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Featured researches published by Espen Boe.


European Journal of Echocardiography | 2015

Non-invasive myocardial work index identifies acute coronary occlusion in patients with non-ST-segment elevation-acute coronary syndrome

Espen Boe; Kristoffer Russell; Christian Eek; Morten Eriksen; Espen W. Remme; Otto A. Smiseth; Helge Skulstad

AIMS Acute coronary artery occlusion (ACO) occurs in ∼30% of patients with non-ST-segment elevation-acute coronary syndrome (NSTE-ACS). We investigated the ability of a regional non-invasive myocardial work index (MWI) to identify ACO. METHODS AND RESULTS Segmental strain analysis was performed before coronary angiography in 126 patients with NSTE-ACS. Left ventricular (LV) pressure was estimated non-invasively using a standard waveform fitted to valvular events and scaled to systolic blood pressure. MWI was calculated as the area of the LV pressure-strain loop. Empirical cut-off values were set to identify segmental systolic dysfunction for MWI (<1700 mmHg %) and strain (more than -14%). The number of dysfunctional segments was used in ROC analysis to identify ACO. The presence of ≥4 adjacent dysfunctional segments assessed by MWI was significantly better than both global strain and ejection fraction at detecting the occurrence of ACO (P < 0.05). Regional MWI had a higher sensitivity (81 vs. 78%) and especially specificity (82 vs. 65%) compared with regional strain. Logistic regression demonstrated that elevated systolic blood pressure significantly decreased the probability of actual ACO in a patient with an area of impaired regional strain. CONCLUSION The presence of a region of reduced MWI in patients with NSTE-ACS identified patients with ACO and was superior to all other parameters. The regional MWI was able to account for the influence of systolic blood pressure on regional contraction. We therefore propose that MWI may serve as an important clinical tool for selecting patients in need of prompt invasive treatment.


American Journal of Physiology-heart and Circulatory Physiology | 2014

Cardiac responses to left ventricular pacing in hearts with normal electrical conduction: beneficial effect of improved filling is counteracted by dyssynchrony

Espen Boe; Kristoffer Russell; Espen W. Remme; Ola Gjesdal; Otto A. Smiseth; Helge Skulstad

Cardiac resynchronization therapy (CRT) has been proposed in heart failure patients with narrow QRS, but the mechanism of a potential beneficial effect is unknown. The present study investigated the hypothesis that left ventricular (LV) pacing increases LV end-diastolic volume (LVEDV) by allowing the LV to start filling before the right ventricle (RV) during narrow QRS in an experimental model. LV and biventricular pacing were studied in six anesthetized dogs before and after the induction of LV failure. Function was evaluated by pressures and dimensions, and dyssynchrony was evaluated by electromyograms and deformation. In the nonfailing heart, LV pacing gave the LV a head start in filling relative to the RV (P < 0.05) and increased LVEDV (P < 0.05). The response was similar during LV failure when RV diastolic pressure was elevated. The pacing-induced increase in LVEDV was attributed to a rightward shift of the septum (P < 0.01) due to an increased left-to-right transseptal pressure gradient (P < 0.05). LV pacing, however, also induced dyssynchrony (P < 0.05) and therefore reduced LV stroke work (P < 0.05) during baseline, and similar results were seen in failing hearts. Biventricular pacing did not change LVEDV, but systolic function was impaired. This effect was less marked than with LV pacing. In conclusion, pacing of the LV lateral wall increased LVEDV by displacing the septum rightward, suggesting a mechanism for a favorable effect of CRT in narrow QRS. The pacing, however, induced dyssynchrony and therefore reduced LV systolic function. These observations suggest that detrimental effects should be considered when applying CRT in patients with narrow QRS.


