Myocarditis. A histopathologic definition and classification.
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Biopsy↗
Biomedical subjects
S M Factor
Publications and source records attributed to S M Factor.
Intrinsic connective tissue abnormalities in the heart muscle of cardiomyopathic Syrian hamsters.
Significant connective tissue abnormalities occurring in hearts of cardiomyopathic Syrian hamsters are reported. These abnormalities include a pronounced loss of the intrinsic connective tissue skeletal framework around foci of myocytolytic necrosis within the non-necrotic myocardium. These changes were demonstrated by a silver impregnation technique, and they were confirmed by scanning electron microscopy. Quantitation demonstrated more than a twofold increase in the area of ventricular wall affected by pathologic changes, when the connective tissue alterations were included with the myocardial necrosis. In addition, the authors also observed focal, thick "tethering" connective tissue fibers at the termini of necrotic lesions, seemingly connecting them to normal muscle. These connective tissue abnormalities may contribute to the progressive loss of ventricular function that occurs in this model of cardiomyopathy. They may permit greater wall thinning than would occur with focal necrosis alone, and they may increase focal mural stiffness in the tethered regions. Further investigation of the pathogenesis of these changes and their mechanical significance is indicated.
Animals↗
Lymphoma with primary cardiac manifestations.
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Aged↗
Comparative study of calcification in the T6-treated and standard Hancock-I porcine xenografts: experimental study in weanling sheep.
We compared the morphological findings in 15 young sheep in which standard Hancock-I cardiac bioprostheses (7 animals) and T6-processed Hancock-I (8 animals) were implanted in the tricuspid position. The animals were sacrificed at intervals from 8 to 47 weeks after valve replacement. No valvular infection was detected. Six of the 7 untreated valves and 5 of the 8 T6-processed valves in the tricuspid position showed calcific deposits in the radiographic examination. Roentgenograms from all specimens showed a fairly uneven distribution of the mineralization sites with the commissures being the structure most frequently involved. Calcium in the aortic wall was more frequent in the T6-processed group while right coronary leaflet involvement more frequent in the control group. Histologic evaluation confirmed the above data and showed a fibrotic reaction with granulomatous degeneration of the muscular shelf in all valves. Comparison of linear regression lines of the evolution of tissue calcium content with time showed no statistically significant difference between the 2 groups. Under the conditions of this study, the T6-treatment does not reduce the extent of calcification in the Hancock-I porcine xenograft after implantation in the tricuspid position in young sheep.
Animals↗
Microvascular spasm as a cause of cardiomyopathies and the calcium-blocking agent verapamil as potential primary therapy.
The origin of cardiomyopathies, a major cause of cardiac disability and death, has been largely unexplained. Pathologic features, common to all cardiomyopathies independent of origin, include ventricular hypertrophy and diffuse scarring with variable amounts of ventricular dilatation. This problem was studied experimentally in 2 models of congestive cardiomyopathy: the hereditary cardiomyopathic Syrian hamster and the hypertensive-diabetic rat. In both the genetic and the acquired disease models, there is focal myocytolytic necrosis followed by healing with focal scars, ventricular wall hypertrophy, ventricular dilatation with congestive heart failure and, ultimately, death. In view of the heterogeneous pathologic features of both diseases, silicone rubber perfusions have been used to study the microcirculation of the heart in these animals; microvascular spasm has been demonstrated early in the disease associated with small areas of myocytolytic necrosis that undergo subsequent fibrosis. Reactive hypertrophy then ensues as a compensatory response to this myocellular necrosis; it is the combination of cell loss and slowly decreasing contractility resulting from the reactive hypertrophy, which culminates in a cardiomyopathy. Administration of verapamil or prazosin to the cardiomyopathic Syrian hamster prevents microvascular spasm and development of cardiomyopathic changes in the myocardium. In view of these and other findings related to the anatomy and hyperreactivity of microcirculation, it is concluded that hypertrophic congestive cardiomyopathies may be caused by focal cell loss due to microvascular spasm and reperfusion injury, with the subsequent development of focal fibrosis and reactive hypertrophy in response to the myocardial necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Extracellular structures in heart muscle.
