Coronary and endocardial fibroelastosis of the ventricles in the hypoplastic left and right heart syndromes [proceedings].
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Coronary Disease↗
Biomedical subjects
C E Essed
Publications and source records attributed to C E Essed.
Coronary and endocardial fibroelastosis of the ventricles in the hypoplastic left and right heart syndromes.
In an autopsy material of 29 cases of the hypoplastic left heart syndrome coronary fibroelastosis was found in 1 case, endocardial fibroelastosis in 8 cases. Figures for 10 cases of the hypoplastic right heart syndrome were 6 cases of coronary fibroelastosis and 1 case of endocardial fibroelastosis. Age ranged from stillborn up to 11-1/2 months. Coronary and endocardial fibroelastosis seemed to be mutually exclusive localizations of congenital fibroelastosis since in our material they did not occur together in the same hearts. In hypoplastic right hearts coronary fibroelastosis was either restricted to the right coronary artery (right circumflex and posterior interventricular branch), or it was found also in the left coronary artery (anterior interventricular branch), with the most serve affections always being situated in the right one. In the only case of coronary fibroelastosis among the hypoplastic left hearts the condition was limited to the anterior interventricular branch of the left coronary artery which communicated with the hypoplastic left ventricle by a fistula. Coronary fibroelastosis was exclusively found in branches supplying the hypoplastic right ventricle and/or in a branch connected by a fistula to the hypoplastic left or right ventricle. Endocardial fibroelastosis was generally found in hypoplastic left ventricles with either no outflow or with severe outflow obstruction. A theory concerning the aetiology of both coronary and endocardial fibroelastosis of the hypoplastic ventricles is proposed. It is argued that development of fibroelastosis may in both localizations be caused or favoured by the coincidence of two factors: abnormal haemodynamic conditions and poor oxygenation of blood and tissues. Observations made in a reference material of 35 hypoplastic left and 24 hypoplastic right hearts were in accordance with this view.
Arteries↗
Echocardiographic diagnosis of overriding tricuspid valve in a child with Ebstein's anomaly.
The M-mode echocardiographic diagnosis of overriding tricuspid valve rests on the ability to demonstrate simultaneously two atrioventricular valves with no intervening septal echo [6, 13]. When scanning inferiorly toward the body of the ventricles, a distinct septal echo at the level of the midportion of the tricuspid valve can be detected. Here we report a case of Ebstein's anomaly, pulmonary stenosis, and ventricular septal defect (VSD), in which the echogram falsely indicated an overriding tricuspid valve.
Child, Preschool↗
MR imaging in assessment of cardiac transplant rejection in humans.
To evaluate the efficacy of myocardial T2 values in the assessment of allograft rejection, we performed magnetic resonance (MR) imaging at 0.5 T serially in seven cardiac transplant recipients and singly in seven normal volunteers. Cardiac-gated multi-echo spin echo images were obtained; T2 values were estimated by a two-point method from regions of interest in the myocardium. Patients underwent MR and cardiac biopsy at various times after transplantation. Forty-two patient exams were performed. All biopsies showed either no rejection or early stages of rejection: grade 0 in 8 examinations, grade 1 in 28, and grade 2 in 6. Myocardial T2 values in patients in early stages of cardiac rejection were slightly higher (but not statistically significant) than those in non-rejecting patients and normal volunteers. Although this study did not allow prospective detection of cardiac rejection in our patient group, it demonstrated a trend toward higher T2 values at higher biopsy grades that may indicate an ability to assess more severe stages of transplant rejection.
Adult↗
The effect of nifedipine on ischemia-induced changes in the biochemical properties of isolated sarcolemmal vesicles and the ultrastructure of myocardium.
To investigate whether slow Ca2+ channel blockers protect against development of changes in properties of the sarcolemma and in the tissue ultrastructure during myocardial ischemia, nifedipine was administered prior to occlusion (up to 3 hours) of the left anterior descending coronary artery in anesthetized pigs. Intravenous doses which reduced arterial blood pressure by 20-25%, had no effect on the time-dependent reduction of Ca2+-calmodulin and cyclic AMP-dependent 32P incorporation into sarcolemmal phospholamban-like protein. Nifedipine blocked the reduction in the activity of sarcolemmal 5'-nucleotidase. Nifedipine had no significant effect on the long-chain fatty acylcarnitine accumulation in sarcolemma. A marked delay in the appearance of ultrastructural indicators of irreversible tissue injury in subepicardial myocardium was observed, when nifedipine was infused. Particularly the reduced appearance of electron-dense bodies in mitochondria suggested a reducing effect of nifedipine on cellular net gain of Ca2+. Apparently, ischemia-induced loss of the ability of the proteinkinases to incorporate phosphate into sarcolemmal phospholamban-like protein is not a process secondary to Ca2+ overload of the myocardium. The involvement of accumulation of long-chain fatty acylcarnitine within the sarcolemma may also be excluded. The membrane defect as indicated by a change in phosphorylation-mediated control of Ca2+ transport may itself be associated with the development of ischemia (-reperfusion)-induced Ca2+ overload.
5'-Nucleotidase↗