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Dive into the research topics where Janne Mykland Hilde is active.

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Featured researches published by Janne Mykland Hilde.


European Respiratory Journal | 2013

Haemodynamic responses to exercise in patients with COPD

Janne Mykland Hilde; Ingunn Skjørten; Viggo H. Hansteen; Morten Nissen Melsom; Jonny Hisdal; Sjur Humerfelt; Kjetil Steine

The present study aimed to explore the prevalence of pre-capillary pulmonary hypertension (PH) and characterise haemodynamic vascular responses to physical exercise in chronic obstructive pulmonary disease (COPD) outpatients, where left ventricular dysfunction and comorbidities were excluded. 98 patients with COPD underwent right heart catheterisation at rest and during supine exercise. Mean pulmonary artery pressure (Ppa), pulmonary capillary wedge pressure (Ppcw) and cardiac output (CO) were measured at rest and during exercise. Exercise-induced increase in mean Ppa was interpreted relative to increase in blood flow, mean Ppa/CO, workload (W) and mean Ppa/W. Pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC) were calculated. PH at rest was defined as mean Ppa at rest ≥25 mmHg and Ppcw at rest <15 mmHg. Prevalence of PH was 5%, 27% and 53% in Global Initiative for Chronic Obstructive Lung Disease stages II, III and IV, respectively. The absolute exercise-induced rise in mean Ppa did not differ between subjects with and without PH. Patients without PH showed similar abnormal haemodynamic responses to exercise as the PH group, with increased PVR, reduced PAC and steeper slopes for mean Ppa/CO and mean Ppa/W. Exercise revealed abnormal physiological haemodynamic responses in the majority of the COPD patients. The future definition of PH on exercise in COPD should rely on the slope of mean Ppa related to cardiac output and workload rather than the absolute values of mean Ppa.


Open Heart | 2017

Mechanisms of ECG signs in chronic obstructive pulmonary disease

Marte Strømsnes Larssen; Kjetil Steine; Janne Mykland Hilde; Ingunn Skjørten; Christian Hodnesdal; Knut Liestøl; Knut Gjesdal

Objective Patients with chronic obstructive pulmonary disease (COPD) often have abnormal ECGs. Our aim was to separate the effects on ECG by airway obstruction, emphysema and right ventricular (RV) afterload in patients with COPD. Methods A cross-sectional study was performed on 101 patients with COPD without left heart disease and 32 healthy age-matched controls. Body mass index (BMI) was measured, and pulmonary function tests, ECG, echocardiography and right heart catheterisation (only patients) were performed. Variables were grouped into (1) airway obstruction by FEV% (percentage of forced expiratory volume)_predicted, (2) emphysema by residual volume/total lung capacity and residual volume (percent of predicted) and (3) RV afterload by mean pulmonary pressure, artery compliance, vascular resistance and RV wall thickness. Results In multivariate regression analysis, emphysema correlated negatively to R+S amplitudes in horizontal and frontal leads, RV/left ventricle (LV) end-diastolic volume ratio to horizontal amplitudes and BMI negatively to frontal amplitudes. Increased airway obstruction, RV afterload and BMI correlated with horizontal QRS-axis clockwise rotation. Airway obstruction, RV afterload, RV/LV end-diastolic volume ratio and BMI correlated to the Sokolow-Lyon Index for RV, and RV afterload negatively to Sokolow-LyonIndex for LV. Several classical ECG changes could, however, not be ascribed to specific mechanisms. Conclusions In COPD, the various pathophysiological mechanisms modify the ECG differently. Increased airway obstruction and RV afterload mainly increase the Sokolow-Lyon Index for RV mass and associate with clockwise rotation of the horizontal QRS-axis, whereas emphysema reduces the QRS amplitudes. BMI is an equally important determinant for the majority of the ECG changes.


COPD: Journal of Chronic Obstructive Pulmonary Disease | 2016

Assessment of Right Ventricular Afterload in COPD

Janne Mykland Hilde; Ingunn Skjørten; Hansteen; Morten Nissen Melsom; Dan Atar; Jonny Hisdal; Sjur Humerfelt; Kjetil Steine