The extracellular matrix of heart muscle contains a considerable variety of structures. We have systematically studied the morphology of these structures using several methods of fixation and microscopy. Endomysial connections between cells are comprised of struts of collagen [1] as well as combinations of elastin fibers, collagen fibers, and microfibrils. The rest of the extracellular matrix is filled with a polyanionic lattice of unit collagen fibrils, microthreads, and granules. In the course of these investigations, we have observed regions of structural continuity across the sarcolemma, from endomysial collagen struts to Z-bands. We have also correlated the mechanical resistance to stretch with orientation of epimysial collagen fibers and sarcomere lengths in living as well as fixed rat papillary muscles. Our observations suggest that the extracellular skeletal framework plays an important role in normal cardiac function.
Animals↗
Familial congestive cardiomyopathy with nemaline rods in heart and skeletal muscle.
Primary familial cardiomyopathy, once exclusively associated with hypertrophic disorders, is now recognized to occur in a dilated or congestive form. In some instances, characteristic myocellular inclusions of varying morphologies have been identified. Nemaline rods are inclusions which typically have been linked with a rather benign and nonprogressive congenital myopathy. We report finding myocellular inclusions consistent with nemaline rods in two brother who died with congestive cardiomyopathy. Although there was no history or clinical evidence of a myopathy, characteristic nemaline rod inclusions were also identified in the skeletal muscle of one sibling.
Aged↗
Lateral border zone: quantitation of lateral extension of subendocardial infarction in the dog.
This study was undertaken to quantitate the lateral extension that occurs concomitantly with the transmural extension of a subendocardial infarction. A subendocardial infarct was produced in 12 dogs by a 40 minute temporary coronary artery occlusion. Infarct extension was induced 7 days later by permanent occlusion of the same vessel. Regional myocardial blood flows confirmed that ischemia had been produced with both coronary artery occlusions. The vascular boundaries between the normally perfused and ischemic beds were defined by perfusion with different-colored Microfil solutions. The extent of subendocardial infarction and subsequent transmural and lateral extensions were assessed by point counting of histologic specimens. The initial temporary occlusion produced a 30.0 +/- 4.2% transmural infarct and the subsequent permanent occlusion a 29.2 +/- 3.5% transmural extension in a risk region of 39 +/- 4 g. Lateral extension was not measured in four dogs because the initial subendocardial infarct was patchy with markedly irregular lateral borders. In eight dogs the size of the measured lateral infarct extension from each lateral margin from two histologic sections was 0.63 +/- 0.013 cm2. The area of both lateral extensions was 1.7 +/- 0.1% of the cross-sectional area of its risk region as determined by planimetry. Using a model of the risk region, the mass of the lateral extension was estimated to be 1.4 +/- 0.3 g or 3.5 +/- 0.6% of the region at risk. Thus, at the lateral margin of a subendocardial infarct there is a border zone that is small relative to the size of the region at risk and infarcted myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Smooth muscle contraction bands in the media of coronary arteries: a postmortem marker of antemortem coronary spasm?
To date, no unequivocal morphologic markers have been described that would allow the diagnosis of coronary artery spasm to be made at autopsy. The coronary arteries of 63 adult patients without myocardial infarction were examined at autopsy, and the presence of medial smooth muscle contraction bands in these vessels was correlated with other vascular changes, myocardial pathologic changes and clinical history. These contraction bands have not been reported previously in human coronary arteries, but they were identified in experimental vascular spasm induced with catecholamines. It was found that 47 of the 63 cases were positive for contraction bands. As evidence of an antemortem process, there was a significant correlation between these changes and the presence of nonocclusive microthrombi, found in 25 cases. Contraction bands were also highly correlated with atherosclerotic plaque ruptures and mural plaque hemorrhages, which may be secondary to coronary spasm. In 78.7% of the cases positive for contraction bands, the cause of death was related to a diagnosis possibly associated with high catecholamine levels. On the basis of experimental evidence and the correlations identified in this study, coronary artery medial smooth muscle contraction bands may represent a postmortem marker of antemortem coronary spasm.
