Impact of Chronic Obstructive Pulmonary Disease in Heart Failure With Preserved Ejection Fraction

Patient phenotype profiling in heart failure with preserved ejection fraction to guide therapeutic decision making. A scientific statement of the Heart Failure Association, the European Heart Rhythm Association of the European Society of Cardiology, and the European Society of Hypertension

“…104 They are also more likely to report more concentric left ventricular geometry, greater left ventricular mass and fibrosis, and greater thoracic aortic stiffness. 106 Chronic obstructive pulmonary disease might mimic HFpEF symptoms (e.g. dyspnoea, exercise limitation) and signs and therefore increase the chance of misdiagnosing HFpEF.…”

“…COPD versus non‐COPD patients hospitalized for HFpEF are more likely to be males, have a history of hospitalizations, be smokers, and use diuretics 104 . They are also more likely to report more concentric left ventricular geometry, greater left ventricular mass and fibrosis, and greater thoracic aortic stiffness 106 …”

Sodium–glucose cotransporter 2 inhibitors in heart failure with preserved ejection fraction and chronic obstructive pulmonary disease — No heterogeneity

“…3 Patients with HFpEF and COPD show a higher degree of systemic large artery stiffening, left ventricular (LV) remodelling and fibrosis compared to patients with either COPD or HFpEF alone. 4 Activated neutrophils may contribute to progressive airway disease as well as COPD exacerbations and chronic systemic inflammation, 5 and cause fibrosis and tissue rarefaction in multiple tissues 6 and myocardial functional impairment. 7 Both syndromes seem to share an important role of extracellular matrix and immune infiltration by macrophages.…”

“…COPD may share underlying pathophysiologic mechanisms that drive both HFpEF and COPD with potential causal relationships where COPD plays a pertinent role both as a consequence and driver of systemic and microvascular inflammation 3 . Patients with HFpEF and COPD show a higher degree of systemic large artery stiffening, left ventricular (LV) remodelling and fibrosis compared to patients with either COPD or HFpEF alone 4 . Activated neutrophils may contribute to progressive airway disease as well as COPD exacerbations and chronic systemic inflammation, 5 and cause fibrosis and tissue rarefaction in multiple tissues 6 and myocardial functional impairment 7 .…”

Exercise intolerance in heart failure with preserved ejection fraction: Causes, consequences and the journey towards a cure

“…The resulting increase in cardiac afterload is associated with diminished myocardial performance (Chirinos, Segers et al., 2019; Reddy et al., 2017), greater PCWP/CO response to exercise, and lower peak $${\dot{V}}_{{{\mathrm{O}}}_2}$$ (Zern et al., 2021). However, the extent to which central arterial stiffness and pressure amplification contribute to exercise intolerance may be considerably heterogeneous due to the presence of specific comorbidities (Chirinos, Bhattacharya et al., 2019; Jain et al., 2021) and biological sex (Lau et al., 2022), and thus additional studies are needed to define the contribution of arterial stiffness to specific HFpEF phenotypes.…”