Abstract Background: We aimed to study whether pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) could be predicted by conventional echo Doppler and novel tissue Doppler imaging (TDI) in a population of chronic obstructive pulmonary disease (COPD) free of LV disease and co-morbidities.Methods: Echocardiography and right heart catheterization was performed in 100 outpatients with COPD. By echocardiography the time-integral of the TDI index, right ventricular systolic velocity (RVSmVTI) and pulmonary acceleration-time (PAAcT) were measured and adjusted for heart rate. The COPD patients were randomly divided in a derivation (n = 50) and a validation cohort (n = 50). Results: PH (mean pulmonary artery pressure (mPAP) ≥ 25mmHg) and elevated PVR ≥ 2Wood unit (WU) were predicted by satisfactory area under the curve for RVSmVTI of 0.93 and 0.93 and for PAAcT of 0.96 and 0.96, respectively. Both echo indices were 100% feasible, contrasting 84% feasibility for parameters relying on contrast enhanced tricuspid-regurgitation. RVSmVTI and PAAcT showed best correlations to invasive measured mPAP, but less so to PVR. PAAcT was accurate in 90- and 78% and RVSmVTI in 90- and 84% in the calculation of mPAP and PVR, respectively. Conclusions: Heart rate adjusted-PAAcT and RVSmVTI are simple and reproducible methods that correlate well with pulmonary artery pressure and PVR and showed high accuracy in detecting PH and increased PVR in patients with COPD. Taken into account the high feasibility of these two echo indices, they should be considered in the echocardiographic assessment of COPD patients.


International Journal of Chronic Obstructive Pulmonary Disease | 2017

Cardiopulmonary exercise test and PaO 2 in evaluation of pulmonary hypertension in COPD

Ingunn Skjørten; Janne Mykland Hilde; Morten Nissen Melsom; Jonny Hisdal; Viggo H. Hansteen; Kjetil Steine; Sjur Humerfelt

Background Exercise tolerance decreases as COPD progresses. Pulmonary hypertension (PH) is common in COPD and may reduce performance further. COPD patients with and without PH could potentially be identified by cardiopulmonary exercise test (CPET). However, results from previous studies are diverging, and a unified conclusion is missing. We hypothesized that CPET combined with arterial blood gases is useful to discriminate between COPD outpatients with and without PH. Methods In total, 93 COPD patients were prospectively included. Pulmonary function tests, right heart catheterization, and CPET with blood gases were performed. The patients were divided, by mean pulmonary artery pressure, into COPD-noPH (<25 mmHg) and COPD-PH (≥25 mmHg) groups. Linear mixed models (LMMs) were fitted to estimate differences when repeated measurements during the course of exercise were considered and adjusted for gender, age, and airway obstruction. Results Ventilatory and/or hypoxemic limitation was the dominant cause of exercise termination. In LMM analyses, significant differences between COPD-noPH and COPD-PH were observed for PaO2, SaO2, PaCO2, ventilation, respiratory frequency, and heart rate. PaO2 <61 mmHg (8.1 kPa) during unloaded pedaling, the only load level achieved by all the patients, predicted PH with a sensitivity of 86% and a specificity of 78%. Conclusion During CPET, low exercise performance and PaO2 strongly indicated PH in COPD patients.


Journal of the American College of Cardiology | 2013

Right ventricular dysfunction and remodeling in chronic obstructive pulmonary disease without pulmonary hypertension.

Janne Mykland Hilde; Ingunn Skjørten; Ole Jørgen Grøtta; Viggo H. Hansteen; Morten Nissen Melsom; Jonny Hisdal; Sjur Humerfelt; Kjetil Steine


Respiratory Medicine | 2013

Pulmonary artery pressure and PaO2 in chronic obstructive pulmonary disease

Ingunn Skjørten; Janne Mykland Hilde; Morten Nissen Melsom; Viggo H. Hansteen; Kjetil Steine; Sjur Humerfelt


Archive | 2013

Pulmonary artery pressure and PaO 2 in chronic obstructive pulmonary disease

Ingunn Skjørten; Janne Mykland Hilde; Morten Nissen Melsom; Viggo H. Hansteen; Kjetil Steine; Sjur Humerfelt


European Respiratory Journal | 2016

Mechanisms of ECG changes in chronic obstructive pulmonary disease

Marte Strømsnes Larssen; Christian Hodnesdal; Ingunn Skjørten; Janne Mykland Hilde; Kjetil Steine; Knut Liestøl; Knut Gjesdal


Respiratory Medicine | 2013

Pulmonary hypertension in COPD; the importance of PaO2

Ingunn Skjørten; Janne Mykland Hilde; Morten Nissen Melsom; Viggo H. Hansteen; Kjetil Steine; Sjur Humerfelt


European Heart Journal | 2013

Reduced systemic arterial compliance and subclinical LV systolic dysfunction in COPD

Janne Mykland Hilde; Jonny Hisdal; Morten Nissen Melsom; Viggo H. Hansteen; Ingebjørg Seljeflot; Harald Arnesen; Kjetil Steine

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Kjetil Steine

Akershus University Hospital

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Morten Nissen Melsom

Akershus University Hospital

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Sjur Humerfelt

Oslo University Hospital

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Jonny Hisdal

Oslo University Hospital

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