Heart Valve Lesions Research Articles

Antiphospholipid antibodies--autoantibodies with a difference.

Antiphospholipid antibodies may be detected by solid phase anticardiolipin antibody tests, the lupus anticoagulant test, or standard tests for syphilis (STS). The occurrence of these antibodies has been associated with venous or arterial thrombosis, fetal loss, and possibly thrombocytopenia. Other suggested features that may be associated with these antibodies include livedo reticularis, migraine, chorea, and heart valve lesions. Uncontrolled studies of small numbers of affected women with recurrent fetal loss suggest that prednisone and aspirin therapy during pregnancy may improve pregnancy outcome. Anticoagulant therapy is recommended for patients with thrombosis for as long as antiphospholipid antibodies persist.

Antiphospholipid Anti-bodies: Autoantibodies With A Difference

Antiphospholipid antibodies may be detected by solid phase anti­ cardiolipin antibody tests, the lupus anticoagulant test, or standard tests for syphilis (STS). The occurrence of these antibodies has been associated with venous or arterial thrombosis, fetal loss, and possibly thrombo­ cytopenia. Other suggested features that may be associated with these antibodies include livedo reticularis, migraine, chorea, and heart valve lesions. Uncontrolled studies of small numbers of affected women with recurrent fetal loss suggest that prednisone and aspirin therapy during pregnancy may improve pregnancy outcome. Anticoagulant therapy is recommended for patients with thrombosis for as long as antiphospho­ lipid antibodies persist.

Q-FEVER ENDOCARDITIS IN ENGLAND AND WALES, 1975-81

Endocarditis was recorded in 92 (11%) of 839 confirmed Q-fever infections reported for the Communicable Disease Report by laboratories between 1975 and 1981; Q-fever endocarditis accounted for approximately 3% of all cases of endocarditis reported. Two- thirds of the 92 reports were of men, and in both men and women endocarditis affected mainly young and middle-aged adults. Only one-third of Q-fever endocarditis patients were noted to have an underlying heart-valve lesion. There were also 30 reports of chronic Q-fever infection, and in 10 the primary clinical feature was liver disease. The laboratory data do not support the view that Q-fever endocarditis is a rare complication of Coxiella burnetii infection, and the condition may be considerably underdiagnosed. Joint veterinary and medical investigations should be undertaken to establish the natural history of Coxiella burnetii infection in the U.K. in order to formulate policies for prevention of acute and chronic infection.

Rate of methicillin penetration into normal heart valve and experimental endocarditis lesions.

Methicillin concentrations were measured in serum, normal heart valves, damaged heart valves, myocardium, and extravascular fluid from 12 New Zealand white rabbits to assess the influence of valvular damage on methicillin penetrations. Fibrin scarring of the aortic valve was induced by the placement of a polyethylene catheter through the aortic leaflet for 4 days. Each rabbit was then given a 40-mg/kg intravenous bolus dose of methicillin. Serum concentrations were collected, and animals were sacrificed 5, 15, 30, and 60 min after the dose. Normal and damaged heart valves from six different rabbits were desiccated to evaluate the fluid content of each. The time course of methicillin in damaged aortic valves was similar to that in serum and followed a bioexponential decline. The pharmacokinetic profile of methicillin in normal heart muscle and normal heart valves was clearly different from that of serum and damaged heart valves. Damaged valves showed a rapid and complete equilibrium with serum, whereas normal heart valve and muscle methicillin concentrations were consistently lower than serum concentrations at all times after the rapid bolus dose. The greater extravascular fluid content in damaged heart valves (P less than 0.001) compared with that in normal heart valves may be associated with the greater extent of penetration into damaged heart valves. Equilibrium between serum and damaged valves may be achieved more rapidly because the damaged area is composed of platelet and fibrin matrix and lacks the membrane integrity of normal heart valve tissue.

