Endothelin-1 polymorphisms involved in impaired exercise tolerance in COPD patients. A pilot study

Eur Rev Med Pharmacol Sci. 2011 Feb;15(2):123-8.

Abstract

Introduction: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide that may lead to impaired exercise tolerance. In this study we exhibit the relationship between two endothelin-1 (+134 3A/4A and G198T) SNPs involved in COPD and their association to impaired exercise tolerance.

Materials and methods: The study population consisted of 22 COPD smokers and 32 smoking controls which underwent pulmonary function tests to assess forced expiratory volume for 1 second (FEV1), forced vital capacity (FVC), as well as cardiopulmonary exercise testing. Single nucleotide polymorphism were isolated using Real-Time PCR.

Results: The distribution of both genotypes (3A3A, 3A4A, 4A4A for the +134 3A/4A and GG, GT, TT for the G198T) did not different among patients and non-COPD smoking controls. Multivariate analysis showed that the 3A4A and GG genotypes in the COPD group were independently associated with better V'O2max values (Odd's Ratio (OR) = 12.5, 95% CI = -0.85-25.1, p = 0.049, and OR = 6.1, 95% CI = 0.83-11.4, p = 0.026, respectively). On the contrary analogous analysis in the non-COPD control group, showed that the 3A3A genotype was independently associated with increased V'O2/pulse (OR = 51.5, 95% CI = 17.2-85.7, p = 0.005) and the 3A4A genotype with increased DVE/DVCO2 value (OR = 3.8, 95% CI = -0.27-7.9, p = 0.054).

Discussion: Our results show that endothelin-1 gene is implicated in exercise performance in COPD patients and might play a role in adaptation of the cardiopulmonary system to exercise.

MeSH terms

  • Adult
  • Aged
  • Endothelin-1 / genetics*
  • Exercise Test*
  • Female
  • Genotype
  • Humans
  • Lung / physiopathology
  • Male
  • Middle Aged
  • Pilot Projects
  • Polymorphism, Single Nucleotide*
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Pulmonary Disease, Chronic Obstructive / physiopathology*

Substances

  • Endothelin-1