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Biomedical subjects

S M Factor

Publications and source records attributed to S M Factor.

At least 73 records · Page 4Linked to original sources
PubMed1991

Pathologic fibrosis and matrix connective tissue in the subaortic myocardium of patients with hypertrophic cardiomyopathy.

To evaluate scar-type and matrix connective tissue and to assess their role in the diastolic dysfunction of hypertrophic cardiomyopathy, surgically resected subaortic myectomy specimens and several autopsy hearts from patients with hypertrophic cardiomyopathy were studied. Eighteen specimens were differentially stained by a newly developed method that precisely determines relative collagen content; these tissues were compared with postmortem hypertrophied and normal control subaortic specimens. Quantitation revealed a 72% higher level (36.5 vs. 22.1 micrograms collagen/mg protein) of stainable collagen in the hearts with hypertrophic cardiomyopathy than in hypertrophied control hearts. The endocardial plaque was quantitated morphometrically, and it constituted only 4.6 +/- 1.7% of the total increased collagen content in the cardiomyopathy specimens. For the matrix studies, the cardiomyopathy specimens were stained by a silver impregnation technique that identifies connective tissue elements not normally visible with routine histologic methods. There was a marked increase in content of all matrix components, both in areas of pathologic scarring and in "normal" zones. Whorls of matrix connective tissue were noted in regions of myocyte whorls, as well as independent of them. Thus, these studies revealed a striking increase of both scar-type and matrix connective tissue in hypertrophic cardiomyopathy. The extensive scarring and the pronounced interstitial and intercellular matrix connective tissue may contribute to the increased ventricular chamber stiffness and impaired relaxation in this disease.

Cardiomyopathy, Hypertrophic↗
PubMed1991

The diabetic heart: clinical, experimental and pathological features.

Patients with diabetes mellitus are particularly vulnerable to cardiovascular disease. Although both the macrovascular and microvascular complications are present in patients with diabetes alone, they are particularly severe in patients with both diabetes and hypertension. While there is no doubt that a primary diabetic cardiomyopathy occurs with functional consequences, considerable evidence--both in humans and in experimental animal models--points to hypertension as of critical importance in the pathogenesis of severe pathological and symptomatic diabetic heart disease. In hypertensive-diabetic cardiomyopathy, the histopathologic myocardial damage has been attributed to hypertension, while the myocellular dysfunction has been attributed to diabetes. Together, the consequences to the myocardium are devastating. Strict control of the hypertension and diabetes mellitus, along with prevention of the microvascular consequences of both conditions, may have an ameliorative effect on the subsequent development of diabetic heart disease.

Animals↗
PubMed1990

Autopsy-documented cure of multiple myeloma 14 years after M2 chemotherapy.

Multiple myeloma was diagnosed in a 65-year-old woman in 1974 who thereafter received five-drug M2 chemotherapy. All protein abnormalities subsequently returned to normal and serial bone marrow studies documented complete bone marrow remission. Destructive bone lesions persisted radiographically, but did not progress. In 1987, a localized sigmoid adenocarcinoma was resected. In 1988, the patient presented with multiple brain metastases associated with a primary pulmonary adenocarcinoma that proved rapidly fatal. At autopsy, no evidence of multiple myeloma was found. This report describes the first tissue-documented cure of multiple myeloma 14 years after diagnosis and initiation of M2 chemotherapy. The possible association of multiple myeloma with other malignancies is also discussed.

Aged↗
PubMed1990

Collagen degradation in ischaemic rat hearts.

Myocardial extracellular matrix is organized into a complex arrangement of intercellular and pericellular fibres and fibrils that serves as a supporting framework for contracting cells. Recent evidence suggests that changes in ventricular shape and function occurring after ischaemic injury may be related to alterations of this matrix. In this report we describe the rapid and extensive loss of collagen in myocardial infarction produced by ligating the left anterior descending coronary artery of the rat for 1-3 h. The total collagen content in the myocardial infarct zones after 1, 2 and 3 h of ligation was 75 +/- 8%, 65 +/- 7% and 50 +/- 10% respectively (mean +/- S.D.) of that of either the non-infarcted tissue controls or of the same regions in sex- and age-matched normal left ventricles. A marked decrease also occurred in the residual collagens which were not extractable with 6 M-guanidine hydrochloride, suggesting that rapid degradation of insoluble collagen fibres may also occur. The decreased collagen content in the 3 h myocardial infarct coincided with the appearance of several enzyme activities. Collagenase, other neutral proteinase and presumed lysosomal serine proteinase activities were increased by 3, 3 and 2 times the control values respectively. These results suggest that the increased activities of collagenase and other neutral proteinases may be responsible for the rapid degradation of extracellular matrix collagen in myocardial infarct.

