RESUMEN

INTRODUCTION: Chronic mitral regurgitation is often accompanied by left atrial and ventricular remodeling and elevated natriuretic peptide levels. Our aim was to examine the relation between severe preoperative left atrial enlargement and changes in hemodynamics and natriuretic peptide levels after mitral valve surgery. METHODS: A prospective study was conducted including 40 consecutive patients in sinus rhythm, with severe degenerative mitral regurgitation. N-terminal protype-B natriuretic peptide levels and hemodynamics were measured at predefined time points. An echocardiographic evaluation was performed the day before valve surgery and six months postoperatively. RESULTS: Patients with left atrial volume index ≥60 mL/m(2), n=26, had higher baseline mean pulmonary capillary wedge pressure (17±9 mmHg vs 9±4 mmHg, p=0.010) and N-terminal protype-B natriuretic peptide (1326±2573 ng/L vs 233±221 ng/L, p=0.002) than patients with left atrial volume index <60 mL/m(2). The mean pulmonary capillary wedge pressure decreased to normal in patients with severe left atrial enlargement early after surgery, while it remained normal in patients without severe left atrial enlargement. The natriuretic peptide levels increased during the early postoperative period and decreased in both groups at 6-month follow-up. CONCLUSIONS: A severe left atrial enlargement in patients with chronic degenerative mitral regurgitation and sinus rhythm indicates higher pulmonary capillary wedge pressure and natriuretic peptide levels than in those without. These findings may support early referral to surgery and may facilitate perioperative management. The potential reversibility of left atrial enlargement after surgery may be associated with postoperative reductions in pulmonary capillary wedge pressure and natriuretic peptide levels.

RESUMEN

It is now generally accepted that adherence of microorganisms to various components of cardiac valve surfaces or vegetation lodging on the heart valves is an important early event in the pathogenesis of infective endocarditis. 120 clinical isolates of S. aureus obtained from patients with endocarditis and wound infections and from nasopharyngeal carriers were quantitatively analysed in vitro for their ability to bind to fibronectin and to produce protein A and alpha-toxin. Both cell-bound and extracellular protein A were measured and alpha-toxin was determined as antigen and as haemolytic activity. The highest fibronectin binding ability was found in carrier strains while no significant differences between strains were observed regarding the production of protein A. Strains isolated from patients with endocarditis produced significantly lower amounts of alpha-toxin than did strains from the other two groups. An inverse relationship between the production of protein A and of alpha-toxin was noticed in the material. Animal passage of five strains in an experimental endocarditis model showed a good reproducibility of the test systems and one strain was upregulated in its fibronectin binding ability and in alpha-toxin production. These in vitro results indicate that the fibronectin binding ability is not the decisive adherence factor and question the role of alpha-toxin as a virulence factor in endocarditis.

Asunto(s)

RESUMEN

A mutant deficient for the 19-kDa extracellular fibrinogen-binding protein (Fib) from Staphylococcus aureus has been constructed. The gene was inactivated by allele replacement. A 2.0-kb fragment from transposon Tn4001 carrying the gene for gentamicin resistance was inserted into the gene encoding Fib (fib). The genotype was verified by PCR analysis, and the loss of Fib was demonstrated by Western blotting (immunoblotting). The mutation has not altered the ability of the strain to bind to fibrinogen or fibronectin compared with that of the isogenic parental strain, FDA486. The mutant, designated K4.3, was compared with strain FDA486 in a wound infection model in rats. Sixty-eight percent of the rats challenged with parental strain FDA486 developed severe clinical signs of wound infection, whereas only 29% of the animals challenged with isogenic mutant K4.3 showed severe symptoms (P < 0.01). The weight loss of animals infected with the wild type was also significantly different from that of animals infected with the mutant strain. The result demonstrates that the extracellular 19-kDa fibrinogen-binding protein from S. aureus contributes to the virulence in wound infection and delays the healing process.

Asunto(s)