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PubMedDate not supplied

[Algorithm for automatic endocardium identification in digital echocardiography image sequences].

The present paper describes an automated procedure for the detection of left ventricular internal wall edges in digital echocardiographic image sequences. The proposed procedure is divided into three steps and programmed in C/UNIX. It includes the use of a specially designed, application-specific adaptive spatio-temporal filter for noise reduction in echocardiographic image sequences, local 3-D histogram equalization for augmented contrast, and segmentation of the left ventricle using a regional growth method. When designing the adaptive spatio-temporal filter, we took into account the fact that the background noise is correlated in tangential orientation due to beam deflection at interfaces characterized by a large impedance "jump". Using the specially designed filter, the background noise is successfully reduced without degrading the ventricular contours. The simulation results presented highlight the performance of the proposed method in an exemplary manner.

Algorithms↗
PubMed1988

Metabolic protection of the reperfused canine endocardium by the thromboxane synthetase inhibitor, dazoxiben.

This study investigated whether dazoxiben, a thromboxane synthesis inhibitor, could reverse regional contractile dysfunction and protect against adenine nucleotide loss in the "stunned myocardium". Hearts from anesthetized dogs were "stunned" by 15 min of left anterior descending coronary artery occlusion followed by 3 hr of reperfusion. Left ventricular segment shortening (%SS) and regional myocardial blood flow (RMBF) were measured by sonomicrometry and the radioactive microsphere technique, respectively. Local coronary venous blood was withdrawn and thromboxane A2 and prostacyclin measured by radioimmunoassay. Transmural biopsies from the reperfused and nonischemic areas were taken at 3 hr following reperfusion for tissue metabolite analysis. During ischemia, %SS, RMBF and area at risk were decreased to similar levels in both control and dazoxiben-treated hearts indicating equivalent degrees of flow deprivation. During reperfusion, %SS recovered only partially and was not significantly improved by dazoxiben. Dazoxiben augmented peak prostacyclin production (123 +/- 31% vs. 292 +/- 49% of preocclusion values) following reperfusion, while it completely blocked thromboxane A2 production. Dazoxiben attenuated the decline in endocardial ATP (69 +/- 5% vs. 92 +/- 9% normalized to the nonischemic zone) and total adenine nucleotides. The results indicate that dazoxiben may elicit a cardioprotective effect on energy metabolism in the reperfused heart, but this is dissociated from any improvement in regional contractile function.

Adenine Nucleotides↗
PubMed2005

Management of left atrial endocardium after extensive thrombectomy.

Thrombosis at the left atrium is a common phenomenon in patients with chronic mitral valve disease and atrial fibrillation. When thrombus organizes and evolves into chronic phase, clean thrombectomy can become a challenge during heart surgery because of dense adhesions and the lack of clean cleavage plane. Leaving residual thrombotic material or roughened endocardial surface after thrombectomy could be a potential source for further thrombosis and a nidus for thromboembolism. We recently managed such a patient successfully using extensive thrombectomy and endocardial coverage with a fresh autologous pericardial patch.

Atrial Appendage↗
PubMed2005

A bronchogenic cyst of the right ventricular endocardium.

In a 73-year-old male patient with a history of prostate cancer, a right ventricular endoluminal tumor was diagnosed by echocardiography. An endocardial papillary fibroelastoma or myxoma appeared possible; a malignant tumor could not be ruled out. The tumor was resected using extracorporeal circulation and cardioplegic arrest. Histopathology study revealed a bronchogenic cyst with ciliated epithelium.

Aged↗
PubMed2004

Septation and shortening of outflow tract in embryonic mouse heart involve changes in cardiomyocyte phenotype and alpha-SMA positive cells in the endocardium.

BACKGROUND: Studies on human, rat and chicken embryos have demonstrated that during the period of outflow tract septation, retraction of the distal myocardial margin of the outflow tract from the junction with aortic sac to the level of semilunar valves leads to the shortening of the myocardial tract. However, the mechanism is not clear. So we investigated the mechanism of outflow tract shortening and remodeling and the spatio-temporal distribution pattern of alpha-SMA positive cells in the outflow tract cushion during septation of the outflow tract in the embryonic mouse heart. METHODS: Serial sections of mouse embryos from embryonic day 9 (ED 9) to embryonic day 16 (ED 16) were stained with monoclonal antibodies against alpha-SCA, alpha-SMA, or desmin, while apoptosis was assessed using the terminal deoxyribonucleotidy transferase-mediated dUTP-digoxigenin nick-end labeling (TUNEL) assay. RESULTS: Between ED 11 and ED 12, the cardiomyocytes in the distal portion of the outflow tract were observed losing their myocardial phenotype without going into apoptosis, suggesting that trans-differentiation of cardiomyocytes into the cell components of the free walls of the intrapericardial ascending aorta and pulmonary trunk. The accumulation of alpha-SMA positive cells in the cardiac jelly began on ED 10 and participated in the ridge fusion and septation of the outflow tract. Fusion of the distal ridges resulted in the formation of the facing walls of the intrapericardial ascending aorta and pulmonary trunk. Fusion of the proximal ridges was accompanied by the accumulation of alpha-SMA positive cells into a characteristic central whorl, in which cell apoptosis could be observed. Subsequent myocardialization resulted in the formation of the partition between the subaortic and subpulmonary vestibules. CONCLUSIONS: The shortening of the embryonic heart outflow tract in mice may result not from apoptosis, but from the trans-differentiation of cells with cardiomyocyte phenotype in the distal portion of the outflow tract into the cell components of the free walls of the intrapericardial ascending aorta and pulmonary trunk. The primary roles of alpha-SMA positive cells in the septation and remodeling of the outflow tract may assure proper fusion of the outflow ridges and form the facing walls of the intrapericardial ascending aorta and pulmonary trunk.

Actins↗