Ultrastructure of crista supraventricularis muscle in patients with congenital heart diseases associated with right ventricular outflow tract obstruction.

Abstract

SUMMARYUltrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, of whom 54 had obstruction to right ventricular outflow. Relationships of anatomic diagnosis, age, peripheral arterial oxygen saturation (PAO2), peak right ventricular systolic pressure gradient and right ventricular end-diastolic pressure (RVEDP) Patients Studied Clinical and hemodynamic data on the 59 patients (age range, 3 to 53 years) with congenital heart disease are shown in table 1. These patients were divided into two groups: those without obstruction to right ventricular outflow (five patients), and those with obstruction to right ventricular outflow (54 patients). In 51 of the latter 54 patients the obstruction was due, at least in part, to hypertrophy of the crista supraventricularis; in one of the three remaining patients the obstruction was due to isolated pulmonic valvular stenosis (patient #54), and in the other two patients, to discrete, fibrous, subvalvular pulmonic stenosis (patients #56 and 57). Systemic-pulmonary arterial shunts had been previously performed in 20 patients, and closed pulmonary valvulotomy with infundibular resection in two of the 59 patients (table 1).

An ultrastructural basis for electrocardiographic alterations associated with Duchenne's progressive muscular dystrophy.

“…The various conditions that produce myofibrillar lysis are customarily divided into three different groups8-depending on the class of myofilament, either myosin (thick filaments) or actin (thin filaments), that is primarily affected. Preferential loss of thin filaments has been typically associated with hypokalemiall with multiple episodes of hypoxia,2 and with the use of antimalarial drugs such as plasmocid.2' By contrast, preferential loss of thick filaments has been reported in the following conditions: congenital heart diseases associated with an obstruction of the right ventricular outflow tract; 22 28 and others.29 The myofibrillar loss in our patients with Duchenne's muscular dystrophy, however, involved both thick and thin filaments. In areas of minimal involvement, the absolute number of myofilaments was decreased, producing a diffuse pattern.…”

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

“…Ultimately, this heterogeneity may dictate differences in pathophysiological response of various neuronal regions (60). As with neuronal tissue studies suggest that mitochondrial spatial location within the myocyte may be associated with a particular response to physiological and pathological stimuli (43,55,65,83,131). With the pioneering development of mitochondrial isolation techniques designed to sequentially fraction spatially distinct subpopulations of mitochondria using both mechanical and enzymatic procedures (96), efforts to define their individual roles in various pathological conditions has been actively pursued.…”

Ultrastructural artefacts in biopsied normal myocardium and their relevance to myocardial biopsy in man.

“…It should be pointed out too that this stricture applies equally to myocardial tissue removed at necropsy from sites that at an earlier time had been subjected to surgical manipulation or other mechanical interference (Reichenbach and Benditt, 1970;Bulkley and Hutchins, 1977). It is moreover unsatisfactory simply to eliminate any tissue that shows these changes assuming them to be artefact as some have (Jones et al, 1975), because they may represent a real pathological change. There is the further danger that minor changes that are in fact artefact are not recognised as such and then included in the interpretation as representative of pathological change (Jones et al, 1975, fig 4b)-where artifactual light and dark cells are shown but not commented on.…”

“…It is moreover unsatisfactory simply to eliminate any tissue that shows these changes assuming them to be artefact as some have (Jones et al, 1975), because they may represent a real pathological change. There is the further danger that minor changes that are in fact artefact are not recognised as such and then included in the interpretation as representative of pathological change (Jones et al, 1975, fig 4b)-where artifactual light and dark cells are shown but not commented on.…”