Damaged Heart Valves Research Articles

L'endocardite infectieuse, ses facteurs de risque, sa prévention

Infective endocarditis, resulting from deposition of circulating microorganisms during a period of bacteremia on damaged endothelial heart valves, remains a serious disease. Its overall incidence did not decline in recent years, 24 cases/year/million inhabitants, in France. This can be explained by a modification of the type of underlying cardiac conditions with regression of rheumatic fever and increase of degenerative heart diseases, prosthetic valves and mitral valve prolapse. The risk of bacterial seeding on a damaged valve remains difficult to evaluate, the highest risk being for patients with prosthetic valve, previous infective endocarditis and cyanotic congenital heart disease. A case-control study, done in 1991, confirmed that procedures are risk factors for infective endocarditis and that the multiplicity of procedures increases the risk. A French consensus conference on the prophylaxis of infective endocarditis has updated the recommendations for antibiotic prophylaxis. Two groups of cardiac patients were identified, based on the incidence and the severity of endocarditis occurring in patients with these conditions, 1) patients considered at risk which require specific prophylaxis, and 2) patients considered non at risk which do not require antibiotic prophylaxis. Procedures which require antibiotic prophylaxis are dental procedures and specific gastrointestinal and urologic procedures. As complex protocols are associated with poor compliance by practitioners and patients, the jury has aimed for simplicity and feasibility.

Dystrophic amyloidosis

Seventeen consecutive patients with dystrophic amyloidosis are reported here (eight Chinese, three Indian, three Iban, two Malay and one Caucasian). Ten were females and seven males, with ages ranging from 12 to 80 years (mean of 48 years). Five instances of dystrophic amyloidosis occurred in areas of tissue damage in the cardiovascular system, including fibrotic cardiac valves and an atheromatous plaque. Three occurred in osteoarthritic joint tissue. Of note were three occurrences in endometriotic cyst walls, four in the fibrotic walls of epidermal cysts, one in a hernial sac and one at the edge of a skin ulcer. All deposits were congophilic and exhibited green-birefringence and permanganate-resistance. Immunohistochemistry did not reveal reactivity for AA protein or immunoglobulin lambda or kappa light-chains. AP protein was detected in 35% of cases. Our results show that, besides the usual sites of osteoarthritic joints and damaged heart valves, dystrophic amyloidosis can complicate other areas of chronic tissue damage and fibrosis such as walls of cysts and ulcers. While the pathogenesis and biochemical nature remain unresolved, immunohistochemistry indicates that neither AA nor AL proteins are present in the deposits, and suggests that a different amyloid protein is involved.

Analysis of adherence of Streptococcus defectivus and endocarditis-associated streptococci to extracellular matrix

Pathogenesis of nutritionally variant streptococcal (NVS) endocarditis initiates with bacterial attachment to and colonization of the damaged heart valve surface. Underlying extracellular matrix (ECM) exposed to the environment during damage to cardiac endothelium provides additional receptors that could be involved in bacterial adherence. The ability of NVS and endocarditis-associated streptococci to bind ECM was investigated by using an enzyme-linked immunosorbent assay system that incorporated ECM secreted by baby hamster kidney and human umbilical vein endothelial cells in culture. Streptococcus defectivus, the major species isolated from NVS endocarditis cases, bound ECM of fibroblasts and endothelial cells, indicating that the ECM molecule involved in the binding was a common constituent of diverse matrices. The specific binding of S. defectivus to ECM was demonstrated by saturation binding and specific antibody inhibition studies. Of the 15 S. defectivus strains analyzed, 13 bound ECM, whereas Streptococcus adjacens and NVS serotype III strains were unable to bind the matrix. This selective binding suggested that S. defectivus binds to heart valves through a mechanism different from those of other NVS in subacute bacterial endocarditis. A survey of non-NVS streptococcal endocarditis isolates demonstrated that S. mutans, S. mitis, S. sanguis, and S. faecalis also bound ECM, whereas other viridans species were unable to bind the matrix.

