Heart failure with preserved ejection fraction (HFpEF) is often detected in chronic obstructive pulmonary disease (COPD) patients, but the relationship of the two entities is less well understood. COPD is a potentially important comorbidity in HFpEF patients as many signs found in COPD are similar to those of heart failure. So defining and identifying HFpEF are controversial and problematic in patients with COPD [1].

In the current issue of the journal, Marcun et al. [2] analyze the prevalence and prognostic implications of co-existing HFpEF in patients hospitalized for acute exacerbation of COPD stating that HFpEF may not be an independent predictor of all-cause mortality.

The entire concept of HFpEF in COPD patients needs to be reconsidered within the framework of pathophysiology. Indeed, the dominant mechanical characteristic of the lung in COPD is an increased stiffness that generates an increased cardiac work. The heart has to push and pull against the lung to allow systole and diastole. When the lung is stiff, as in COPD patients, the work of the heart increases, and HFpEF is the unavoidable consequence [3–5]. Therefore it is inevitable that there is a high frequency of left ventricular diastolic dysfunction (LVDD) in hospitalized patients with COPD, and LVDD in the context of the HFpEF may occur at the early stages of COPD, prior to changes in right ventricular function and pulmonary hypertension.

Similarly, Marcun et al. report that patients with HFpEF have elevated NT-proBNP levels compared to patients without HFpEF. Actually, previous results show that there is no difference in LVDD between the mild/moderate and severe/very severe COPD groups, but NT-proBNP levels remain significantly different, suggesting that NT-proBNP levels increase with the severity of COPD, and that the mechanisms for these changes may be independent from HFpEF [6]. Elevated NT-proBNP levels in patients with COPD can be explained within the above described lung and heart interdependency. In details, COPD causes significant extrapulmonary effects, and is associated with comorbidities that can contribute to the severity of the disease and prognosis. An explanation for the close association between COPD and HFpEF involves coupling between impaired LV filling and pulmonary venous changes due to lung parenchymal abnormalities [7, 8]. Pulmonary hypertension is often present in patients with HFpEF and COPD, and its presence is associated with worse survival. Some analysis in the HFpEF population, based on exclusion of HFpEF patients with a diagnosis of COPD or known significant lung disease, demonstrates that HFpEF still has a higher proportion of pulmonary hypertension, and is still a strong predictor of mortality [9], in opposition to the current study wherein HFpEF is not identified as an independent predictor of mortality.

Overall, evidence suggests that HFpEF is not merely a disease of old age and multiple comorbidities, but is a distinct entity associated with a poor prognosis and severe cardiovascular dysfunction. Unfortunately the overlapping symptom of dyspnea with both HFpEF and COPD may lead to misapplication of therapy. HF patients with COPD are less likely to receive beta-blockers compared to those without COPD, possibly due to clinicians’ concerns about precipitating bronchoconstriction [10]. HF patients with COPD also tend to have higher levels of creatinine, and underuse of angiotensin converting enzyme (ACE) inhibitors and mineralocorticoid receptor antagonists [11]. These characteristics likely contribute to the increased mortality risk in patients affected by COPD and HFpHF. An accurate examination of the influence of therapy on the results is lacking in the current paper.

In conclusion, in a population with COPD, HFpEF should be considered as an unavoidable comorbidity to identify the most beneficial therapies and improve its prognosis.