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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 649 records · Page 36Linked to original sources
PubMed1976

Intracellular collagen fibrils in prolapsed ("floppy") human atrioventricular valves.

Ultrastructural study of prolapsed atrioventricular valves from five patients, one of whom also had the Marfan syndrome, disclosed granular cells that were characterized by numerous membrane-bound, electron-dense inclusions resembling those in the Hurler syndrome. Collagen fibrils were present within some of these inclusions. The intracellular collagen deposits may form as a consequence of abnormal interactions between newly secreted collagen and acid mucopolysaccharides.

Adolescent↗
PubMed1975

Cardiac pathology after aortic valve replacement using Hufnagel trileaflet prostheses: a study of 20 necropsy patients.

Necropsy observations are described in 20 patients dying between October 1967 and March 1973 after replacement of the aortic valve with a Hufnagel trileaflet prosthesis. Seven patients died within two months of operation and 13, between 2.1 and 58 months (average 22). Four of seven patients dying early had extensive prosthetic thrombus causing obstruction of one coronary arterial ostium in each. Of the 12 patients surviving six months or longer after valve replacement, death in eight resulted from degeneration (tearing) of the prosthetic cusps causing severe aortic regurgitation in each, and from thrombosis of the prostheses in three, probably causing prosthetic stenosis and defintely causing narrowing of at least one coronary ostium. Thus, prosthetic degeneration or thrombosis caused death in 11 of the 12 patients surviving six months or longer. In conclusion, this trileaflet aortic prosthesis, although similar in design to the normal aortic valve, is composed of materials not durable enough to withstand the stresses created by blood flow in this position.

Adult↗
PubMed1975

Systemic lupus erythematosus as a cause of severe mitral regurgitation. New problem in an old disease.

Clinical and morphologic observations in three patients with systemic lupus erythematosus and severe mitral regurgitation are described. Attention is called to the "healing" of Libman-Sacks endocarditis, an infrequent occurrence in patients with systemic lupus erythematosus in the era before steroid therapy. The mitral regurgitation in our patients appears to have resulted from "healing" of the Libman-Sacks vegetations by scarring and calcification. The healing is attributed to long-term corticosteroid therapy.

Adolescent↗
PubMed1975

Myocardial ultrastructure in patients with chronic aortic valve disease.

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severly degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.

Adolescent↗
PubMed1975

Cardiac pathology after valve replacement by disc prosthesis. A study of 61 necropsy patients.

Clinical and necropsy observations are described in 61 patients who had one or more cardiac valves replaced with a discoid prosthesis of the Hufnagel type. The most common (31 percent) cause of death among the 45 patients who died early (less than 65 days after operation) appeared to be prosthetic disproportion; that is, the prothesis was too big for the aorta or ventricular cavity into which it was inserted so that inadequate space was present between the margins of the disc and the endocardium of ventricle or intima of aorta. Prosthetic thrombosis occurred in only 3 of the 45 patients who died early, but poppet movement appeared considerably altered in each. In contrast, thrombi were observed on a prosthesis in 14 of the 16 patients who died late (4 to 47 months [average 21] postoperatively), but in none did the thrombi appear of sufficient size to alter poppet function. Escessive bleeding occurred in 11 (24 percent) of the 45 early deaths and was primarily related to the insertion of a patch in the root of the aorta. Uncorrected valvular disease either by itself or by its ability to alter function of the prosthesis appeared responsible for death in 6 (13 percent) of the 45 patients who died early and in 2 (6 percent) of the 16 who died late. Insertion of a mitral poppet disc in a patient with uncorrected aortic regurgitation, even of mild degree, may be hazardous because the aortic regurgitant jet stream may interfere with proper function of the mitral disc. Likewise, insertion of a poppet disc only in the aortic valve position in a patient with combined aortic and mitral regurgitation may considerably increase the degree of mitral incompetence because the aortic prosthesis is intrinsically obstructive. Disc wear or variance was observed in all but one prosthesis in place for more than 1 year. Although hemolytic anemia of significant degree was not observed in any of the 16 patients who died late, the occurrence of renal hemosiderosis in 13 of the 16 patients indicates that the poppet disc prosthesis is considerably traumatic to erythrocytes. Thus, this type of prosthesis is not an ideal substitute cardiac valve. It clots, despite anticoagulant therapy, it is intrinsically stenotic, portions of it, that is, the disc, degenerate, and it causes hemolysis to erythrocytes.

Adult↗
PubMed1975

Unruptured sinus of Valsalva aneurysm.

An unruptured congenital sinus of Valsalva aneurysm (behind the right aortic valve cusp) is described as an incidental necropsy finding in an 82 year old man. Review of previous reports on aneurysms involving only one of the three aortic sinuses discloses that few cases have been described, and that these lesions are rarely diagnosed during life. It is probable, however, that unruptured aortic sinus aneurysm (involving only one sinus) is more common than previous reports indicate, but that, among patients with congenital sinus aneurysm, rupture is likely to occur.

Aged↗
PubMed1975

Heterografts as aortocoronary bypass conduits in human beings.