Reduced adherence to traumatized rat heart valves by a low-fibronectin-binding mutant of Staphylococcus aureus

Isogenic strains of Staphylococcus aureus, differing in fibronectin binding, were constructed for studies of the contribution of fibronectin binding to the in vivo pathogenesis of staphylococcal disease. Mutagenesis of S. aureus 879R4S was accomplished by mating with Enterococcus faecalis FA378 that carried the transposon Tn918. Four low-fibronectin-binding mutants were identified that bound 24- to 35-fold less fibronectin than the parent strain did. A spectinomycin-resistant strain, R4SSp, was transduced by a bacteriophage (80 alpha) lysate propagated on a low-binding mutant of 879R4S to produce R4SSp/1536, which bound less fibronectin, contained a single copy of the transposon, and grew on spectinomycin-containing medium. Using a rat model of endocarditis, we determined the distribution of S. aureus R4SSp and its transductant in normal and cardiac catheterized rats. Cultures of heart tissue showed that catheterized rats challenged with the fibronectin-binding parent strain had over 250-fold more organisms in the left heart than did rats challenged with the low-binding transductant. The ability to bind fibronectin had no effect on the number of S. aureus cells cultured from other tissues. These data suggest that the ability of S. aureus to bind fibronectin is an important factor in establishing adherence to damaged heart valves in vivo.

Characterisation of and polysaccharide production by amoxycillin-resistant streptococci.

Small numbers of bacteria capable of growing on agar supplemented with amoxycillin 40 mg/L were isolated from the saliva of 9 out of 20 adult volunteers in a previous study. All the bacteria were identified as Streptococcus sanguis although no strains produced dextran in conventional tests. However, using a specific assay, all the antibiotic-resistant strains were found to secrete glucosyltransferases (GTF), the enzymes that synthesise these extracellular polysaccharides; the production of GTF-S, the enzyme that synthesizes dextran, was 22-43% less than that of an antibiotic-sensitive control strain. Enzyme production by both antibiotic-resistant and sensitive bacteria was markedly inhibited by dextran primer. The amoxycillin-resistant bacteria were resistant to other penicillins; their resistance to erythromycin was variable but they were uniformly sensitive to cephalothin and clindamycin. As dextran production has been proposed as a key factor in the colonisation of damaged heart valves by bacteria such as S. sanguis, these highly resistant bacteria may not pose a threat to the susceptible individual.

Role of culture conditions and immunization in experimental nutritionally variant streptococcal endocarditis.

The nutritionally variant streptococci (NVS) are usually isolated from patients with NVS endocarditis and recently have been serotyped into three groups. In the past, studies on microbial endocarditis have not analyzed the effect of the growth medium or growth phase on the bacteria used to induce the disease in the experimental rabbit model. Therefore, in this study various bacterial growth parameters were examined, including growth in semisynthetic or complex medium to the exponential or stationary phase of growth. The 50% infective dose ranged from 3.7 X 10(5) to 8.5 X 10(6) CFU for representative strains from each of the three serotypes grown under these conditions, indicating that there was no significant difference. The role of immunization was also examined in this model using organisms grown to the exponential phase in semisynthetic medium. Rabbits were immunized with heat-killed whole cells, high titres of specific antibody were produced as demonstrated by enzyme-linked immunosorbent assay, and then the rabbits were challenged with 20- to 100-fold 50% infective dose of the homologous strain. A total of 90 to 100% of the rabbits were protected from the disease process, as shown by the absence of the organisms from the heart valve 3 days after the challenge. Rabbits immunized with the amphiphile that replaces lipoteichoic acid in these organisms were not protected from challenge, demonstrating that another surface component is responsible for adherence or colonization or both. Finally NVS were incubated with radioiodinated fibronectin, fibrinogen, or laminin to determine whether these molecules aided in the adherence of the organisms to the heart valve. Only minor amounts of these components were bound to NVS as compared with controls. Therefore, NVS bind directly to the damaged heart valve or through an unknown mechanism.

Variation in responsiveness of BALB/c sublines and congenic mice to phase I Coxiella burnetii infection and vaccination.

