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Biomedical subjects

S M Factor

Publications and source records attributed to S M Factor.

At least 127 records · Page 7Linked to original sources
PubMed1984

Primary arteriopathy in Takayasu's disease.

Three patients with classic Takayasu's arteritis affecting the aorta and its major branches were found to have a unique small pulmonary arteriopathy characterized by deficiency of the outer media, with capillary ingrowth both here and in the thickened fibrosed intima. In one patient there was also evidence of a mononuclear cellular arteritis of the affected arteries and widespread focal angiomatoid like lesions. Another patient had similar, but less well-defined dilatation lesions. This patient's major coronary arteries showed an active arteritis with ingrowth of reparative granulation tissue capillaries into both media and intima, yielding an appearance not dissimilar to that seen in the small pulmonary arteries. The outer pulmonary artery medial defects observed in our patients bear some similarity to experimental acute immune-complex arteritis and may thus provide tenuous evidence for an autoimmune basis for Takayasu's disease.

Adult↗
PubMed1984

Long-term follow-up of the Ionescu-Shiley mitral pericardial xenograft.

In a group of 40 patients discharged from the hospital after mitral valve replacement with an Ionescu-Shiley pericardial xenograft from January, 1977, to December, 1980, seven instances of valve failure occurred. This unprecedented incidence of bioprosthetic dysfunction after mitral valve replacement with the Ionescu-Shiley pericardial xenograft led us to update the follow-up of our patients receiving this valve in the mitral position. The results of our survey showed, at 6 years postoperatively, an actuarial survival rate of 72%, an actuarial probability of being free from emboli of 62%, and an actuarial freedom from prosthetic failure of 60%. The explanted valves showed complete absence of the neoendothelial lining of the Dacron-covered frame and lesions resembling those observed in Ionescu-Shiley pericardial xenografts removed from our fatigue test system after a mean of 29 +/- 17 X 10(6) cycles. This similarity prompted a classification of tears occurring in the mitral Ionescu-Shiley pericardial xenograft, which is of extreme importance, since the clinical presentation and outcome of patients with a failing valve differs according to the type of rupture. The lesions of the cusp observed in clinical specimens were possibly related to the continuous trauma of the tissue against the bare Dacron cloth during closure of the valve. It is concluded that (1) actual durability and thrombogenicity of the Ionescu-Shiley pericardial xenograft in the mitral position needs to be carefully reassessed, (2) close follow-up of such patients by clinical and two-dimensional echocardiographic evaluation is advisable after the third postoperative year, and (3) failure of the mitral Ionescu-Shiley pericardial xenograft may occur suddenly, and awareness of this complication is the clue to prompt recognition and treatment of such patients.

Adult↗
PubMed1984

Coronary microvascular abnormalities in the hypertensive-diabetic rat. A primary cause of cardiomyopathy?

The authors have continued their investigation of the hypertensive-diabetic (HD) rat by evaluating changes in the myocardial microvasculature in this model. Perfusion of HD animals in vivo with a silicone rubber solution revealed numerous areas of microvascular tortuosity, focal constrictions, and microaneurysm formation. These alterations were present to a lesser extent in normoglycemic hypertensive (H) rats, and were distinctly rare in normotensive diabetic rats and unaffected control animals. Quantitation of these vascular lesions revealed highly significant differences between HD animals and the other three groups, with hypertensive rats intermediate between HD rats and diabetic control rats. Areas of pronounced arteriolar constriction were also identified in the HD and H animals with the use of serial sections of Epon-embedded myocardium. It is believed that these lesions represent dynamic changes in the microcirculation, which may cause segmental reperfusion injury to the myocardium, leading to focal replacement fibrosis. Interstitial scarring may result from increased leakiness of small vessels exacerbated by the combined disease. The authors propose that the additive effects of hypertension and diabetes mellitus on the myocardial microcirculation may be a primary cause of cardiomyopathy in this model of human disease.

Animals↗
PubMed1983

Fatal pulmonary and cerebral fat embolism in systemic lupus erythematosus.

A patient with an eight-year history of systemic lupus erythematosus (SLE) and recent onset of recurrent psychosis died after acute deterioration of cardiopulmonary status and level of consciousness. Autopsy disclosed massive pulmonary hemorrhage and unsuspected fat emboli in the lungs, kidney, and brain. This article discusses the significance of systemic fat embolism in SLE, with reference to corticosteroid therapy, fatal pulmonary hemorrhage, and lupus psychosis.

Adult↗
PubMed1983

Hypertensive diabetic cardiomyopathy in the rat: ultrastructural features.

