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. 2011 Jul-Sep;1(3):377-82.
doi: 10.4103/2045-8932.87303.

Pulmonary hemodynamic responses to inhaled NO in chronic heart failure depend on PDE5 G(-1142)T polymorphism

Thibaud Damy  1 , Pierre-François Lesault, Soulef Guendouz, Saadia Eddahibi, Ly Tu, Elisabeth Marcos, Aziz Guellich, Jean-Luc Dubois-Randé, Emmanuel Teiger, Luc Hittinger, Serge Adnot
Affiliations

Pulmonary hemodynamic responses to inhaled NO in chronic heart failure depend on PDE5 G(-1142)T polymorphism

Thibaud Damy et al. Pulm Circ. 2011 Jul-Sep.

Abstract

To evaluate the vasoconstrictor component of PH in CHF by investigating the hemodynamic response to inhaled nitric oxide (iNO) and to determine whether this response was influenced by the phosphodiesterase 5 gene (PDE5) G(1142)T polymorphism. CHF patients underwent right heart catheterization at rest and after 20 ppm of iNO and plasma cGMP and PDE5 G(1142)T polymorphism determinations. Of the 72 included CHF patients (mean age, 53±1 years; mean left ventricular ejection fraction, 29±1%; and mean pulmonary artery pressure, 25.5±1.3 mmHg), 54% had ischemic heart disease. Proportions of patients with the TT, GT, and GG genotypes were 39%, 42% and 19% respectively. Baseline hemodynamic characteristics were not significantly different across PDE5 genotype groups, although pulmonary capillary wedge pressure (PCWP) tended to be lower in the TT group (P=0.09). Baseline plasma cGMP levels were significantly lower in the TT than in the GG and GT patients. With iNO, PVR diminished in TT (-33%) but not GG (-1.6%) or GT (0%) patients (P=0.002); and PCWP increased more in TT than in GT (P<0.05) or GG (P<0.003) patients. The PDE5 G(-1142) polymorphism is therefore a major contributor to the iNO-induced PVR decrease in CHF.

Keywords: heart failure; nitric oxide; phosphodiesterase.

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Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Plasma cGMP concentration depending on PDE5 G(1142)T polymorphism.
Figure 2
Figure 2
Percent of change between baseline and after inhaled NO in transpulmonary gradient, mean pulmonary artery pressure, pulmonary capillary wedge pressure and cardiac output.
Figure 3
Figure 3
Change between baseline and after inhaled NO in pulmonary vascular resistance.
Figure 4
Figure 4
Change between baseline and after inhaled NO in pulmonary vascular resistance depending on mean pulmonary artery pressure subgroup.
Figure 5
Figure 5
Plasma cGMP concentration depending on PDE5 G(1142)T polymorphism at baseline and after inhaled NO.
See this image and copyright information in PMC

References

    1. Kjaergaard J, Akkan D, Iversen KK, Kjoller E, Kober L, Torp-Pedersen C, et al. Prognostic importance of pulmonary hypertension in patients with heart failure. Am J Cardiol. 2007;99:1146–50. - PubMed
    1. Damy T, Goode K, Kallvikbacka-Bennet A, Lewinter C, Hobkirk J, Nikitin N, et al. Determinants and prognostic value of pulmonary artery pressure in patients with chronic heart failure. Eur Heart J. 2010. [Last accessed on 2010 Aug 05]. Available from: http://eurheartj.oxfordjournals.org/content/early/2010/08/05/eurheartj.e... . - PubMed
    1. Guglin M, Khan H. Pulmonary hypertension in Heart Failure. J Cardiac Fail. 2010;16:461–74. - PubMed
    1. Simmoneau G, Robins I, Beghetti M, Channick R, Delcroix M, Denton CP, et al. Updated Clinical Classification of Pulmonary Hypertension. J Am Coll Cardiol. 2009;54:S43–54. - PubMed
    1. Badesch D, Champion HC, Gomez Sanchez M, Hoeper M, Loyd J, Manes A, et al. Diagnosis and Assessment of Pulmonary Artery Hypertension. J Am Coll Cardiol. 2009;54:S55–66. - PubMed