formation: in zebrafish embryos lacking Tal1, endocardial cells form a disorganized mass within the ventricle and do not populate the atrium. Through blastomere transplantation, we find that tal1 plays a cell-autonomous role in regulating endocardial extension, suggesting that Tal1 activity influences the behavior of individual endocardial cells. The defects in endocardial behavior in tal1-deficient embryos originate during the earliest steps of endocardial morphogenesis: tal1-deficient endocardial cells fail to generate a cohesive monolayer at the midline and instead pack tightly together into a multi-layered aggregate. Moreover, the tight junction protein ZO-1 is mislocalized in the tal1-deficient endocardium, indicating a defect in intercellular junction formation. In addition, we find that the tal1-deficient endocardium fails to maintain its identity; over time, a progressively increasing number of tal1-deficient endocardial cells initiate myocardial gene expression. However, the onset of defects in intercellular junction formation precedes the onset of ectopic myocardial gene expression in the tal1-deficient endocardium. We therefore propose a model in which Tal1 has distinct roles in regulating the formation of endocardial intercellular junctions and maintaining endocardial identity.

Endoventriculoplasty using autologous endocardium for anterior left ventricular aneurysms.

BACKGROUND: There is currently consensus that endoventriculoplasty is the treatment of choice for an anterior left ventricular aneurysm. We describe here a new technique of endoventriculoplasty using autologous endocardium for left ventricular anterior aneurysm. METHOD: From 1990 until 2003, 49 patients underwent endoventriculoplasty using autologous pericardium at the Thoraxcenter of the University Hospital of Groningen in the Netherlands (28 patients) and at the Department of Cardio Thoracic Surgery of the University Hospital of Pisa in Italy (21 patients). Mean logistic EuroSCORE and mean ejection fraction were 15.7 +/- 6.7 and 31 +/- 9 %, respectively. RESULTS: Overall 30-day mortality was 4.1 %. Causes of in-hospital mortality were low output syndrome (1 patient) and ventricular fibrillation (1 patient). Postoperative complications were myocardial infarct (4.1 %), low output syndrome (6.1 %), renal failure (4.1 %), neurological events (2.0 %), atrial fibrillation (14.3 %), ventricular fibrillation or tachycardia (6.1 %), ARDS (4.1 %), re-operation for bleeding (4.1 %), and major wound infection (2.0 %). CONCLUSION: Our analysis shows that endoventriculoplasty with autologous endocardium is a safe procedure and improves the outcome in high-risk patients with ventricular aneurysm.

[Surgical repair of postinfarction ventricular septal perforation by endocardial patch with infarction exclusion].

UNLABELLED: We evaluated the surgical results of postinfarction ventricular septal perforation by endocardial patch with infarction exclusion. MATERIALS AND METHODS: We reviewed 8 patients complicating AMI who underwent surgical treatment at our institution from July 1997 to August 2000 (6 males, 2 females, mean age 73.9 +/- 9, range 57-87). The localization of AMI and VSP was anterior in 6 patients, inferior in 2. All patients had coronary angiography preoperatively. And 7 patients had the percutaneous transluminal coronary angioplasty of the infarct artery. RESULTS: There were 2 hospital deaths due to cerebral infarction and pulmonary hemorrhage. All deaths occurred in patients with cardiogenic shock. CONCLUSION: Good results were obtained by infarction exclusion technique. Better operative results may be expected with the preoperative coronary angioplasty of the infarct artery.

Influence of the mesenchymal microenvironment on myocardial and endocardial cell behaviour in experimental interaction with chick limb mesenchyme.

In an attempt to clarify the possible influence of the mesenchymal microenvironment in the differentiation of myocardial and endocardial cells, an "in vivo" transplantation experiment was performed in which the ventricular region of the heart (chick or quail) was placed in close association to the mesenchyme of the anterior chick limb to create an experimental interaction between myocardium and foreign mesenchyme. The results showed that after 48 h of tissue interactions the ventricular myocardium is incorporated into the mesenchyme of the anterior chick limb, changing its organization and cytological appearance. The myocytes tend to dissociate, exhibiting a less organized myofibrillar pattern. In addition, abundant extracellular matrix components made up of granular and fibrillar material were observed associated with the myocardial and the mesenchymal cell membranes as well as distributed in their surrounding microenvironment. The endocardium became discontinuous, due to detachment of the cells and emitted multiple pseudopodia and filopodia. These observations indicate that the mesenchyme from the anterior chick limb modifies the cellular behaviour and organization of the neighbouring myocardium and endocardium with which it interacts. We suggest that this might occur through participation of extracellular matrix components such as glycosaminoglycans, fibronectin and collagen which are known to act as macromolecular mediators in cell to cell interactions, cell migration and differentiation.