Adult↗
Prazosin, an alpha 1-adrenergic receptor antagonist, suppresses experimental autoimmune encephalomyelitis in the Lewis rat.
Prazosin, an antagonist of alpha 1-adrenergic receptors, has been found to suppress the clinical and histological expression of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. Suppression was more significant in females than in males and was a dose-dependent phenomenon. Analysis of the effect of other adrenergic receptor antagonists supports the conclusion that the suppressive effect of prazosin is a consequence of blockade of the alpha 1-receptor since treatment with either the alpha 2-antagonist yohimbine or the beta-antagonist propranolol exacerbated the disease, whereas treatment with the long-acting mixed alpha 1/alpha 2-antagonist phenoxybenzamine had some suppressive activity. Treatment with prazosin was also able to suppress clinical and histological signs of EAE in animals sensitized by adoptive transfer with activated spleen or lymph node cells. Whether prazosin acts through altering vascular permeability or the immune response, or both, remains to be determined.
Animals↗
Abnormalities of the coronary microcirculation in acute murine Chagas' disease.
Chronic Chagasic heart disease has many features characteristic of other congestive cardiomyopathies, including ventricular and atrial chamber enlargement, hypertrophy, focal scarring, and mural thrombi. Histologically, there is often lymphocytic inflammation, spotty necrosis, and few parasites. Although immunologic mechanisms have been invoked to explain the development of myocardial degeneration, there have been suggestions that the focal alterations in the heart are secondary to abnormalities of the coronary microcirculation. Based on work from our laboratories which has demonstrated microvascular hyperreactivity in several other models of congestive cardiomyopathy, we investigated whether the cardiac microcirculation of mice acutely infected with Trypanosoma cruzi was also abnormal. We perfused animals at 15-17 days post-infection with silicone rubber which fills the arterioles, capillaries, and venules of the beating heart. After clearing the tissue, we observed numerous areas of focal vascular constriction, microaneurysm formation, dilatation, and proliferation of microvessels which were not present in control animals. These lesions were similar to those we have observed in other congestive cardiomyopathies. Since at this stage of infection there is minimal cardiac degeneration or fibrosis, the presence of these vascular lesions even early in Chagas' disease, may be significant for the pathogenesis of focal myocardial damage. These observations during acute infection provide additional support for the suggestions of others that the myocardial microcirculation is abnormal in Chagas' disease.
Aneurysm↗
Coronary lesions in neurofibromatosis associated with vasospasm and myocardial infarction.
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Adult↗
The Meadox unicusp pericardial bioprosthetic heart valve: new concept.
To obtain a valve with better hemodynamic performance and longer durability than the currently available bioprostheses, a single-cusp pericardial xenograft has been developed. This valve has been tested extensively both in vitro, in a pulse duplicator and in a fatigue-testing system, and in vivo, in a series of dogs and sheep. Hemodynamic studies showed improved hemodynamic performance compared with other biological and mechanical valves. Effective orifice areas were larger and performance indexes higher, especially in the small sizes. Accelerated fatigue testing showed durability significantly superior to that of other biological devices. Animal experiments have established that the single cusp remains pliable even after more than two years of insertion. There is a low incidence of calcification and good preservation of the collagen matrix. This preliminary experience demonstrates that the unicusp pericardial xenograft has superior hemodynamics, increased resistance to fatigue-induced lesions, and a low incidence of calcification. These results might indicate an extended in vivo durability for this device.
Actuarial Analysis↗
Replacement of mitral valve chordae with autologous pericardium in dogs.
Glutaraldehyde-tanned autogenous pericardium was compared with untreated autogenous pericardium as a tissue for replacement of anterior chordae tendinae of the mitral valve. Tanned autogenous pericardial chordae have a marked fibrous reaction at their healing ends but retain central pliability. Untreated autogenous pericardial chordae become uniformly fibrosed and stiff. Both retain their length, heal well to the papillary muscle and cusp, and are considered as potentially useful chordal substitutes in the right circumstances. Some of the response of the host to implanted tanned xenograft tissue must be related to the consequences of tanning rather than a reaction to foreign tissue.
Animals↗
Haemodynamics and durability of mitral bioprostheses--an in vitro study.
