Skeletal muscle dysfunction is well recognised in chronic obstructive pulmonary disease (COPD) and is associated with increased morbidity and mortality. Considerable circumstantial evidence supports a role for renin-angiotensin systems in skeletal muscle turnover. Angiotensin II (ATII) administration causes cachexia through several biological mechanisms. Angiotensin converting enzyme inhibitors (ACE-I) block the conversion of angiotensin I to ATII. Previous pilot studies have shown that the administration of ATII receptor blockers (ARB) or ACE-I to COPD patients may increase quadriceps strength and peak work rate (Andreas et al, 2006; Di Marco et al, 2010). We hypothesised that in an unselected COPD population referred for pulmonary rehabilitation (PR), those receiving ARB or ACE-I drugs would have preserved muscle mass.Methods
Data from 373 consecutive COPD patients (213M: 160F; mean age 68.3; median FEV1 41% predicted) referred to an outpatient pulmonary rehabilitation programme were analysed. Patients were divided into those receiving either an ARB or ACE-I and controls (those receiving neither drug). Fat free mass (FFM; measured by bioelectric impedance analysis), incremental shuttle walk (ISW), Chronic Respiratory Disease Questionnaire (CRDQ), MRC Dyspnoea score (MRC) and COPD assessment test (CAT) were measured. Between group differences were compared using Mann–Whitney U or unpaired t-test.Results
Data are presented as median (25th, 75th centiles), and summarised in Abstract P37 table 1. 130 COPD patients from this cohort were taking either an ACE-I (n=82), ARB (n=45) or both (n=3). The groups were matched for gender distribution and long-term oral corticosteroid use. Compared with the control COPD patients, those on ACE-I or ARB were older, had better FEV1 % predicted but similar ISW, CRDQ, MRC and CAT. However, the patients receiving ACE-I or ARB had significantly higher fat free mass (FFM) and fat free mass index (FFMI).Conclusions
In an unselected COPD cohort referred for pulmonary rehabilitation, patients on ACE-I or ARB appear to have increased muscle mass compared with those receiving neither drug. Future longitudinal studies and randomised controlled trials are required to further define the effect of ACE-I and ARB in COPD.