Animals↗
PubMed1990

Endomyocardial biopsy diagnosis of small vessel disease: a clinicopathologic study.

We reviewed the clinical history of 191 patients undergoing endomyocardial biopsy and correlated signs and symptoms of heart disease with the presence or absence of small vessel disease. Idiopathic congestive heart failure (78%), arrhythmia (35%), and chest pain (25%) were the most frequent indications for biopsy. Small vessel disease was noted in 61% of the biopsies (67% female, 56% male): 10% severe, 36% moderate, and 15% mild small vessel disease. Patients with hypertension were twice as likely to have small vessel disease than those without hypertension. Of the 27 females with hypertension, 85% had small vessel disease, 67% with either severe or moderate small vessel disease. Small vessel disease was almost twice as frequent in patients with chest pain compared to patients without chest pain. Chest pain was significantly more common in patients with severe small vessel disease than in those with normal small vessels. Of all patients with chest pain, 18% had severe small vessel disease; however, of 20 patients with severe small vessel disease, 45% had chest pain. This analysis suggests that small vessel disease seen in endomyocardial biopsy is more common in women and is related to hypertension. When severe, it is likely to be associated with atypical chest pain.

Adult↗
PubMed1990

AIDS cardiomyopathy: first rule out other myocardial risk factors.

Consecutive autopsies of 59 male AIDS patients revealed that 21 had other myocardial risk factors: 17 were alcohol abusers and 6 had hypertension or coronary artery disease. AIDS patients with these myocardial risk factors were older (mean age 45 versus 35 years, P less than 0.01), and were more likely to have cardiomegaly (mean heart weight 397 grams versus 350 grams, P = 0.06) than patients with AIDS alone. When evaluating patients for AIDS cardiomyopathy, other myocardial risk factors must be considered.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Hypertensive-diabetic cardiomyopathy in rats.

Left ventricular papillary muscle function, transmembrane action potentials, myosin adenosinetriphosphatase (ATPase) and isoenzyme distribution, and myocardial pathology were studied in hypertensive (H), diabetic (D), hypertensive-diabetic (HD), and control (C) rats. There was approximately 50% relative left ventricular hypertrophy in H and HD rats. Relative lung and liver weights were greater in HD rats. Peak velocity of shortening tended to decrease progressively in H, D, and HD rats. The duration of contraction and relaxation was markedly prolonged in Ds and HDs. The length-developed tension relation was blunted in HDs. The negative inotropic effect of verapamil was similar in all groups. Resting membrane potential and amplitude were decreased in D and HD rats. Action potential duration was increased in H, D, and especially HD rats. The shortening of action potential duration with increased stimulus frequency was greater in H, D, and especially HD rats than in Cs. Left ventricular myosin ATPase and V1 isoenzyme content decreased progressively in H, D, and HD rats. Right ventricular V1 isoenzyme content was not affected in H rats but was markedly decreased in D and HD rats. Left (and right) ventricular pathology was unchanged in rats with diabetes but was increased in rats with hypertension. These data suggest that the combination of myocardial pathology (due to hypertension) and cellular dysfunction (caused mainly by diabetes) may result in cardiomyopathy and congestive heart failure in the HD rat.

Analysis of Variance↗
PubMed1990

A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease.

The hearts obtained at autopsy of 67 patients with hypertension, diabetes mellitus, or both were examined microscopically and histochemically, and the amount of fibrosis was determined. Significant differences in heart weight, interstitial fibrosis, replacement fibrosis, and perivascular fibrosis were found among the groups. The mean heart weight of the hypertensive-diabetic patients was significantly greater than that of the hypertensive patients and the diabetic patients. The amount of microscopic fibrosis increased between the groups, the lowest in hypertensive hearts, midrange in diabetic hearts, and highest in hypertensive-diabetic hearts. Total fibrosis correlated with heart weight among diabetic and hypertensive-diabetic patients and was significantly greater among patients with congestive heart failure, most of whom had histories of both hypertension and diabetes. The microscopic grade of fibrosis correlated significantly (p less than 0.01) with a quantitative, histochemical determination of the amount of collagen per milligram of total noncollagenous protein in the heart tissue. Myocardial fibrosis may contribute to the diastolic dysfunction typical of hypertensive-diabetic cardiomyopathy, in which congestive heart failure is a common sequela. The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed.

Adult↗
PubMed1990

Swimming causes myosin adaptations in the rat cardiac isograft.

