138 research outputs found

    Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis

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    In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 ± 2 (mean ± SEM) to 19 ± 2 mm Hg (p < 0.005). The mean diastolic transmitral pressure gradient (12.6 ± 1.2 mm Hg before and 11.5 ± 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 ± 0.3 to 4.1 ± 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 ± 0.1 to 1.1 ± 0.2 cm2(p < 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 ± 0.2 cm2larger than it was before drug administration (p < 0.05).Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients. Nitroglycerin may add diagnostic accuracy without transseptal catheterization. Whether this response to nitroglycerin has direct therapeutic value in patients with mitral valve obstruction has yet to be determined

    Recombination in West Nile Virus: minimal contribution to genomic diversity

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    Recombination is known to play a role in the ability of various viruses to acquire sequence diversity. We consequently examined all available West Nile virus (WNV) whole genome sequences both phylogenetically and with a variety of computational recombination detection algorithms. We found that the number of distinct lineages present on a phylogenetic tree reconstruction to be identical to the 6 previously reported. Statistically-significant evidence for recombination was only observed in one whole genome sequence. This recombination event was within the NS5 polymerase coding region. All three viruses contributing to the recombination event were originally isolated in Africa at various times, with the major parent (SPU116_89_B), minor parent (KN3829), and recombinant sequence (AnMg798) belonging to WNV taxonomic lineages 2, 1a, and 2 respectively. This one isolated recombinant genome was out of a total of 154 sequences analyzed. It therefore does not seem likely that recombination contributes in any significant manner to the overall sequence variation within the WNV genome

    Reduced fecundity is the cost of cheating in RNA virus phi6.

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    Co-infection by multiple viruses affords opportunities for the evolution of cheating strategies to use intracellular resources. Cheating may be costly, however, when viruses infect cells alone. We previously allowed the RNA bacteriophage phi6 to evolve for 250 generations in replicated environments allowing co-infection of Pseudomonas phaseolicola bacteria. Derived genotypes showed great capacity to compete during co-infection, but suffered reduced performance in solo infections. Thus, the evolved viruses appear to be cheaters that sacrifice between-host fitness for within-host fitness. It is unknown, however, which stage of the lytic growth cycle is linked to the cost of cheating. Here, we examine the cost through burst assays, where lytic infection can be separated into three discrete phases (analogous to phage life history): dispersal stage, latent period (juvenile stage), and burst (adult stage). We compared growth of a representative cheater and its ancestor in environments where the cost occurs. The cost of cheating was shown to be reduced fecundity, because cheaters feature a significantly smaller burst size (progeny produced per infected cell) when infecting on their own. Interestingly, latent period (average burst time) of the evolved virus was much longer than that of the ancestor, indicating the cost does not follow a life history trade-off between timing of reproduction and lifetime fecundity. Our data suggest that interference competition allows high fitness of derived cheaters in mixed infections, and we discuss preferential encapsidation as one possible mechanism
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