O7.2.1 Heart failure

The diagnosis of heart failure coexisting with COPD is complicated by symptom overlap and the technical challenges of echocardiography in COPD. The natriuretic peptides, including BNP and NT-proBNP, can assist in identifying heart failure in the setting of acute breathlessness, but do not exclude comorbid COPD, and currently have an unclear diagnostic role in stable disease. The prevalence of heart failure in COPD patients is estimated at 20 to 32%. For the converse situation in heart failure, COPD prevalence has been previously quoted as 10 to 33%. A prospective multicentre sub study of patients admitted with heart failure (Iversen 2008) [evidence level III-2] confirmed COPD in 35% of participants using spirometry. Self-reported COPD diagnosis had poor sensitivity to identify these individuals. Prevalence of COPD was higher in those heart failure patients with preserved left ventricular ejection fraction (LVEF), but was also substantial in those with reduced LVEF (41% versus 31%, p = 0.03). Potential mechanisms contributing to the high rates of heart failure in COPD include coronary artery disease (CAD), hyperinflation, sympathetic nervous system and renin-angiotensin system activation, pulmonary hypertension and right heart dysfunction.  A study by Labaki et al found levels of the natriuretic peptide, NT-proBNP to be an independent risk factor for COPD exacerbations (Labaki 2018).

Barr and colleagues investigated a subgroup from the Multi-ethnic Study of Atherosclerosis (MESA): a multi-centre, prospective, cross-sectional study of cardiovascular disease (CVD). The group initially reported a linear relationship between extent of emphysema and impairment of LV filling, reduction of stroke volume and of cardiac output, without a threshold effect, in “healthy” patients prospectively assessed for cardiac disease with magnetic resonance imaging (MRI) (Barr 2010) [evidence level III-2]. The same association was not present for left ventricular ejection fraction. Smoking status was an effect modifier, with a greater effect seen for current smokers. Similar relationships were obtained for measures of airflow limitation. Mechanisms have been further explored (Stone 2016) in a randomised crossover trial of combination ICS/LABA (fluticasone furoate/vilanterol) versus placebo in patients with at least moderate COPD and bronchodilator-responsive gas trapping. Compared with placebo, active treatment was associated with significantly reduced residual volume -429 ml, 95% CI 2.74-8.91, improved right and left ventricular filling indices and cardiac index. In COPD, heart failure adversely impacts on morbidity and prognosis. A prospective cohort study (Boudestein 2009) [evidence level III-2] further clarifies this relationship; Boudestein’s group sought to quantify heart failure and its prognostic implications in 405 Dutch general practice patients identified as having COPD. Extensive diagnostic testing revealed occult heart failure in 20.5%, of which half was systolic, half diastolic and none was cor pulmonale. Similar proportions were found in the subset of 244 patients meeting GOLD criteria for COPD. Not unexpectedly, comorbid heart failure proved a strong predictor of all cause mortality over the mean follow up duration of 4.2 years for the whole cohort (adjusted HR 2.1, 95% CI 1.2-3.6, p=0.01) and for “GOLD COPD patients” (adjusted HR 2.0, 95% CI 1.0-3.7, p=0.04).

Since COPD and heart failure present with similar symptoms and frequently do coexist, the clinical implication is that the opportunity for intervention will be missed unless both diagnoses are specifically sought using careful clinical assessment in conjunction with appropriately directed investigations.