To investigate the contributions of humoral and hemodynamic factors to cardiac adaptations associated with chronic exercise, female Fischer 344 rats were subjected to chronic swimming, infrarenal cardiac transplantation, or both. Swimming resulted in hypertrophy (11-12%) of the in situ hearts in both the unoperated and operated animals compared with the matched sedentary controls. The cardiac isograft exhibited atrophy (32-35%), which was not attenuated by swimming. The cardiac isograft was also associated with a decrease in the percent of V1 myosin isoenzyme, which was attenuated by swimming (45 +/- 5% versus 66 +/- 6%). Swimming also increased the percent of this isomyosin in the in situ hearts of operated rats. These data suggest that hemodynamic load and/or neural innervation are necessary for hypertrophy associated with chronic conditioning by swimming, whereas myosin isoenzyme control is significantly mediated by humoral factors.

Adaptation, Physiological↗
PubMed1990

Enhanced platelet adherence and aggregation in Chagas' disease: a potential pathogenic mechanism for cardiomyopathy.

Spasm and thrombosis of the coronary microcirculation has been implicated in the pathogenesis of the cardiomyopathy of Chagas' disease. We demonstrate that increases in platelet adherence and aggregation accompany Trypanosoma cruzi infection and may contribute to the observed microvascular pathology. Scanning electron microscopy and radiolabeled platelets studies revealed that platelet adherence to T. cruzi-infected human endothelial cells was significantly increased when compared to controls (P = 0.024). In in vitro experiments, we determined the influence of infection on prostacyclin production, a marker of endothelial cell perturbation. The basal levels of 6-keto-prostaglandin F1 alpha was significantly greater in the supernatant of infected endothelial cells than in those of uninfected endothelial cells (P less than 0.05). The influence of infection was assessed on platelet aggregation at days 5 and 12 post-infection in A/J mice. Platelets from T. cruzi-infected mice were 2-6-fold more sensitive to aggregation induced by adenosine diphosphate and sodium arachidonate than controls. Thromboxane B2 levels in the plasma of infected mice were greater than controls. These data support the hypothesis that heightened platelet reactivity and endothelial cell dysfunction are associated with acute Chagas' disease and may cause coronary microvascular spasm and/or occlusion.

Animals↗
PubMed1990

Immunogenicity of glutaraldehyde-tanned bovine pericardium.

Glutaraldehyde-tanned bovine pericardium was tested for its ability to induce immunologic responses in vivo. Sections of glutaraldehyde-tanned bovine pericardium were implanted between the abdominal muscles of rats and guinea pigs. Control animals received Dacron implants. Lymphocytes and sera from animals were isolated at 2 and 4 weeks after implantation (four animals per group per time). Tritiated thymidine incorporation and an enzyme-linked immunosorbent assay were used to measure T- and B-lymphocyte responses to glutaraldehyde-tanned bovine pericardium antigens. At the same time points, implants and surrounding tissue from all animals were processed for histologic data. Results show that T-lymphocytes from animals with glutaraldehyde-tanned bovine pericardium implants responded significantly (p less than 0.001) to glutaraldehyde-tanned bovine pericardium antigens in vitro but not to Dacron. In contrast, lymphocytes from animals with Dacron implants failed to respond to glutaraldehyde-tanned bovine pericardium or Dacron preparations. Results of enzyme-linked immunosorbent assay show that animals with glutaraldehyde-tanned bovine pericardium implants produced antibody directed against glutaraldehyde-tanned bovine pericardium antigens. Histologic study revealed a dense mononuclear and multinuclear giant cell infiltrate at the interface between glutaraldehyde-tanned bovine pericardium and surrounding host tissues, with focal degradation of implant collagen. Dacron elicited a nonspecific lymphocytic and foreign body-type reaction. These results indicate that glutaraldehyde-tanned bovine pericardium can induce immunologic responses in vivo consistent with a host-versus-graft reaction.

Abdominal Muscles↗
PubMed1989

Diabetic heart disease: the clinical and pathological spectrum--Part I.

Diabetes mellitus is a significant condition affecting major segments of all population groups studied. With the introduction of insulin and oral hypoglycemic therapy, and with better understanding of diet and weight control over the past half century, the primary causes of diabetic morbidity and mortality have shifted in varying proportions from metabolic derangements, infection, and renal insufficiency to different types of cardiovascular disease. Despite extensive clinical and laboratory research on the etiology, pathogenesis, and even the existence of cardiovascular disease associated with diabetes mellitus, however, considerable debate is still apparent in this field. Our purpose is to present an overview of the subject of diabetic heart disease, with a critical analysis of epidemiologic, clinical, and pathological data. Some of this material will be addressed from the perspective of research in this area over the past decade by one of us (SMF), particularly in experimental hypertensive and diabetic cardiomyopathy. However, overall, an attempt will be made to provide an objective and balanced analysis, in order to answer the question: does diabetic heart disease exist?

