Left Ventricular Endocardial Fibroelastosis Research Articles

Morphological variations in pulmonary atresia with intact ventricular septum.

The morphological features of a series of 37 specimens of pulmonary atresia with intact ventricular septum were reviewed with particular emphasis on features which might influence the results of pulmonary valvotomy. The degree of right heart hypoplasia was quantified by measuring right and left heart dimensions and comparing them with 20 normal infant hearts. Right ventricular cavity size was usually smaller than normal but constituted a spectrum ranging from tiny to a dilated ventricle larger than normal. There was a positive correlation between triscuspid annular size and right ventricular size but no correlation between the size of the pulmonary artery and the right ventricle. Successful pulmonary valvotomy with subsequent adequate right ventricular function would have been precluded by a tiny right ventricular cavity or infundibular atresia in 14 specimens and by severe tricuspid stenosis or regurgitation in an additional 4. Severe right or left ventricular endocardial fibroelastosis may have adversely affected ventricular function in several others. Ten specimens displayed convex bulging of the left ventricular septal surface. If these these anatomical findings are representative for the condition as a whole, they provide a good explanation for its disastrous prognosis.

Pathologic anatomy of cardiac valve replacement: A study of 224 necropsy patients

Necropsy observations are described in 224 patients who died from 1963 through October 1972 after replacement of one or more cardiac valves by prostheses: 128 patients died within 2 mo of operation, and 96 patients at later periods up to 116 mo. Of the 281 valves replaced, Starr-Edwards prostheses were used in 250. Prosthetic dysfunction continues to be the most common cause of death (approximately 30%) in patients dying either early or late after valve replacement. It is hoped that the metal balls and cloth-covered struts will decrease the late frequency of prosthetic dysfunction, but not enough time has elapsed for this altered prosthesis to be tested adequately. Present data indicate that the frequency of clinical embolism and prosthetic thrombosis after use of the clothcovered prostheses is less than that observed in the noncloth-covered prostheses. Cloth wear with possible dislodgement and increased intravascular hemolysis, however, remains of concern. The frequencies of peribasilar fistulae, infection at sites of attachment of prostheses, and aneurysm formation at sites of excision of left ventricular papillary muscles are decreasing. It appears that secondary left ventricular endocardial fibroelastosis after mitral replacement, aortic root and coronary ostial intimal proliferation after aortic valve replacement and calcification of valve anuli will only increase with time after valve replacement. The latter changes may prove to be major long-term problems. It is clear after a decade of cardiac valve replacement that the ideal valve prosthesis is not yet available, or if available, not adequately tested. Thus, valve replacement at this time must be reserved for the patient severely disabled by cardiac valve disease.

Fetal cardiac failure resulting from congenital anomalies of the heart

Cardiac failure during fetal life is uncommon, even among subjects with cardiovascular malformations. The occurrence of fetal cardiac failure appears to depend upon the presence of some condition which places a burden upon the right ventricle. Classically, premature closure of the foramen ovale is such a condition. In the three cases of fetal cardiac failure reported the malformations represented were (1) right ventricular endocardial fibroelastosis, (2) Ebstein's malformation of the tricuspid valve, and (3) left ventricular endocardial fibroelastosis and mitral insufficiency.