Pulmonary function in chronic heart failure - Changes after heart transplantation

Citation
Cs. Ulrik et al., Pulmonary function in chronic heart failure - Changes after heart transplantation, SC CARDIOVA, 33(3), 1999, pp. 131-136
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
SCANDINAVIAN CARDIOVASCULAR JOURNAL
ISSN journal
14017431 → ACNP
Volume
33
Issue
3
Year of publication
1999
Pages
131 - 136
Database
ISI
SICI code
1401-7431(1999)33:3<131:PFICHF>2.0.ZU;2-Y
Abstract
To investigate the impact of chronic heart failure on pulmonary function in heart transplant recipients, pulmonary function was evaluated in 41 consec utive patients (mean age 43 years, range 15-57 years) before and 6 months a fter successful heart transplantation. The pulmonary function tests include d measurements of forced vital capacity [FVC], forced expiratory volume in 1.s [FEV1], FEV1/FVC ratio, total lung capacity [TLC], and diffusion capaci ty for carbon monoxide [T-LCO] and KCO [T-LCO per 1 alveolar volume]. Compared to pretransplant values, spirometry after transplantation revealed modest improvements in FVC (from 77 +/- 16 to 88 +/- 21% of predicted [%pr ed]; p < 0.001) and FEV1 (from 75 +/- 16 to 85 +/- 22%pred; p < 0.001), whe reas the FEV1/FVC ratio was unchanged (81% +/- 11 and 80% +/- 10; p = NS). A slight but statistically significant increase in TLC (from 78 +/- 15 to 8 6 +/- 18%pred, p < 0.001) was also observed. Prior to transplantation the m ean T-LCO was 76 +/- 17%pred; 7 of the patients had a T-LCO below 60%pred ( mean 51% pred). In 33 of the 41 patients a reduction in T-LCO was observed after transplantation; for all 41 patients the mean fall in T-LCO was 14% o f the predicted value (SD 12%pred) (p < 0.0001). Likewise, a significant re duction in KCO was noted (p < 0.0001). Multiple regression analysis reveale d that high pretransplant T-LCO %pred (p = 0.02) and FVC %pred (p = 0.04) w ere associated with a less favorable outcome concerning posttransplant T-LC O %pred. Although normalization of FEV1, FVC and TLC can be anticipated after correc tion of severe chronic left ventricular failure by heart transplantation, t he pronounced concomitant decline in diffusion capacity observed in this st udy may be explained by underlying pulmonary disease caused by factors othe r than long-standing heart failure. Our findings support the notion that pu lmonary function abnormalities attributable to chronic heart failure should not preclude consideration for heart transplantation.