Rupture of the ventricular septum as a complication of myocardial infarction.
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Aged↗
Biomedical subjects
J J Fenoglio
Publications and source records attributed to J J Fenoglio.
Right atrial ultrastructure in congenital heart disease. II. Atrial septal defect: effects of volume overload.
Portions of operatively resected right atrium from 15 patients with atrial septal defect were studied ultrastructurally to determine whether the cell hypertrophy in the right atrium of patients with increased right atrial blood flow and increased right atrial pressure is caused by the increased blood flow. In 12 patients with normal right atrial mean pressure but increased right atrial blood flow the atrium was dilated but no atrial arrhythmias were noted clinically. Ultrastructurally, the atrial myocardial cells in these patients were normal, measuring 6 to 10 mu in diameter, and there was no evidence of cell hypertrophy or degeneration. The remaining three patients had elevated right atrial mean pressure and increased right atrial blood flow. Ultrastructurally, the atrial myocardial cells in all three patients were hypertrophied, and two patients had evidence of focal cell degeneration; the atrium was markedly dilated, but atrial arrhythmias were not noted. The lack of cell hypertrophy in the right atrium of the 12 patients with increased blood flow but normal mean pressure suggests that in congenital heart disease volume overload alone does not lead to cell hypertrophy of the right atrial myocardium.
Adult↗
Drug related vasculitis. Clinicopathologic correlations in 30 patients.
Drug related vasculitis has variously been described as necrotizing hypersensitivity or allergic angiitis or microscopic panarteritis nodosa. We reviewed tissue sections from 30 patients with validated drug hypersensitivity and vasculitis in order to precisely define this entity. No evidence of necrotizing vascular lesions or of fibrinoid associated with necrosis was found. The vascular lesions in all 30 patients involved small arteries, arterioles, capillaries, and venules. The inflammatory infiltrate consisted primarily of mononuclear cells and prominent numbers of eosinophils and was present in all three layers of the involved vessel walls. Clinically the patients developed either localized or systemic vasculitis, which could not be predicted on the basis of the associated drug. The findings of a skin rash, fever, or eosinophilia and the development of symptoms consistent with a hypersensitivity reaction while medication was being taken were all suggestive of the diagnosis of drug related vasculitis.
Adolescent↗
Time course of infarct growth toward the endocardium after coronary occlusion.
Transmembrane potentials and ultrastructure of subendocardial Purkinje and ventricular muscle fibers, isolated 1, 3, 5, 6, 14, and 24 h after coronary occlusion were investigated. Action potentials were recorded from progressively fewer layers of muscle cells as the age of the infarct increased. At 14 h little viable muscle remained. The decrease in the number of electrophysiologically viable muscle fibers correlated with structural evidence that the infarct moved with time toward the endocardial surface until only viable Purkinje fibers remained. Purkinje and surviving ventricular muscle fibers demonstrated a progressive decrease in resting potential, action potential amplitude, and Vmax and a progressive increase in action potential duration. Spontaneous diastolic depolarizations were found in Purkinje fibers only in 24-h infarcts and occasionally in cells deep to the endocardial surface, which may have been muscle cells. We hypothesize that during the first 24 h after coronary occlusion arrhythmias originate near the interface of infarcted and ischemic myocardium. As this interface moves toward the endocardium, this site of origin of arrhythmias moves with it until the Purkinje network is reached.
Animals↗
Ultrastructure and transmembrane potentials of cardiac muscle in the human anterior mitral valve leaflet.
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Acetylcholine↗
Protracted ventricular tachcardia induced by premature stimulation of the canine heart after coronary artery occlusion and reperfusion.
The effects of premature ventricular stimuli were studied in two groups of dogs with infarcts, one group subjected to permanent occlusion of the left anterior descending coronary artery and the other to temporary occlusion for 2 hours. In dogs with permanent occlusion, spontaneous ventricular arrhythmias occurred after 3-6 hours. In 13 dogs with temporary occlusion, ventricular arrhythmias occurred immediately after reperfusion and then persisted. In five dogs with temporary occlusion, ventricular arrhythmias did not occur spontaneously until 13-15 hours after occlusion. On days 2-9 after surgery, after sinus rhythm had returned, the ventricles of each awake dog were stimulated. After permanent occlusion, premature stimuli occurring on the T wave usually induced from one to 10 repetitive responses on days 2-4. Protracted ventricular tachycardia (lasting greater than 10 seconds) was induced in only two of 10 dogs. The response to premature stimuli was similar after temporary occlusion when ventricular arrhythmias did not occur spontaneously until 13-15 hours after occlusion. Protracted tachycardia was not induced. In the dogs with temporary occlusion, which initially had continuous arrhythmias, premature stimuli occurring on the T wave on days 3-5 after surgery induced both repetitive responses and protracted ventricular tachycardia. Stimuli applied to the ventricles during tachycardia terminated it. Histological studies on all infarcts showed that, after permanent occlusion, necrosis was uniform; after temporary occlusion, viable myocardium survived in the necrotic region. These salvaged myocardial fibers may provide reentrant pathways, causing long-lasting tachycardia.
