Heart failure and chronic obstructive pulmonary disease: common partners, common problems

Heart failure (HF) and chronic obstructive pulmonary disease (COPD) are common partners with common problems. Both are chronic systemic disorders incurring significant morbidity and mortality. Although around one third of patients with HF have concurrent COPD,1 remarkably few reports have addressed this often ignored combination. The systematic review presented within this thesis defines the diagnostic challenges, prevalence and prognostic implications of HF with coexistent COPD. I then critically appraise the twin controversies of β-blockade in COPD and β-agonists in HF. The two are inextricably linked, each therapy exerting the reverse pharmacologic activity of the other. The evidence for symptomatic or prognostic benefit from either therapy is limited, and in the case of β-agonists adverse consequences appear more likely. A Cochrane meta-analysis concluded that long term cardioselective β-blockade is safe and well tolerated in patients with moderate to severe or reversible COPD.2 Although often cited,3 these conclusions are simply not true. Of the 20 randomised controlled trials included in the meta-analysis, 11 involved single doses and only one lasted longer than a month. The 9 ‘long term’ studies (defined as more than a single treatment dose) involved 147 young, predominantly male patients with moderate airways obstruction (mean forced expiratory volume in 1 second (FEV1) 1.8 litres). The effect on health status has never been assessed in any cohort with COPD. The long term impact of β-blockade on pulmonary function, symptoms and quality of life is therefore largely unknown. Most importantly, no study has included patients with HF. I randomised 27 patients with HF and coexistent moderate or severe COPD to receive bisoprolol or placebo, titrated to maximum tolerated dose over 4 months. Patients were elderly and predominantly male. Cardiovascular comorbidity, smoking history and pulmonary function were similar in each group (mean FEV1 1.37L vs 1.26L). There were several key findings. A reduction in FEV1 occurred after 4 months following treatment with bisoprolol compared with placebo (–70 ml vs +120 ml, p=0.01). Reversibility following inhaled β2-agonist and static lung volumes were not impaired by bisoprolol. All measures of health status exhibited a consistent non-significant improvement, including the Short Form 36 physical and mental component scores, Minnesota Living with Heart Failure Questionnaire, and Chronic Respiratory Questionnaire. The mean number of COPD exacerbations was similar in the bisoprolol and placebo groups. Although recruitment was limited, the results pose crucial questions and provide direction for larger randomised controlled trials. I analysed cross-sectional data from 61 primary care practices (377,439 patients) participating in the Scottish Continuous Morbidity Recording scheme. The prevalence of COPD in patients with HF increased year on year from 19.8% in 1999 to 23.8% in 2004. These changes may previously have been attributed to an ageing population or increasing age of presentation. However, the trend remained significant after age standardisation. A clear socioeconomic gradient was observed, with prevalence greatest in the most deprived. Consultation rates for HF or COPD in those with both conditions were greater than disease specific contact rates in patients with either condition alone. Cardiovascular comorbidity was similar in HF patients with and without COPD, despite differences in smoking history (respectively 76% vs 47%, p<0.001). This is concerning and suggests that common cardiovascular conditions are being under diagnosed (and likely under treated) in patients with HF and COPD. Although overall β-blocker prescribing increased over time, the adjusted odds of β-blocker prescription in patients with COPD was low (odds ratio 0.30 [95% CI 0.28–0.32], p