We previously described a cohort of diabetic patients with typical congestive cardiomyopathy, in whom myocardial lesions were related to concomitant high blood pressure. To evaluate the association of diabetes mellitus and hypertension in more detail, we studied 4 groups of rats with either no disease, streptozotocin-induced diabetes mellitus, renovascular hypertension, or a combination of hypertension and diabetes. Analysis revealed significant myocardial fibrosis and degeneration in the hypertensive-diabetic group when compared to controls, without an obvious relationship to small vessel lesions. The myocardial alterations appeared similar to those observed in patients with hypertension and diabetes mellitus. Of note, although hypertensive animals had focal moderate lesions, diabetic animals had no pathological changes. To further characterize these histological changes, we performed electron microscopy on the 4 animal groups, which we are reporting in this study. Our analysis of the ultrastructural alterations confirms the previous histological observations. Diabetic animals only had increased cellular lipid, and mild, focal areas of myofibrillolysis, with no significant increases in perivascular and perisarcolemmal basal lamina. Consistent with our light microscopic finding that PAS positive material was associated with interstitial or replacement fibrosis, we noted basal lamina proliferation in the hypertensive and hypertensive-diabetic groups, particularly in areas of scarring. Pericapillary basal lamina was increased to the greatest extent in the hypertensive-diabetics. Qualitative alterations of myocardial cells and muscular blood vessels were similar in both the hypertensive and hypertensive-diabetic animals; however, there were more extensive changes in the latter group. This study provides further evidence that the combination of diabetes mellitus and hypertension produces significantly greater myocardial lesions than with either disease alone, not only at the light microscopic level, but ultrastructurally as well. Although the pathogenesis of this cardiomyopathy is unknown it may be related to abnormalities of the cardiac microcirculation. The prevalence of hypertension in the diabetic population suggests that greater attention should be paid to the combination of these 2 conditions and their effects on the heart.

Animals↗
PubMed1983

Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

In this study we quantitated the region of preserved myocardium between a subendocardial myocardial infarct (SEMI) and the endocardium in dogs and determined whether this preserved zone was within the region at risk and whether infarct extension could occur in this region. We also evaluated whether a similar subendocardial region exists in patients with SEMI. A 40-minute temporary occlusion of the left anterior descending coronary artery (LAD) in eight dogs resulted in a 35 +/- 5% transmural infarct with 8 +/- 1% subendocardial preservation as assessed by point-counting of the histologic specimens. In vivo perfusion of coronary vessels with Microfil showed that this preserved subendocardial zone was within the region at risk. The preserved subendocardial zone had significantly fewer cell layers in the dogs ventilated with room air than in dogs ventilated with 100% oxygen (8 +/- 4 vs 19 +/- 4, p less than 0.001), which suggests that diffusion from the ventricular cavity was the mechanism of cell preservation. In contrast, the inspired oxygen concentration did not influence the size of the SEMI. Reocclusion of the LAD for 24 hours in an additional eight dogs, 1 week after a SEMI had been created by a 40-minute temporary occlusion, resulted in both subendocardial and subepicardial extension involving 5 +/- % and 29 +/- 9%, respectively, of the transmural myocardium at the infarct center. Subendocardial infarct extension of a similar dimension to that in dogs ventilated on 100% oxygen was observed in postmortem material from eight patients with infarct extension. The preserved layers of subendocardium presumably receive sufficient nutrients from the ventricular cavity to maintain the viability of this region during temporary, but not permanent, reduction of blood supply from the coronary arteries.

Aged↗
PubMed1983

Results of endomyocardial biopsy in patients with spontaneous ventricular tachycardia but without apparent structural heart disease.

To evaluate possible occult myocardial disease in 18 patients whose only major manifestation of heart disease was spontaneous ventricular tachycardia or fibrillation, right ventricular endomyocardial biopsies were performed. None of the patients had symptoms of ischemic or congestive heart disease, and at catheterization none had significant lesions of the coronary arteries or regional wall motion abnormalities of the left ventricle. The mean left ventricular ejection fraction (65 +/- 7%), mean right ventricular ejection fraction (55 +/- 9%), mean cardiac index (3.0 +/- 0.5 1/min/m2), mean right atrial pressure, mean pulmonary capillary wedge pressure, and mean pulmonary artery systolic pressure were normal. However, right ventricular endomyocardial biopsy specimens were abnormal in 16 of 18 (89%) patients: nine (50%) had changes of a significant, although nonspecific, cardiomyopathy with myocellular hypertrophy, interstitial and perivascular fibrosis, and vascular sclerosis; three (17%) had subacute inflammatory myocarditis; two (11%) had diffuse abnormalities of the intramyocardial arteries; and two (11%) had pathologic changes consistent with arrhythmogenic right ventricular dysplasia. In the two (11%) patients with normal biopsy specimens, one had Wolff-Parkinson-White syndrome and the other had mitral valve prolapse. Although histologic abnormalities were found in 89% of these patients, performance of right ventricular endomyocardial biopsies in this group of patients should be considered a research procedure. We conclude that the majority of patients who have serious ventricular arrhythmias but no apparent structural cardiac abnormalities have abnormal right ventricular biopsy specimens and that the arrhythmias may be the first manifestation of a variety of primary myocardial abnormalities.