Clinical and necropsy observations are described in a man in whom two sheep carotid arterial heterografts were inserted as aortocoronary bypass conduits 30 months before death, and in whom a canine saphenous vein heterograft was inserted several hours before death. All three grafts failed. The lumens of the sheep carotid arterial heterografts had closed by the time of catheterization 6 months after operation; at necropsy both grafts were totally occluded at their coronary and aortic ends and their media and adventitia were infiltrated by granulomatous inflammatory cells. Little information is available regarding the use of heterografts as coronary bypass conduits. Examination of previous reports describing heterografts for vascular reconstruction or bypass in both man and experimental animals and observations in our patient suggest that heterografts are unsatisfactory as aortocoronary bypass conduits.

Adult↗
PubMed1975

Dilatation of the mitral anulus. A rare cause of mitral regurgitation.

To confirm or deny the thesis that mitral anular dilatation is a cause of mitral regurgitation, this anulus was measured in 102 patients, 24 of whom had normal hearts and 78 of whom had dilated left ventricles, some associated with mitral regurgitation, others not. The circumference of the mitral anulus in the 24 patients with normal hearts averaged 9 cm (range 7 to 11 cm); in 24 patients with idiopathic cardiomyopathy of the ventricular dilated type, both with (12 patients) and without (12 patients) mild to moderate regurgitation, 11 cm (range 10 to 14 cm); and in 31 patients with severe mitral regurgitation, 12 cm (range 8 to 18 cm). Among the latter 31 patients with severe mitral regurgitation, the anulus was only mildly dilated in the 15 with rheumatic disease (average 11 cm) and in the six with ruptured chordae tendinease on previously normal valves (average 10 cm); in contrast, in the 10 patients with floppy mitral valves with or without the Marfan syndrome the mitral anulus was greatly dilated (average 15.5 cm). Thus, only in patients with floppy valves with or without the Marfan syndrome or both does anular dilatation by itself appear great enough to cause mitral regurgitation. It appears, therefore, that dilatation of the mitral anulus is a rare cause of mitral regurgitation and that abnormality of the fibrous skeleton of the heart is necessary for the mitral anulus to dilate enough to cause mitral regurgitation.

Adult↗
PubMed1975

The hypertensive diseases. Evidence that systemic hypertension is a greater risk factor to the development of other cardiovascular diseases than previously suspected.

This report summarizes the clinical frequencies of systemic hypertension and necropsy evidence of cardiomegaly in various cardiovascular conditions (Table I), termed "the hypertensive diseases" because of their frequent association with systemic hypertension. Although long recognized as a major risk factor, systemic hypertension appears to be an even greater risk factor to the development of various cardiovascular conditions than previously appreciated. Hypertension by itself appears to be the sole underlying factor in most cases of nontraumatic cerebral arterial or aortic (dissection = partial rupture) rupture. In association with hyperlipidemia, hypertension clearly accelerates atherosclerosis and its devastating consequences.

Angina Pectoris↗
PubMed1975

The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients.

The natural history of the cardiovascular manifestations of systemic lupus erythematosus (SLE) have been altered by corticosteroids which exert their own cardiovascular effects. This study describes clinical and necropsy observations in 36 corticosteroid-treated patients with SLE and compares them to necropsy observations in patients with SLE reported before the use of corticosteroid therapy. The 36 patients averaged 32 years of age, and 33 were women. Systemic hypertension was present in 25 (69 per cent) and left ventricular hypertrophy in 23 (64 per cent) patients. Hypertension was twice as common in the 19 patients who received this drug for more than 12 months (average 38 months) than in the 17 patients who received this drug for less than 12 months (average 6 months), and was almost five times more common among our patients than in patients with SLE in the presteroid era. Congestive cardiac failure occurred in 15 patients (43 per cent), eight times more frequent than that reported in noncorticosteroid-treated patients with SLE. Subepicardial and myocardial fat was increased in all 36 patients. Lupus carditis was similar in frequency but differed morphologically in our patients compared to those not treated with corticosteroids. Libman-Sacks-type endocardial lesions, present in 18 (50 per cent) of our patients, were smaller, fewer in number, univalvular rather than multivalvular, and mainly left-sided. Most verrucae were either partly or completely healed, and some were calcified. Pericarditis, present in 19 (53 per cent) patients, was predominantly of the fibrous type. Myocarditis was present in three patients, each of whom also had endocarditis and pericarditis. The lumen of at least one of the three major coronary arteries was narrowed more than 50 per cent by atherosclerotic plaques in 42 per cent of the 18 patients who received corticosteroids for more than 1 year, but in none of the 17 patients who received corticosteroids for less than 1 year. Four of the eight patients with narrowed coronary arteries had myocardial infarcts. Although vital to the management of SLE, corticosteroids have an over-all deleterious effect on the heart. Systemic hypertension and left ventricular hypertrophy appear or, when present, worsen; congestive cardiac failure increases; epicardial apartment of Me