Adult↗
PubMed1989

Diabetic heart disease--Part II: The clinical and pathological spectrum.

Diabetes mellitus is a significant condition, affecting major segments of all population groups studied. With the introduction of insulin and oral hypoglycemic therapy, together with better understanding of diet and weight control gained over the past half century, the primary causes of diabetic morbidity and mortality have shifted in varying proportions from metabolic derangements, infection, and renal insufficiency to different types of cardiovascular disease. Despite extensive clinical and laboratory research on the etiology, pathogenesis, and even the existence of cardiovascular disease associated with diabetes mellitus, however, considerable debate is still apparent in this field. Our purpose is to present an overview of the subject of diabetic heart disease, with a critical analysis of epidemiologic, clinical, and pathological data. Some of this material will be addressed from the perspective of research in this area over the past decade by one of us (SMF), particularly in experimental hypertensive and diabetic cardiomyopathy. However, overall, an attempt will be made to provide an objective and balanced analysis in order to answer the question: does diabetic heart disease exist?

Cardiovascular Diseases↗
PubMed1989

ACE inhibitors in acute and chronic ischaemia: current status and future promise.

1. Myocyte loss, reactive hypertrophy, dynamic ischaemia with 'stunning', and ventricular wall remodelling are all involved in the initiation and progression of myocardial failure which is ischaemic in origin. 2. The effects of ACE inhibitors to reduce preload and afterload has potentially salutary effects in these settings. Moreover, sulphyl containing ACE inhibitors may have further actions in reducing free radicals and their damage in the acute phases of these events. 3. These promising initial studies warrant further exploration.

Acute Disease↗
PubMed1989

Compensatory hypertrophy and failure in gradual pressure-overloaded guinea pig heart.

Left ventricular hypertrophy has been produced in the guinea pig by a procedure that gradually increases left ventricular afterload. A mildly constricting band was placed around the ascending aortas of very young guinea pigs (225-275 g). With growth to 500-1,000 g, left ventricular systolic pressure increased and left ventricular hypertrophy developed. In approximately 50% of these animals, the hypertrophy was associated with normal left ventricular function and with no unusual symptoms or evidence of heart failure. The other animals developed dyspnea, which appeared an average of 41 days after banding. Dyspneic animals had normal body weight, markedly increased right ventricular and lung weights, decreased left ventricular norepinephrine content, diminished maximum left ventricular pressure generating capacity, and a significantly higher incidence of left ventricular interstitial and perivascular fibrosis. These findings demonstrate that even when left ventricular overload is imposed gradually by banding the aortas of young animals, myocardial decompensation ultimately ensues in a significant proportion of such animals. The slow imposition of loading, the slow rate of decompensation, and the ability to identify animals in heart failure by clinical dyspnea make this model uniquely valuable for studies on the mechanisms of heart failure.

Adaptation, Physiological↗
PubMed1989

Effect of verapamil on the development of chronic experimental Chagas' disease.

In previous work, we have shown that the chronic administration of verapamil, a calcium channel blocker, ameliorated the mortality, pathology, and biochemical alterations associated with acute murine Chagas' disease. To extend these studies to an established chronic model, C3H/Hej mice were infected with the Sylvio X10/4 clone. This clone does not cause symptomatic acute disease but does induce cardiac pathology incorporating several pathological features of human chagasic cardiomyopathy. Cardiac pathology was assessed at 60, 90, and 180 days postinfection. There was a significant decrease in the degree of inflammation and fibrosis in the group infected and treated with verapamil. Myocardial beta-adrenergic adenylate cyclase (AC) activity was determined 180 days postinfection. In the infected group not treated with verapamil, there was no significant change in the maximum rate of conversion of ATP to cAMP (Vmax) or in the concentration of agonist giving 50% of Vmax (apparent Kact) for isoproterenol (ISPN)-dependent AC activation. The increase in Vmax for ISPN determined in the presence of 5'-guanylylimidodiphosphate (Gpp[NH]p) was consistently lower in infected than in uninfected mice, suggesting that infection altered the potential synergistic activation of AC by the guanine nucleotide. In the infected group treated with verapamil, there was a slight increase in the Vmax for ISPN. However, there was a marked enhancement of the synergistic contribution of Gpp(NH)p. These observations suggest that verapamil had preserved that aspect of the AC complex mediating guanine nucleotide sensitive activation of AC. Collectively, the observations in the acute and chronic models of murine Chagas' disease suggest that verapamil may be a useful adjunct in treatment.

Adenylyl Cyclases↗