Adult↗
PubMed1983

Skeletal framework of mammalian heart muscle. Arrangement of inter- and pericellular connective tissue structures.

We have studied the connective tissue of mammalian heart muscle in order to obtain an integrated description of extracellular structures and their dispositions relative to cardiac myocytes. Light microscopy and several types of electron microscopy have been employed in these investigations. The epimysium, the sheath of connective tissue that surrounds the muscle, contains relatively large fibers of collagen and elastin. In papillary muscles of rat, the large collagen fibers of the epimysium form a weave pattern at slack length (sarcomere lengths 1.8 to 2.0 micron) but are well aligned in states of stretch along the long axis of the muscle (sarcomere length 2.3 to 2.5 micron). We propose that the epimysial collagen network protects the sarcomeres from being stretched beyond lengths favorable to maximal force production. The endomysium is defined as the connective tissue that surrounds and interconnects myocytes; it consists of intercellular struts (bundles of collagen fibrils, often attached near Z-band level), a weave of bundles of collagen fibrils that envelopes myocytes, and a collagen fibril-microthread-granule lattice that bridges cells and fills the extracellular matrix. In contracted muscles festoons of sarcolemma are attached to Z-bands, thus forming regions for transmission of force across the sarcolemma. Perimysial bundles of collagen connect epimysium to endomysium and surround groups of myocytes. Collagen fibers often have a twisted configuration, probably for enhanced tensile strength. Superimposed on the large extracellular structures is the polyanion-rich lattice comprised of unit collagen fibrils, microthreads, and granules. Amorphous ground substance forms a matrix in which the fibrils of collagen fibers are embedded; it appears continuous with the cell coat in regions of fiber attachment. Elastic fibers interconnect cells and helically wind around myocytes. Circumferential forces from elastin stretched about shortened, thickened myocytes in systole should promote elongation in tandem with intramyocyte forces of elongation.

Animals↗
PubMed1983

Catecholamine-induced myocardial necrosis in experimental diabetes mellitus.

The pathogenesis of the cardiomyopathy associated with diabetes mellitus is unknown. Among several suggested mechanisms, myocardial necrosis induced by endogenous catecholamines may play a role. Therefore, the sensitivity of the heart to the effect of varying doses of isoproterenol hydrochloride and norepinephrine bitartrate was examined in diabetic and control rats given streptozocin. The dose of isoproterenol hydrochloride ranged from 0.008 to 30 mg/kg of body weight. Norepinephrine bitartrate was given in doses from 0.2 to 1.0 mg/kg of body weight. Each dose was given twice, 24 hours apart. Animals were killed 48 hours after the first dose, and their hearts were examined pathologically. Diabetes did not significantly alter the pathological response of the heart to either drug. We conclude that the diabetic heart is not intrinsically hypersensitive to catecholamines.

Animals↗
PubMed1982

The cardiomyopathy of Wilson's disease. Myocardial alterations in nine cases.

Though myocardial alterations are well recognized in haemochromatosis, little attention has been paid to the cardiac changes in Wilson's disease. To define the extent of myocardial degeneration in newly diagnosed or chronically treated Wilson's disease, we reviewed the autopsy findings in 9 cases with this condition. We compared our observations with those in 3 control cases, selected for comparable age and with liver disease having no known association with cardiac degeneration. Our results revealed cardiac hypertrophy in 5 out of 9 cases of Wilson's disease. There was evidence of interstitial and replacement fibrosis, intramyocardial small vessel sclerosis and focal inflammatory cell inflammation to a variable degree in all cases. One case had AV nodal degeneration, and a 15 year old boy had severe atherosclerosis of the left main coronary artery. Two patients died suddenly, presumably secondary to an arrhythmia; one of these patients had the most marked myocardial alterations. We could not correlate these changes specifically with the tissue levels of copper, treatment with D-penicillamine, or the presence of cirrhosis. We conclude that there are definite morphological abnormalities in the hearts of patients with Wilson's disease consistent with a cardiomyopathy. Though the myocardial changes were non-specific, the fact that 2 patients died suddenly, suggests the need for a prospective study of cardiac function in these patients in the future.

Adolescent↗
PubMed1982

Hypothesis: is congestive cardiomyopathy caused by a hyperreactive myocardial microcirculation (microvascular spasm)?

