Relationship between COPD and heart failure
Heart failure is a complex syndrome owing to the inability of the heart to pump sufficient blood to meet the needs of the body’s tissues. It represents the end stage of cardiac disease, mostly following coronary disease or hypertension. Two distinct clinical syndromes have been identified: heart failure with reduced ejection fraction (HFrEF), i.e. EF <40%, which is characterised by abnormalities in left ventricular systolic function, progressive chamber dilation and eccentric remodelling, and heart failure with preserved ejection fraction (HFpEF), i.e. EF ≥50%, which presents normal or near normal systolic function and evidence of diastolic dysfunction with concentric remodelling or hypertrophy [19]. Heart failure with mid-range EF (i.e. EF range 40%-49%) has recently been labelled [19]. About half of patients with heart failure have a normal ejection fraction [20].
Although patients with heart failure present similar clinical signs and symptoms, it is important to distinguish the various forms of heart failure because they differ in pathophysiology, structural changes in the cardiac muscle, neuro-humoral and inflammatory molecular mechanisms, epidemiology, potential susceptibility to environmental triggers and response to treatment [19]. Some biomarkers have been linked to the heart failure subtypes. For example, plasma B-natriuretic peptide concentration in patients with HFpEF was lower than in patients with HFrEF, and highly sensitive troponin T was significantly associated with development of HFrEF; in contrast, growth factor GDF, cystatin C and urinary albumin excretion were significantly associated with the development of HFpEF [21]. Opportunities and challenges of old and new pharmacological treatments of heart failure patients have been updated in the clinical guidelines [22]. However, the role of both beta-blockers and ACE/ARB (angiotensin-converting enzyme/angiotensin receptor blocker) in HFpEF is not well established and there is no evidence-based optimal therapeutic protocol for HFpEF [22].
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In this respect, the finding from the study by Suissa et al. [6], that concomitant use of long-acting bronchodilators influences the incidence of new heart failure (hazard ratio 1.21 among those with no heart failure diagnosis before cohort entry), suggests that these drugs play a role in the development of heart failure in COPD patients in a 1-year follow-up period. Accurate identification of COPD subgroups that are potentially more vulnerable to cardiac drug toxicity is crucial. Measuring coexisting cardiac diseases, subtypes and severity of heart failure, conditions/comorbidities associated with poor prognosis such as peripheral artery disease or diabetes, and severity of lung function impairment is challenging, but cannot be fully achieved in large observational studies based on healthcare electronic databases. Because clinical presentation is fundamental to the diagnosis of heart failure, and heart failure and COPD share both risk factors and clinical presentation, making the correct diagnosis may be difficult [23]. Acute respiratory symptoms may have mixed pulmonary and cardiac origin [24]. Echocardiography is the cornerstone for the diagnosis of heart failure, but in patients with pulmonary emphysema, air trapping may alter echocardiographic acoustic windows, leading to poor image quality in many COPD patients [25]. Moreover, N-terminal pro-brain natriuretic peptide may improve the diagnostic accuracy of heart failure in stable COPD [26].
Rigorous measurement of drug use that is potentially dangerous for the heart is another crucial point in pharmacological safety research, with a particular focus on potential interaction between drugs and a consideration of patients’ adherence to medical prescription and how this changes over time. The increased risk of heart failure resulting from the addition of a LABA rather than tiotropium (hazard ratio 1.28 versus 1.11) compared with the risk of monotherapy is another interesting finding from the work of Suissa et al. [6], and the hypothesis of a trigger action of LABAs in precipitating heart failure cannot be ruled out. Longer follow-up studies could elucidate this aspect. Mechanisms for decompensated heart failure are complex and not fully understood. Multiple risk factors have been proposed and include ischaemia, arrhythmia, respiratory infections, COPD exacerbations and air pollution [19, 27].
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