Adipose Tissue↗
PubMed1975

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

Ultrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, or 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) to hypertrophic changes, abnormalities of cellular and myofibrillar orientation, and degenerative alterations were determined. Changes directly related to hypertrophy were: cell diameters greater than 20 mu, irregular cell shape, lobulated nuclei, multiple intercalated discs, dilated T tubules, abnormal Z bands, and increased numbers of ribosomes. Abnormalities of cellular or myofibrillar orientation were focal in distribution and occurred in 12 patients, most of whom had elevated RVEDP, decreased PAO2, markedly enlarged cells, and interstitial fibrosis. Interstitial fibrosis was prominent in 19 patients and was associated with cellular hypertrophy, elevation of RVEDP, and increased age of the patients. Degenerative changes (myofibrillar lysis, abnormally small mitochondria, myelin figure formation, and proliferation of sarcoplasmic reticulum in cardiac muscle cells ocurred in six patients and correlated with increased age, decreased PAO2, and elevated RVEDP. Mitochondria containing glycogen deposits were present in 17 patients, most of whom had decreased PAO2. The variability of morphologic manifestations of chronic cardiac hypertrophy and the relationships of hypertrophic changes to orientation abnormalities and degenerative alterations are discussed.

Adolescent↗
PubMed1975

Late postoperative anatomic observations after insertion of Hufnagel caged-ball prostheses in descending thoracic aorta.

Clinical and necropsy observations are described in two patients who died 11 and 13 years, respectively, after implantation of Hufnagel prostheses (the first ever used successfully in humans to treat cardiac valve disease) in descending thoracic aorta. Despite the long implantation periods, there was no evidence of prosthetic degeneration or thrombosis or intravascular hemolysis. Although approximately 4000 Hufnagel descending aortic prostheses were distributed by the manufacturer for human use, data in only 55 patients in whom these prostheses were inserted were found in previous publications, and 26 of them had died. Of the 13 late deaths previously reported, no evidence of prosthetic degeneration or thrombosis was described in the three patients surviving greater than 3 years (8, 10, 12.5 years, respectively). Since neither our patients nor any of the other three reported long-term survivors had prosthetic-related complications and since the dangers of excising the descending aortic prosthesis are considerable, it appears most reasonable, as a rule, not to remove the descending aortic prosthesis at any time in these patients if aortic valve replacement is subsequently performed.

Adult↗
PubMed1975

Endocardial papillary elastofibromas. Histologic, histochemical, and electron microscopical findings.

The organization of cellular and extracellular components appeared similar and was distinctive in three endocardial papillary elastofibromas studied. Each tumor papilla contained (1) a dense, central core of collagen and elastic tissue, (2) a peripheral, myxomatous layer with deposits of acid mucopolysaccharides, and (3) an overlying, hyperplastic layer of endothelial cells. Ultrastructural study of one tumor showed that the cells in all three zones had numerous cytoplasmic filaments, 100 Angstroms in diameter, and dilated cisterns of endoplasmic reticulum; endothelial cells also had intercellular junctions and numerous pinocytotic vesicles. The myxomatous stroma varied from amorphous to fibrillar, and the collagenous cores showed focal degeneration. The name "endocardial papillary elastofibroma" is suggested to emphasize those features which are most conspicuous and which serve to differentiate this tumor from myxoma.

Endocardium↗
PubMed1975

Long-term morphologic and hemodynamic evaluation of the left ventricle after cardiopulmonary bypass. A comparison of normothermic anoxic arrest, coronary artery perfusion, and profound topical cardiac hypothermia.

In order to assess the long-term effects of cardiopulmonary bypass (CPB) in combination with pupular methods of myocardial protection, 37 dogs were placed on CPB for 100 minutes with the use of a bubble oxygenator without hemodilution. A separate group (I) of eight normal dogs served as a control for assessment of hemodynamic changes. The operative groups were as follows: II, continuous coronary perfusion with an empty, beating heart for 60 minutes at 35 degrees C.; III, hypothermic anoxic arrest (aortic occlusion) for 60 minutes with topical cold saline lavage (4 degrees C.); IV, anoxic arrest for 60 minutes at 35 degrees C. Subgroups of Groups III and IV received intracoronary perfusion with Ringer's lactate or Sacks' solution during aortic occlusion and were compared with those animals receiving no perfusion. Survival in Groups II and III was significantly better than in Group IV (82 and 92 per cent vs. 45 per cent). Coronary perfusion with Ringer's lactate or Sack's solution did not influence survival. The 23 survivors from all groups underwent left heart catheterization and LV cineangiography 5 months after operation. All three operative groups had significant elevation of LVEDP and depression of maximum developed dp/dt when compared with normal dogs. Ejection fraction was significantly depressed in Groups III and IV, and there was evidence of left ventricular hypokinesia and/or akinesia in all three operative groups. Differences in function between Groups II, III, and IV were not significant. The use of intracoronary solutions during anoxic arrest did not significantly influence these functional alterations. Evidence of subendocardial fibrosis was found in each of the operative groups, with the most marked changes found in the normothermic arrest group. Moderate fibrosis was present, however, in some survivors in both the continuous coronary perfusion and topical hypothermic arrest groups. These data indicate that although survival is greatly enhanced when coronary artery perfusion or topical hypothermia is used, neither method prevents chronic deterioration in ventricular function nor the development of subendocardial fibrosis.

Animals↗