The haemodynamic characteristics and durability of mitral bioprostheses were evaluated and compared in vitro in a pulse duplicator and in a fatigue test system. Porcine xenografts were shown to be the most stenotic of all bioprostheses, studied at rates simulating both rest and exercise; on the other hand the new generation of biological valves showed a clear improvement in haemodynamics compared with the standard porcine and pericardial prostheses so far used clinically. Durability tests performed at a rate of 1600 to 1800 beats per minute and with a closing pressure ranging from 80 to 100 mmHg showed that the Ionescu-Shiley and Edwards pericardial xenografts last significantly longer than the Hancock and Carpentier Edwards porcine valves and Hancock pericardial bioprosthesis. Correlation between the mode of failure of pericardial and porcine valves in vitro and in vivo clearly demonstrates that a major role in valve failure is played by mechanical stress. This can be either a consequence of the continuous trauma sustained by the tissue hitting against the bare dacron cloth of the sewing ring during the movements of the cusps. or a result of fatigue occurring and the bending points of the leaflets. The results of this study underline the importance of a continued in vitro evaluation of both haemodynamics and durability of bioprostheses, since some of the pericardial valves which had the best haemodynamic performance showed the worst resistance to fatigue-induced failure. A careful selection of the tissue, modification of the stent design and avoidance of a dacron covered frame are suggested to improve long-term durability of biological prostheses.
Bioprosthesis↗
Combined renovascular hypertension and diabetes in rats: a new preparation of congestive cardiomyopathy.
Myocardial function, electrophysiologic characteristics, and structure were studied in rats with both renovascular hypertension and streptozotocin-induced diabetes (HD). Ventricular papillary muscles from untreated rats with HD showed a marked slowing of isometric and isotonic contractions. Peak developed tension and peak shortening were preserved, except in one animal with findings of congestive heart failure. Transmembrane action potentials increased fivefold in duration. Myocardial interstitial fibrosis was frequently observed. Physiologic parameters of rats with HD treated by left nephrectomy, captopril, and insulin were very similar to those of age-matched controls. The mortality rate of rats with HD was 43% over 5 to 6 months in the first study. In a second study, spontaneously dying rats with HD were compared with those deliberately killed. A 55% mortality was observed over 7 months. Myocardial structural damage and histologic evidence of congestive heart failure were more frequent in spontaneously dying rats with HD. Combined renovascular hypertension and diabetes in rats appears to be a new preparation of congestive cardiomyopathy.
Action Potentials↗
Myocardial micronecrosis produced by microsphere embolization. Role of an alpha-adrenergic tonic influence on the coronary microcirculation.
Microspheres approximately 25 or 50 micrometers in diameter were systemically embolized from the left ventricular cavity. The number of microspheres given was empirically chosen to minimize the possibility of more than one microsphere lodging in an arteriole (3 mg/kg), yet was sufficient to allow for adequate histological assessment. The dogs were sacrificed after 24 hours, and focal areas of myocytolytic necrosis were noted in the myocardium. Groups of dogs were given pretreatment with drugs 10 minutes before embolization. Dogs pretreated with phentolamine (n = 8) and prazosin (n = 2) did not reveal any areas of myocardial necrosis after embolization with 25-micrometers microspheres. Cardiac lesions were also prevented in four of five dogs pretreated with verapamil. In contrast, cardiac lesions were not prevented by pretreatment with yohimbine (n = 2), dipyridamole (n = 3), propranolol (n = 2), or atropine (n = 2). Drug pretreatment with phentolamine or verapamil was not able to prevent cardiac lesions after embolization with 50-micrometers microspheres. Furthermore, despite a greater number of microspheres physically present in the subendocardial layer, the necrotic lesions were more frequent in the mid-wall and epicardial layers. Lesions produced by 25- or 50-micrometers emboli were also significantly smaller in the endocardium. Systemic embolization with microspheres excluding the coronary circulation did not produce cardiac lesions. We conclude that mechanical interruption of the coronary circulation with a 25-micrometers microsphere may be a necessary but not sufficient condition to produce cardiac necrosis. An alpha 1-adrenergic mechanism is also involved in the production of these lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