Experimental streptococcal endocarditis in the pig: The development of lesions 3 to 14 days after inoculation

Endocarditis was produced in 18 of 36 pigs within 14 days of a single intravenous inoculation of a group L streptococcus; in several pigs the lesions were well established within 5 days. Valves on the left side of the heart were affected 3 times as often as those on the right. Myocardial infarction was found in 10, renal infarction in 13 and polyarthritis in all the 18 pigs that developed endocarditis. In most pigs with endocarditis there was a persistent bacteraemia but in those that did not have endocarditis, bacteraemia was of shorter duration. Possible reasons for the occurrence of endocarditis in 50 per cent of inoculated pigs are discussed and experimentally-induced and naturally occurring heart valve lesions in pigs are compared.

Changes in experimental atherosclerotic lesions of rat heart valves following long-term regression

Regression of experimental atherosclerotic lesions of rat heart valves was studied in a long-term experiment. Following a period of regression of 12 months duration, the thick superficial layers of foam cells disappeared completely. Persisting masses of cholesterol crystals did not seem to be accompanied by any cellular proliferation or fibrous reaction. Such cholesterol deposits showed peculiar transparent cystoid areas probably representing local cholesterol dissolution. The structural differences between arterial and valvular plaques can be hypothetically explained by small numbers of smooth muscle cells in the heart valves.

Development of heart valve lesions during methysergide therapy.

Development of heart valve lesions during methysergide therapy.

Transitional forms of Corynebacterium acnes in disease.

A clear-cut triad of sequential Corynebacterium acnes transitional forms from disease has been discovered. This entity includes three major forms which are capable of stabilization in culture, the spherical, the intermediate, and the definitive C. acnes. During conversion or reversion among the three forms, a variety of forms with mixed characteristics was observed. The spherical form was gram-negative and osmotically fragile, but it possessed a vestigial cell wall and mesosomes which excluded it from the L forms. In lieu of the L-form designation, the term "transitional" was adopted for all forms leading up to the definitive C. acnes. Culture of the spherical form was successful only on Mycoplasma-type media. The intermediate form was gram-negative, had mixed spherical and filamentous morphology, and bore a striking resemblance to Streptobacillus moniliformis. Like the spherical form, it was nutritionally exacting. The definitive form of C. acnes was preceded by gram-positive transitional forms of C. acnes morphology. It lacked, however, the carbohydrases and proteinases of C. acnes and susceptibility to C. acnes bacteriophages. Reversion was often blocked at this stage. A series of blood cultures from a patient with endocarditis was studied. Postmortem stain sections of the heart-valve lesion included intracellular masses of gram-negative spherical organisms. Indirect fluorescent antibody staining of these masses was strongly positive with antiserum to the spherical form and weakly positive with antiserum to the intermediate form.

Adenovirus endocarditis in mice.

Viral endocarditis developed in 24 percent of 50 newborn mice 6 to 8 days after intraperitoneal inoculation with murine adenovirus. Typical adenovirus intranuclear inclusions were seen in heart-valve lesions, and high titers of virus were recovered from heart tissue. Furthermore, adenovirions were directly visualized by electron microscopy within endothelial cells and fibroblasts of the heart valves.

The Relationships between Dyspnea, Pulmonary Function and Intracardiac Pressures in Adults with Left Heart Valve Lesions

SUMMARY Sixty-nine patients with left heart valve lesions have been studied in order to define a sequence of events relating raised intracardiac pressure to abnormalities of pulmonary function and dyspnea. Mitral valve disease was present in 50, aortic valve disease in 12 and both valves were abnormal in seven patients. Evidence is presented that the raised left atrial pressure causes a generalized thickening of the alveolar capillary membrane which usually shows its effect by a decreased pulmonary elasticity (low compliance) and abnormal gas exchange (low fractional carbon monoxide uptake). In some patients the raised pulmonary artery pressure is transmitted, by anastomoses, to the bronchial capillaries and this results in exudation of fluid or edema of the mucous membrane of the smallest air passage causing an obstruction to air flow (high non-elastic resistance). These pulmonary abnormalities may result in difficulty in obtaining the oxygen required for exercise. In some patients the hyperventilation during exercise is an attempt to compensate for this abnormality of gas exchange. In other patients abnormal hyperventilation during exercise is related to nervous causes. Where there is not an abnormally high minute ventilation during exercise, this may be due to gas exchange being normal or due to ventilation being limited by the very high work of breathing. Dyspnea is best related to the amount of respiratory work related to the uptake of oxygen and appears to be associated with this increased respiratory work in the presence of difficulty in gas exchange.

