Responses to incremental exercise and the impact of the coexistence of HF and COPD on exercise capacity: a follow-up study

Our aim was to evaluate: (1) the prevalence of coexistence of heart failure (HF) and chronic obstructive pulmonary disease (COPD) in the studied patients; (2) the impact of HF + COPD on exercise performance and contrasting exercise responses in patients with only a diagnosis of HF or COPD; and (3) the relationship between clinical characteristics and measures of cardiorespiratory fitness; (4) verify the occurrence of cardiopulmonary events in the follow-up period of up to 24 months years. The current study included 124 patients (HF: 46, COPD: 53 and HF + COPD: 25) that performed advanced pulmonary function tests, echocardiography, analysis of body composition by bioimpedance and symptom-limited incremental cardiopulmonary exercise testing (CPET) on a cycle ergometer. Key CPET variables were calculated for all patients as previously described. The [Formula: see text] (E)/[Formula: see text] CO(2) slope was obtained through linear regression analysis. Additionally, the linear relationship between oxygen uptake and the log transformation of [Formula: see text] (E) (OUES) was calculated using the following equation: [Formula: see text] O(2) = a log [Formula: see text] (E) + b, with the constant ‘a’ referring to the rate of increase of [Formula: see text] O(2). Circulatory power (CP) was obtained through the product of peak [Formula: see text] O(2) and peak systolic blood pressure and Ventilatory Power (VP) was calculated by dividing peak systolic blood pressure by the [Formula: see text] (E)/[Formula: see text] CO(2) slope. After the CPET, all patients were contacted by telephone every 6 months (6, 12, 18, 24) and questioned about exacerbations, hospitalizations for cardiopulmonary causes and death. We found a 20% prevalence of HF + COPD overlap in the studied patients. The COPD and HF + COPD groups were older (HF: 60 ± 8, COPD: 65 ± 7, HF + COPD: 68 ± 7). In relation to cardiac function, as expected, patients with COPD presented preserved ejection fraction (HF: 40 ± 7, COPD: 70 ± 8, HF + COPD: 38 ± 8) while in the HF and HF + COPD demonstrated similar levels of systolic dysfunction. The COPD and HF + COPD patients showed evidence of an obstructive ventilatory disorder confirmed by the value of %FEV(1) (HF: 84 ± 20, COPD: 54 ± 21, HF + COPD: 65 ± 25). Patients with HF + COPD demonstrated a lower work rate (WR), peak oxygen uptake ([Formula: see text] O(2)), rate pressure product (RPP), CP and VP compared to those only diagnosed with HF and COPD. In addition, significant correlations were observed between lean mass and peak [Formula: see text] O(2) (r: 0.56 p < 0.001), OUES (r: 0.42 p < 0.001), and O(2) pulse (r: 0.58 p < 0.001), lung diffusing factor for carbon monoxide (D(LCO)) and WR (r: 0.51 p < 0.001), D(LCO) and VP (r: 0.40 p: 0.002), forced expiratory volume in first second (FEV(1)) and peak [Formula: see text] O(2) (r: 0.52; p < 0.001), and FEV(1) and WR (r: 0.62; p < 0.001). There were no significant differences in the occurrence of events and deaths contrasting both groups. The coexistence of HF + COPD induces greater impairment on exercise performance when compared to patients without overlapping diseases, however the overlap of the two diseases did not increase the probability of the occurrence of cardiopulmonary events and deaths when compared to groups with isolated diseases in the period studied. CPET provides important information to guide effective strategies for these patients with the goal of improving exercise performance and functional capacity. Moreover, given our findings related to pulmonary function, body composition and exercise responses, evidenced that the lean mass, FEV(1) and D(LCO) influence important responses to exercise.