Coxiella burnetii is a Gram-variable staining, sporogenic, obligate intraphagolysomal parasite of eukaryotic cells where it proliferates in a wide range of vertebrate and invertebrate hosts (Baca and Paretsky 1983). The disease in humans is known as Q fever which can occur in clinical presentations (i) as a severe flu-like syndrome often accompanied by pneumonitis and hepatitis (Salmon et al 1982), (ii) or as a chronic process involving low grade fever, weight loss, granulomatous hepatitis and sometimes endocarditis (Turck et al 1976). Persistent granulomatous hepatitis may last for one or more years and may resolve without specific chemotherapy (i.e., tetracycline, chloramphenicol). Whereas, infection of normal or damaged heart valves produces endocarditis following a long incubation period, and the disease is usually resistant to conventional chemotherapy (Turck et al 1976).

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.

Methicillin distribution in serum and extravascular fluid and its relevance to normal and damaged heart valves.

We evaluated the distribution of methicillin into normal and damaged heart valves and the accuracy with which subcutaneous plastic chambers reflected tissue uptake of this antibiotic. A total of 24 male New Zealand rabbits were given constant infusion doses of methicillin through central venous catheters. Five of these animals had their aortic and mitral valves damaged by catheterization of the left ventricle. A total of 19 rabbits had perforated plastic chambers inserted subcutaneously 7 to 10 days before methicillin infusion. In all animals more than 80% of the total infused dose of methicillin was accounted for in the serum, urine, and tissues. In the 12 animals infused to steady state (less than 7 h), the steady-state serum concentrations (11 to 120 micrograms/ml) were equal to the concentrations attained in either peritoneal or tissue chamber fluids. In the 12 animals sacrificed before 7 h, tissue chamber concentrations lagged behind serum and heart tissue concentrations in attaining steady state. Steady-state concentrations in normal heart valves and heart muscles failed to increase proportionally to increased constant infusion doses (8.7 to 87.2 mg/kg per h). The steady-state methicillin concentrations in fibrin-scarred heart valves were invariably higher than the steady-state concentrations in the normal right heart of the same animals (P less than 0.05). Tissue uptake of methicillin was altered in scarred heart valves as compared to normal heart valves, and large-volume subcutaneous tissue chambers misrepresented the uptake rate of methicillin into heart tissues and valves.

Effects of molecular weight of dextran on the adherence of Streptococcus sanguis to damaged heart valves.

Dextran-producing streptococci such as Streptococcus sanguis are the organisms most frequently associated with infective endocarditis in humans. A series of experiments was designed to study how the molecular weight of dextrans affects the adherence of an endocarditis strain of S. sanguis to canine heart valves covered with platelets and fibrin. The data indicated that this adherence was dependent on dextrans of high molecular weight, such as dextran T-2000 or glucans isolated from S. sanguis or S. mutans. The adherence properties of the strain studied were not modified by prior exposure of the bacterial cells of valve leaflets to high-molecular-weight dextrans. Preexposure of bacterial cells or valve leaflets to low-molecular-weight dextrans decreased their adherence. Low-molecular-weight dextrans interfered with adherence of dextran-positive strains to damaged heart valves.

Adherence of glucan-positive and glucan-negative streptococcal strains to normal and damaged heart valves.

The adherence of 18 strains of streptococci to sections of normal canine and human aortic, mitral, and tricuspid valves and to canine interatrial septum was compared in an in vitro system. Quantitative measurements of adherence ratios were performed by two independent methods. Adherence ratios for Streptococcus mutans, S. sanguis, S. bovis, and Group D streptococci were higher (0.0058-0.0101) than for the other streptococcal strains studied (0.0025-0.0041). With the exception of Group D streptococci, adherence ratios for each bacterial strain were similar with the aortic, mitral, and tricuspid valve sections. Adherence ratios with normal human and canine valve leaflets were similar, but adherence ratios with interatrial septum were lower than with normal valve sections. Adherence ratios for glucan-positive and glucan-negative strains of streptococci with normal and with damaged aortic valve leaflets were also compared. The adherence ratios of the glucan-positive streptococci (S. mutans, S. sanguis, and S. bovis) and one glucan-negative enterococcal strain (KG-3) were approximately five times higher with damaged aortic valves (0.039-0.051) than with normal aortic valves (0.009-0.010). For glucan-positive strains, adherence ratios with normal aortic leaflets were similar when bacteria were grown in media which contains or lacks sucrose. In striking contrast, growth of the glucan-positive strains in medium which lacks sucrose, with resultant deficiency of glucan production, decreased the adherence ratios with damaged aortic valve leaflets to those found with normal aortic leaflets. Treatment of glucan-positive strains with dextranase resulted in a decrease in their adherence ratios to levels seen with bacteria grown in medium lacking sucrose, but the higher adherence ratios could be restored in the presence of exogenous dextran.It is concluded that glucan production is one quantitatively important factor that contributes to the greater adherence of glucan-positive streptococci to damaged rather than to normal aortic heart valve leaflets. However, glucan production is not the only factor that determines preferential adherence of streptococci to damaged heart valves, because glucan-negative strains may also show some degree of increased adherence to damaged valves. Thus, bacterial glucan production is one of the factors that could contribute to the pathogenesis of bacterial endocarditis.