Animals↗
Right atrial ultrastructure in congenital heart disease. I. Comparison of ventricular septal defect and endocardial cushion defect.
Ultrastructural studies were performed on portions of the operatively resected right atrium from six patients with a ventricular septal defect and six patients with an endocardial cushion defect. The six patients with a ventricular septal defect had normal right atrial mean pressure and no evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients appeared normal and measured 6 to 12 mu in diameter. The six patients with an endocardial cushion defect had elevated right atrial mean pressure and evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients were generally larger than 12 mu in diameter. The cells were irregular and had multiple and occasionally widened intercalated discs. In addition, there were degenerative changes in two patients with markedly increased atrial pressure. These changes included extensive loss of contractile elements, aggregation of small irregular mitochondria and proliferation of tubules of the sarcoplasmic reticulum. The structural changes suggest that hypertrophy of the right atrium may be secondary to volume overload of the atrium, whereas degenerative changes may be secondary to increased right atrial pressure.
Basement Membrane↗
Congenital aortic stenosis secondary to dysplasia of congenital bicuspid aortic valves without commissural fusion.
The hearts of nine children with clinical evidence of congenital valve stenosis and a congenital bicuspid aortic valve were reviewed. Aortic stenosis was diagnosed on the basis of cardiac catheterization data in four patients, operative findings in two and auscultatory findings in three. The patients were 1 month to 9 years old; six were male and three female. In each patient the two commissures of the valve were free to the aortic wall. The cusps were thickened, rolled and redundant; microscopic studies revealed that they consisted of immature loose connective tissue consistent with a dysplastic or incompletely differentiated valve. The valve orifice was obstructed by the dysplastic cusps, and dysplastic changes rather than the commissural fusion were responsible for the observed aortic stenosis. These valves do not appear amenable to valvotomy because obstruction is due to the abnormal valve tissue. These findings may explain the occasional poor results of valvotomy in infants and children with congenital aortic valve stenosis.
Aortic Valve↗
Ultrastructure of the mesothelioma of the atrioventricular node.
In order to determine the histogenesis of tumors of the atrioventricular node, so-called conduction tumors, two such tumors were serially blocked for electron microscopy. Ultrastructurally these tumors were composed of nests of cells arranged in small channels and tubules set in a connective tissue stroma. The cells lining the tubules were flattened or low cuboidal and had abundant microvilli over the lumen surface. The cells were joined by specialized junctions along their lateral adjacent borders, especially at the luminal surfaces, and intercellular spaces delineated by specialized junctions were frequent. Microvilli, intercellular spaces bounded by tight junctions, and complex intercellular junctions are features of mesothelial cells, and especially of benign mesothelioma of the genital tract. These results strongly suggest that the cardiac conduction tumor is derived from mesothelial cells and is in fact a mesothelioma of the atrioventricular node.
Atrioventricular Node↗
Cardiomyopathy with skeletal myopathy.
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Adult↗
Congenital bicuspid aortic valve after age 20.
The bicuspid aortic valve is recognized as a frequent cause of aortic stenosis in adults. Aortic stenosis has been reported to occur in as many as 72 percent of adults with a congenital bicuspid aortic valve, with peak incidence occurring in the 5th and 6th decades of life. Review of the clinical records of 152 patients aged 20 years and older found to have a bicuspid aortic valve at autopsy revealed aortic stenosis in only 28 percent. The incidence of aortic stenosis increased progressively with age; 46 percent of patients over age 50 years and 73 percent over age 70 years had some degree of stenosis. The stenotic valves were obstructed by nodular, calcareous masses but commissural fusion was present in only eight cases. The largest group of patients in the series (40 percent) died of infective endocarditis; 77 percent of these were under age 50 years. Primary aortic regurgitation without infective endocarditis was uncommon. Thirty-two percent of the patients in this series had an apparently normally functioning aortic valve, and this rate remained relatively constant with increasing age; 37 percent of patients over age 50 years and 27 percent over age 70 years had an apparently normal valve. The bicuspid aortic valve in patients over age 20 does not invariably become stenotic or insufficient.
Adult↗
Ultrastructure of a cardiac rhabdomyoma.
Electron microscopic study of a cardiac rhabdomyoma removed at open heart operation revealed large rounded or polygonal cells that contained large amounts of monoparticulate glycogen. Myofibrils in these cells were few and located either subjacent to the plasma membranes or radiating from central areas. Leptofibrils and masses of anomalous Z band material were abundant. Shallow tubular sarcolemmal invaginations and elements of free and junctional sarcoplasmic reticulum were associated with the myofibrils. Desmosomes and nexuses were evident in intercellular junctions, which were extensive and randomly distributed throughout the cell surfaces. It is concluded that cardiac rhabdomyomas probably are hamartomas.