In most congested, dilated cardiomyopathies, pathologic analysis reveals focal myocardial necrosis, microscopic scarring, interstitial fibrosis, and myocellular hypertrophy. The focal nature of these processes indicates that the cardiomyopathies may not be due to diffuse abnormalities of cardiac muscle cells, at least in the early stages, but that the changes may represent focal events affecting discrete, small volumes of tissue. Experimental evidence of microvascular hyperreactivity (spasm), both in the hereditary cardiomyopathy of the Syrian hamster and in the acquired cardiomyopathy of the hypertensive-diabetic rat, suggests that transient spasm of the myocardial microcirculation may lead to focal myocellular necrosis and scarring, which then causes the unaffected myocardial cells to undergo compensatory hypertrophy in order to normalize the increased load per unit of myocardium. When enough myocardium is lost and the compensatory hypertrophy results in decreased contractility, congestive heart failure ensues as a systemic response to altered ventricular function. The efficacy of verapamil therapy in the Syrian hamster in preventing microvascular spasm, cell necrosis, and the subsequent development of a cardiomyopathy has provided hope that similar preventive treatment can be applied to patients with early stages of cardiomyopathy.

Animals↗
PubMed1982

Microvascular spasm in the cardiomyopathic Syrian hamster: a preventable cause of focal myocardial necrosis.

The cardiomyopathic Syrian hamster develops focal myocardial necrosis beginning at 1 month of age, which leads to eventual ventricular failure within 1 year. The pathogenesis of this myocytolytic necrosis is unknown. Based on the nature of the cell necrosis, cytochemical evidence of vascular alterations, and the sensitivity of the hamsters to catecholamines and other vasoactive substances, we believe that the cardiomyopathy may be mediated by abnormalities of the microcirculation. Nonetheless, until the present study, no significant changes have been observed in these vessels. To elucidate the pathogenesis of this disease, we perfused living cardiomyopathic hamsters with silicone rubber solutions, which revealed numerous areas of microvascular constriction, diffuse vessel narrowing and luminal irregularity. Fixed structural lesions in these vessels could not be demonstrated. Pretreatment of young hamsters with verapamil during the period when they normally develop myocardial necrosis prevented myocytolytic lesions and abolished microvascular hyperreactivity. We believe that focal, transient spasm of small blood vessels, probably secondary to vasoactive substances, may cause myocytolytic necrosis (a form of reperfusion injury) in this model. This may also be a multifactorial disease with myocellular as well as vascular abnormalities leading to myocardial degeneration. The similarity of this disease to human and experimental cardiomyopathy suggests that microvascular spasm may be a common denominator of many different cardiomyopathic syndromes.

Animals↗
PubMed1982

The microcirculation of the human heart: end-capillary loops with discrete perfusion fields.

We studied 10 autopsied human hearts by perfusing colored Microfil into separate coronary arteries to define organization of capillaries at the borders between two perfusion fields. Sections of "cleared" myocardium were examined with epiillumination at the grossly identified borders of Microfil perfusion. In two- and three-color-injected hearts, the capillaries were arrayed in a pattern of arcades and loops without connections between separately perfused capillary beds. In hearts perfused through only one coronary artery, the capillaries were organized into tufted loops at the border. These findings contrast with the microcirculatory pattern in canine skeletal muscle and brain, in which heterologous capillaries are focally interconnected. We conclude that the human microcirculation is composed of end-capillary loops that supply discrete perfusion fields. This pattern of unconnected heterologous capillary beds suggest that there is no obvious anatomic arrangement of the microcirculation that could account for a significant ischemic lateral border zone in human myocardial infarctions.

Animals↗
PubMed1981

The histological lateral border of acute canine myocardial infarction. A function of microcirculation.

Studies from this laboratory have shown that the border of a 24-hour canine infarct is histologically sharp and is composed of numerous interdigitating peninsulas of necrotic and normal tissue. To see if this sharp boundary is spatially related to the capillary beds of occluded and non-occluded arteries, the left anterior descending artery (LAD) was ligated in five mongrel dogs. Twenty-four hours later, white silicone rubber (Microfil) was injected into the LAD distal to the ligature; simultaneously and under the same pressure, red Microfil was injected into the left main coronary artery (LMCA). In hematoxylin and eosin sections from the border of the infarct, capillaries supplied by the LAD (white) were either in areas of necrosis, in normal epicardium or, rarely, in normal tissue along the lateral boundary; those supplied by the LMCA (red) were almost always in normal regions. Quantitative evaluation of this relationship revealed that the majority of the vessels in the normal and necrotic tissue were concordant (i.e., that normal tissue was supplied by the LMCA, and necrotic tissue by the LAD). However, a small zone of vascular discordance, averaging approximately 30 micrometers in width, was present along the infarct boundary, possibly representing a narrow border zone of little consequence. Hence, the complex interdigitation of normal and necrotic tissue in the lateral border of an infarct is predominantly a function of the interdigitation of the capillary beds supplied by the occluded and nonoccluded arteries.

Acute Disease↗