Jorien Hannink

Heart failure and COPD: partners in crime?

Chronic obstructive pulmonary disease (COPD) and heart failure (HF) are both common diseases with major impact and seem to coexist more frequently than expected from their separate population prevalences. However, estimates of combined prevalence must be interpreted carefully because of imperfections and difficulties in assessment of both diseases. This review aims to highlight HF prevalence in patients with COPD and vice versa, with a critical analysis of studies performed. First, definition, diagnosis, and prevalence of COPD and of HF will be discussed. Subsequently, an overview of important studies concerning combined prevalence with their limitations will be presented. Finally, pathogenic mechanisms and diagnostic considerations in clinical practice will be discussed.

Dynamic hyperinflation after metronome-paced hyperventilation in COPD– A 2 year follow-up

UNLABELLED In contrast to the decline in FEV(1), the behavior of dynamic hyperinflation (DH) over time is unknown in patients with COPD. Metronome-paced hyperventilation (MPH) is a simple applicable surrogate for exercise to detect DH. OBJECTIVE To evaluate changes in MPH-induced DH during two years follow-up in mild-to-severe COPD patients. Additionally, influence of smoking status on DH and the relation between DH and other lung function parameters were assessed. METHODS Patients were recruited from a randomized controlled trial conducted in general practice. Measurements of lung function and DH were performed at baseline and after 12 and 24 months. DH was assessed by MPH with breathing frequency set at twice the baseline rate. Change in inspiratory capacity after MPH was used to reflect change in end-expiratory lung volume and therefore DH, presuming constant total lung capacity. RESULTS During follow-up, 68 patients completed all measurements. DH increased by 0.23±0.06L (p≤0.001). No significant changes in FEV(1) %pred were seen. Smokers had lower FEV(1) and a more rapid decline than non-smokers. DH in smokers increased more over time compared to non-smokers. The amount of DH correlated positively with resting inspiratory capacity. CONCLUSION After two years, a significant increase in MPH-induced DH in COPD patients was demonstrated, which was not accompanied by a decline in FEV(1). It might be that DH is a sensitive measure to track consequences of changes in airflow obstruction.

Validity of Oxycon Mobile in measuring inspiratory capacity in healthy subjects.

Introduction:  Inspiratory capacity (IC) assessments have been performed mainly in laboratory settings, because of fixed measurement devices. Oxycon Mobile® (OM) is the mobile and wireless version of Oxycon Pro® (OP), a commonly used fixed measurement device. The purpose of this study was to examine IC agreement between OM and OP at rest and during steady‐state exercise. Also, the within‐ and between‐days variability of IC’s were determined.

Similar Dynamic Hyperinflation during Arm and Leg Exercise at Similar Ventilation in Chronic Obstructive Pulmonary Disease

PURPOSE Patients with chronic obstructive pulmonary disease (COPD) report more dyspnea during arm than during leg exercise. One of the major causes of dyspnea is dynamic hyperinflation (DH), which is caused by airflow limitation as well as increase in ventilation. The aims of our study were to compare DH at equal ventilation (isoventilation) during arm and legwork and to investigate the effects of breathing pattern on DH. METHODS Thirteen clinically stable patients with mild to very severe COPD (forced expiratory volume in 1 s = 59% ± 21%) participated in this study. Arm and leg constant work rate (CWR) ergometry were performed in random order with ventilation equal to that at 50% of peak armload. The corresponding leg load of that level of ventilation was determined from the incremental leg test. Respiratory physiology was measured breath-by-breath. Change in inspiratory capacity, measured at rest and at 2-min intervals, was used to reflect DH. RESULTS At steady-state isoventilation (37 ± 2 and 36 ± 2 L · min for arm and leg CWR tests, respectively, P > 0.05), armload was 29 ± 5 W and leg load was 52 ± 6 W (P < 0.001). The level of DH, 0.32 ± 0.09 and 0.27 ± 0.08 L during arm and leg exercises, respectively, was not significantly different. However, breathing frequency was greater during arm than during leg exercise (24 ± 1 vs 21 ± 1 breaths per minute, P < 0.01), and the opposite was true for tidal volume (1.56 ± 0.15 vs 1.69 ± 0.14 L, P < 0.01). CONCLUSIONS At similar ventilation, we found a similar degree of DH during arm and leg CWR tests in patients with mild to very severe COPD. Although differences in breathing pattern were observed between arm and leg exercises, these did not affect the level of DH.

Non-invasive ventilation abolishes the IL-6 response to exercise in muscle-wasted COPD patients: A pilot study

Systemic inflammation in patients with chronic obstructive pulmonary disease (COPD) has been related to the development of comorbidities. The level of systemic inflammatory mediators is aggravated as a response to exercise in these patients. The aim of this study was to investigate whether unloading of the respiratory muscles attenuates the inflammatory response to exercise in COPD patients. In a cross‐over design, eight muscle‐wasted stable COPD patients performed 40 W constant work‐rate cycle exercise with and without non‐invasive ventilation support (NIV vs control). Patients exercised until symptom limitation for maximally 20 min. Blood samples were taken at rest and at isotime or immediately after exercise. Duration of control and NIV‐supported exercise was similar, both 12.9 ± 2.8 min. Interleukin‐ 6 (IL‐6) plasma levels increased significantly by 25 ± 9% in response to control exercise, but not in response to NIV‐supported exercise. Leukocyte concentrations increased similarly after control and NIV‐supported exercise by ∼15%. Plasma concentrations of C‐reactive protein, carbonylated proteins, and production of reactive oxygen species by blood cells were not affected by both exercise modes. This study demonstrates that NIV abolishes the IL‐6 response to exercise in muscle‐wasted patients with COPD. These data suggest that the respiratory muscles contribute to exercise‐induced IL‐6 release in these patients.