Cell Membrane↗
Pericardial cysts. A radiologic-pathologic correlation and review.
Pericardial cysts are generally described as round radiodensities typically found at the right cardiophrenic angle in asymptomatic individuals. A review of all cases of pericardial cysts from the files of this Institute reveals that approximately one third of the cysts are found in other locations and that approximately one third of patients have symptoms of chest pain, dyspnea, or persistent cough. The radiographs of 41 patients show that in all but 6 of the cases the cyst is visualized as a round radiodensity touching both the hemidiaphragm and the anterior chest wall. Surprisingly, 15 of the 41 occurred on the left border of the heart. The six cysts significantly above the diaphragm were difficult to diagnosis radiologically and were usually mistaken for thymomas or pulmonary masses; two such cysts caused bronchial obstruction. In general, the possibility that a mass in either anterior cardiophrenic angle is a pericardial cyst should be strongly considered, even if the mass is on the left side and even if the patient is symptomatic.
Adolescent↗
Quadricuspid semilunar valves.
Forty-seven cases of quadricuspid semilunar valves which were autopsied were reviewed. The ratio of quadricuspid pulmonic valve to quadricuspid aortic valve was 5:1. Among the 35 patients with quadricuspid pulmonic valves, there were ten patients with clinical and pathologic evidence of coexisting congenital cardiac defects, eight of which resulted in severe cyanotic heart disease in infancy. In the remaining 25 patients the quadricuspid pulmonic valve was an incidental finding at autopsy. Three of the seven patients with quadricuspid aortic valves had aortic insufficiency, while the remaining four had no other clinical or pathologic evidence of congenital heart disease.
Adult↗
Myocardial changes in malignant hyperthermia.
Although consideral information is available concerning the structural and biochemical changes in the skeletal muscles of patients with malignant hyperthermia, little is known of the cardiac changes in this disease. However, ventricular fibrillation and cardiac arrest are frequent in these patients. In 3 patients with malignant hyperthermia, contraction bands and foci of myofiberlysis were found in the heart at necropsy. Ultrastructurally, areas of myofiber overstretching adjacent to contraction bands and foci of extensive myofiberlysis were associated with disruptions of the sarcolemma. Similar ultrastructural findings have been reported in the skeletal muscles of these patients and are thought responsible for the hyperkalemia which is a constant feature of malignant hyperthermia. Our findings suggest that the ventricular arrhythmias, frequent in this disease, are the result of direct damage to cardiac muscle rather then secondary to elevated plasma levels of potassium.
Adult↗
Cardiac rhabdomyoma: a clinicopathologic and electron microscopic study.
Cardiac rhabdomyomas are rare tumors of infancy. In a series of 36 patients 78 percent were under 1 year of age, and only one patient was over age 15 years. Ninety percent of the rhabdomyomas were multiple and occurred with nearly equal frequency in the right and left ventricles. Although reportedly infrequent in the atria, rhabdomyomas involved either one or both atria in 30 percent of patients. In 50 percent of patients at least one of the tumor masses was intracavitary and obstructed 50 percent or more of one of the cardiac chambers or valve orifices. Symptoms referable to obstruction of intracardiac blood flow were present in nine patients, none of whom had tuberous sclerosis, and all of whom would appear to have been good surgical candidates. Histologically the rhabdomyomas were composed of classic "spider cells". Electron microscopic studies revealed scattered bundles of myofibrils ringing these cells and radiating toward the center; glycogen was present both free in the cytoplasm and within mitochondria. Distinct intercellular junctions resembling intercalated discs with well defined desmosomes and nexuses were present. Many of the cells contained leptofibrils, arranged either peripherally or in spiraled clusters in the center of the cell. Rhabdomyomas derive from cardiac muscle cells and appear to represent hamartomas rather than true tumors.
Adult↗
Structural basis of ventricular arrhythmias in human myocardial infarction: a hypothesis.
The present study was undertaken using light and electron microscopic techniques to determine whether Purkinje fibers survive in the subendocardial region of anteroseptal infarcts in humans. Tissue was obtained for this purpose from 11 patients with 12 documented infarctions at the time of autopsy; six patients died within 72 hours of the infarction and five had healed infarcts. Seven of the 11 patients had ventricular arrhythmias. Light microscopic study indicated that intact cells with a normal appearance remained on the subendocardial surface, although the underlying ventricular muscle either was necrotic or was replaced by fibrous tissue. Electron microscopy demonstrated that these intact surviving cells over the surface of the infarct had few randomly oriented myofibrils, abundant glycogen, and other characteristics of Purkinje fibers. These cells could be readily distinguished from normal or infarcted ventricular muscle cells. Purkinje fibers, the most peripheral part of the conduction system, survive in extensive anteroseptal infarcts and may be the site of origin of ventricular arrhythmias.
Animals↗