Global Lung Function Initiative 2012 reference equations for spirometry in the Norwegian population.

We studied the fit of the Global Lung Function Initiative (GLI) all-age reference values to Norwegians, compared them with currently used references (European Community for Steel and Coal (ECSC) and Zapletal) and estimated the prevalence of obstructive lung disease.Spirometry data collected in 30 239 subjects (51.7% females) aged 12-90 years in three population-based studies were converted to z-scores.We studied healthy non-smokers comprising 2438 adults (57.4% females) aged 20-90 years and 8725 (47.7% female) adolescents aged 12-19 years. The GLI-2012 prediction equations fitted the Norwegian data satisfactorily. Median±sd z-scores were respectively 0.02±1.03, 0.01±1.04 and -0.04±0.91 for forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC in males, and -0.01±1.02, 0.07±0.97 and -0.21±0.82 in females. The ECSC and Zapletal references significantly underestimated FEV1 and FVC. Stricter criteria of obstruction (FEV1/FVC GLI-2012 LLN. Corresponding comparison regarding myocardial infarction showed a four-fold higher risk for women.The GLI-2012 reference values fit the Norwegian data satisfactorily and are recommended for use in Norway. Correspondingly, the FEV1/FVC GLI-2012 LLN identifies higher risk of obstructive characteristics than FEV1/FVC <0.7.

Left ventricular dysfunction in COPD without pulmonary hypertension.

OBJECTIVES: We aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance. METHODS: 100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21-24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume. RESULTS: LV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH. CONCLUSIONS: Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices.

Abnormal blood lactate accumulation during repeated exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome.

Post-exertional malaise and delayed recovery are hallmark symptoms of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Studies on repeated cardiopulmonary exercise testing (CPET) show that previous exercise negatively affects oxygen uptake (VO2 ) and power output (PO) in ME/CFS. Whether this affects arterial lactate concentrations ([Laa ]) is unknown. We studied 18 female patients (18-50 years) fulfilling the Canadian Consensus Criteria for ME/CFS and 15 healthy females (18-50 years) who underwent repeated CPETs 24 h apart (CPET1 and CPET2 ) with [Laa ] measured every 30th second. VO2 at peak exercise (VO2peak ) was lower in patients than in controls on CPET1 (P < 0.001) and decreased in patients on CPET2 (P < 0.001). However, the difference in VO2peak between CPETs did not differ significantly between groups. [Laa ] per PO was higher in patients during both CPETs (Pinteraction  < 0.001), but increased in patients and decreased in controls from CPET1 to CPET2 (Pinteraction  < 0.001). Patients had lower VO2 (P = 0.02) and PO (P = 0.002) at the gas exchange threshold (GET, the point where CO2 production increases relative to VO2 ), but relative intensity (%VO2peak ) and [Laa ] at GET did not differ significantly from controls on CPET1 . Patients had a reduction in VO2 (P = 0.02) and PO (P = 0.01) at GET on CPET2 , but no significant differences in %VO2peak and [Laa ] at GET between CPETs. Controls had no significant differences in VO2 , PO or %VO2peak at GET between CPETs, but [Laa ] at GET was reduced on CPET2 (P = 0.008). In conclusion, previous exercise deteriorates physical performance and increases [Laa ] during exercise in patients with ME/CFS while it lowers [Laa ] in healthy subjects.