Experimental Bacterial Endocarditis and Proliferative Glomerulonephritis: Description of Method of Production Utilizing Bilateral Lower Extremity or Single Aorta-Vena Cava Arteriovenous Fistulas

SUMMARY AND CONCLUSIONS 1)By combining the effects of systemic cardiovascular stress produced by large arteriovenous fistula loads with bacteremia, a new method has been described for the experimental production of endocarditis and acute diffuse proliferative glomerulonephritis in dogs. 2)Bilateral lower extremity (iliac and femoral), or single aorta-vena cava fistulas are effective for use in this experimental method. 3)Seventeen unoperated normal dogs were given injections of bacterial organisms in numbers up to 14,000 times the numbers of bacteria of the same species and strains as were followed by heart valve or kidney lesions in the dogs with large arteriovenous fistula loads. There was in no instance the occurrence of either endocarditis nor glomerulonephritis in these normal dogs. 4)Likewise, in 10 dogs with single femoral arteriovenous anastomoses receiving intravenous injections of bacteria in comparable numbers, neither endocarditis nor glomerulonephritis occurred. 5)Because of the absence of lesions in the unoperated normal dogs and dogs with single femoral arteriovenous shunts given the same bacteria in the same or much larger numbers than given to the animals with large fistulas subsequently showing valvular or renal lesions, it is concluded that the increased work of the heart plays a major role in determining the susceptibility of these animals to endocarditis and glomerulonephritis. 6)The pathogenesis of these experimental observations depends upon the fact that increasing the work of the heart by means of large arteriovenous fistula loads create or set in motion certain mechanical and, or endocrine alterations which in turn produce a specific and significant increase (up to 14,000 times) in the susceptibility of the endothelial surfaces of the heart and kidneys to bacterial infection. The factual data supporting these conclusions are presented. 7)By utilizing these experimental methods, it may be possible to identify more precisely the physiological alterations which occur in response to increased cardiovascular work and which are apparently responsible for this great increase in susceptibility to bacterial infection observed in these studies. Such accomplishments, might forecast the development of more effective methods of prophylaxis and therapy for endocarditis, glomerulonephritis, and possibly for bacterial infections in general.

Clinical varieties of chronic myocardial insufficiency.

CHRONIC myocardial insufficiency, already clinically of great importance, is becoming increasingly so with the current increase of old persons in our population. By chronic myocardial insufficiency I mean that form of heart disease in which myocardial insufficiency with or without myocarditis has developed in the absence of lesions of heart valves or pericardium. Another term for the condition is chronic nonvalvular heart disease. The form or type of heart disease here discussed always has been of much importance because, beginning at about the age of 40, it steadily increases in frequency until in the later years of life it accounts for the great majority of patients consulting physicians or coming into hospitals because of symptoms and signs of heart disease. Furthermore, as people live longer, as now increasingly they do, there will be more and more patients with this form of heart disease. Only a few of these patients are

A study of two distinct strains of streptococcus isolated from the same heart-valve lesion

Journal Article A study of two distinct strains of streptococcus isolated from the same heart-valve lesion Get access Katherine M. Howell Katherine M. Howell Nelson Morris Institute for Medical Research, Michael Reese Hospital, Chicago Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 30, Issue 3, March 1922, Pages 299–307, https://doi.org/10.1093/infdis/30.3.299 Published: 01 March 1922 Article history Received: 28 October 1921 Published: 01 March 1922