Clinical aspects of ‘Q’ fever

Summary ‘Q’ fever is an acute febrile illness seen mainly among members of the farming community. The infection is contracted from sheep and cows mainly by inhalation of infected dust, but can be spread by raw milk. The symptoms bear a marked resemblance to influenza and in the majority of cases the illness clears up spontaneously. A firm diagnosis can best be made by demonstrating a rise in complement fixing antibodies. Patchy consolidation of the lungs is seen on X-ray in about one-third of the cases and occasionally the infection becomes implanted on previously damaged heart valves and gives rise to subacute bacterial endocarditis. Treatment with tetracycline or trimethoprim sulphamethoxazole is indicated.

Early Surgery for the Damaged Heart Valve

Early Surgery for the Damaged Heart Valve

Severe Mechanical Hemolytic Anemia Due to Valvular Heart Disease Without Prosthesis

Excerpt Anemia, after the replacement of a damaged heart valve, was first reported in 1954 when Rose and associates (1) described it after the insertion of a prosthetic valve of the Hufnagel type i...

Bacteremia after prophylaxis

Much investigative work has demon­ strated that transient bacteremias are often caused by tooth removal and other oral surgical procedures.113 A great deal of presumptive evidence and, in recent years, many definitive studies indicate bacteremias result from procedures em­ ployed in treating periodontal disease and, indeed, even from routine pro­ phylaxis.8'10, 12,14-29 Bacteremias thus pro­ duced are of short duration and are not clinically significant in most instances. However, in individuals who have a background of acute rheumatic fever, rheumatic heart disease or other valvular heart disease, bacteremias, however tran­ sient, are potentially dangerous. This should be taken into account when any oral surgical or periodontal procedure is contemplated. Rheumatic heart disease is a compli­ cation of acute rheumatic fever and is the most common cause of organic heart dis­ ease in persons under the age of 40. One of the severe complications of rheumatic heart disease is subacute bacterial endo­ carditis. Before the advent of antibiotics this was almost always fatal. The major­ ity of individuals thus affected now re­ cover, but usually only after prolonged illness. Approximately 20 per cent of cases of subacute bacterial endocarditis develop within several weeks after dental procedures.30,31 This occurs because of the relative frequency of transient bac­ teremias after removal of teeth, other oral surgical procedures, treatment of peri­ odontal disease and prophylaxis. In indi­ viduals affected with heart disease, bac­ teria may localize and multiply on deformed or damaged heart valves, re­ sulting in further damage to already in­ volved structures.

The dentist's responsibility in the management of the patient with rheumatic heart disease

The management of the “cardiac” requires certain fundamental knowledge and the need for closer cooperation between the physician and dentist. This discussion limits consideration specifically to the management of the patient with rheumatic heart disease. Bacteremias have been shown frequently to follow manipulation and trauma of surgical procedures, especially following the extraction of teeth. From such a bacteremia the patient with valvular heart disease (usually resulting from rheumatic fever) may develop subacute bacterial endocarditis as a result of the localization of bacteria on previously damaged heart valves. The prophylactic use of sulfathiazole, if given in doses sufficient to raise the blood levels above 4 mg. per 100 c.c., reduces markedly the incidence of positive blood cultures. It is in a large part the dentist's responsibility to manage the patient with valvular heart disease by treatment with sulfonamides. It is thought that prophylactic premedication with sulfathiazole may prevent the individual with valvular heart disease from developing a subacute bacterial endocarditis.