Heart failure in COPD

Abstract

The main aim of the thesis was to assess the prevalence of heart failure in patients with a diagnosis of chronic obstructive pulmonary disease (COPD). Furthermore, to explore diagnostic strategies (including natriuretic peptides and cardiovascular magnetic resonance imaging (CMR)) to identify heart failure in COPD patients. Finally, to document common mechanisms and possible interactions in the development of the two syndromes.

The prevalence of previously unknown heart failure was assessed in 405 patients ≥ 65 years with a GP diagnosis of COPD, in a stable phase of their disease. All participants underwent an extensive systematic diagnostic work-up and an expert panel established the presence of heart failure and/or COPD during consensus meetings. Of 405 participating patients with a diagnosis of COPD, 83 (20.5%) had previously unrecognised heart failure (42 patients systolic, and 41 'isolated' diastolic, and none 'isolated' right sided heart failure). In total 244 (60.2%) patients had COPD according to the GOLD criteria; in 50 (20.5%) patients combined with unrecognised heart failure. The prevalence of heart failure in stable COPD patients is therefore about four times as high as in subjects aged 65 years or over in the population at large.

Independent clinical determinants of the presence of concomitant heart failure were a history of ischaemic heart disease, body mass index, laterally displaced apex beat, and heart rate. The ROC-area of this multivariate 'clinical model' with these four predictors was 0.70. The ROC area of amino-terminal pro B-type natriuretic peptide (NT-proBNP) as a single test was 0.72. Addition of NT-proBNP to the 'clinical model' significantly increased the ROC-area to 0.77 (95% CI 0.71-0.83). Addition of electrocardiography to the 'clinical model' increased the ROC-area to 0.75 (95% CI 0.69-0.81). Thus, a limited number of easy available items from history and physical examination with addition of NT-proBNP and/or electrocardiography can increase the confidence of the clinician about the presence or absence of concomitant heart failure in patients with stable COPD.

In a nested-case control study we assessed the diagnostic value of cardiovascular magnetic resonance (CMR) imaging for detecting or excluding heart failure in COPD patients. The diagnostic value of CMR was higher than that of electrocardiography or natriuretic peptide measurements. CMR may serve as an alternative in case of uninterpretable echocardiographic results.

We reviewed the literature for etiological and pathophysiological pathways that could be involved in the development of heart failure in the presence of COPD or vice versa. The relationship between COPD and heart failure seems multi-factorial, with tobacco smoking as a common etiologic factor. Local and systemic inflammation, and possibly local and systemic atherosclerosis are common pathways. An important starting point for both diseases seems to be dysfunction of the alveolar-capillary membrane, resulting in decreased oxygen diffusion, and (in more severe cases) sympathetic and structural changes in heart and lungs, which could promote the development of COPD and heart failure. At the moment, much of the interrelation between both syndromes is still unknown.

Conclusion: Clinicians should be aware of the high prevalence of previously unknown heart failure in elderly patients with COPD. Intensified co-operation between general practitioners, pulmonologists and cardiologists is needed in clinical practice and research to extend the diagnostic strategies, further explore common pathways and treatment options, and eventually increase the prognosis of this large patient population.