Journal of Applied Physiology | 2018

Dysfunction of the Systemic Right Ventricle After Atrial Switch: Physiological Implications of Altered Septal Geometry and Load

Petter Storsten; Morten Eriksen; Espen W. Remme; Espen Boe; Gunnar Erikssen; Otto A. Smiseth; Helge Skulstad

Atrial switch operation in patients with transposition of the great arteries (TGA) leads to leftward shift and changes the geometry of the interventricular septum. By including the implications of regional work and septal curvature, this study investigates if changes in septal function and geometry contribute to reduced function of the systemic right ventricle (RV) in adult TGA patients. Regional myocardial work estimation has been possible by applying a recently developed method for noninvasive work calculation based on echocardiography. In 14 TGA patients (32 ± 6 yr, means ± SD) and 14 healthy controls, systemic ventricular systolic strains were measured by speckle tracking echocardiography and regional work was calculated by pressure-strain analysis. In TGA patients, septal longitudinal strain was reduced to -14 ± 2 vs. -20 ± 2% in controls ( P < 0.01) and septal work was reduced from 2,046 ± 318 to 1,146 ± 260 mmHg·% ( P < 0.01). Septal circumferential strain measured in a subgroup of patients was reduced to -11 ± 3 vs. -27 ± 3% in controls ( P < 0.01), and a reduction of septal work (540 ± 273 vs. 2,663 ± 459 mmHg·%) was seen ( P < 0.01). These reductions were in part attributed to elevated afterload due to increased radius of curvature of the leftward shifted septum. To conclude, in this mechanistic study we demonstrate that septal dysfunction contributes to failure of the systemic RV after atrial switch in TGA patients. This is potentially a long-term response to increased afterload due to a flatter septum and suggests that medical therapy that counteracts septal flattening may improve function of the systemic RV. NEW & NOTEWORTHY We have demonstrated that transposition of the great arteries patients with systemic right ventricles (RVs) have reduced function of the interventricular septum (IVS). Since the IVS is constructed to eject into the systemic circulation, it may seem unexpected that it does not maintain function when being part of the systemic RV. By applying the principles of regional work, wall tension, and geometry, we have identified unfavorable working conditions for the IVS when the RV adapts to systemic pressures.


Jacc-cardiovascular Imaging | 2018

Afterload Hypersensitivity in Patients With Left Bundle Branch Block

John Aalen; Petter Storsten; Espen W. Remme; Per A. Sirnes; Ola Gjesdal; Camilla Kjellstad Larsen; Espen Boe; Helge Skulstad; Jonny Hisdal; Otto A. Smiseth


European Cardiology Review | 2012

Heart Failure with Preserved Ejection Fraction – A Review

Otto A. Smiseth; Anders Opdahl; Espen Boe; Helge Skulstad


European Heart Journal | 2018

P4709Left ventricular free wall pacing causes excessive work load in septum and right ventricular free wall-a mirror image of left bundle branch block

P Storsten; Espen Boe; J Aalen; Espen W. Remme; Ola Gjesdal; O S Andersen; Otto A. Smiseth; Helge Skulstad


European Heart Journal | 2018

P4707Cardiac resynchronization therapy - Always right for the right ventricle?

P Storsten; J Aalen; Espen Boe; Espen W. Remme; C K Larsen; Ola Gjesdal; O S Andersen; Jürgen Duchenne; Jens-Uwe Voigt; Otto A. Smiseth; Helge Skulstad


European Heart Journal | 2017

P736Relative downregulation of septal function and metabolism in TGA patients with atrial switch

P Storsten; Jan Gunnar Fjeld; A.G. Sherwani; Espen Boe; Espen W. Remme; Ola Gjesdal; Gunnar Erikssen; Otto A. Smiseth; Helge Skulstad


Circulation | 2015

Abstract 12002: Increasing Heart Rate in Left Bundle Branch Block Results in Incomplete Relaxation and Increases Left Ventricular Diastolic Stiffness

O S Andersen; Espen Boe; Helge Skulstad; Petter Storsten; Hans Henrik Odland; Otto A. Smiseth; Espen W. Remme


Circulation | 2013

Abstract 15734: Coronary Artery Occlusion in N-STEMI Patients Can Be Identified by Assessing Segmental Work Which Incorporates the Effects of Afterload on Strain Measurements

Espen Boe; Kristoffer Russell; Christian Eek; Morten Eriksen; Bjørnar Grenne; Harald Brunvand; Otto A. Smiseth; Helge Skulstad

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Helge Skulstad

Oslo University Hospital

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Espen W. Remme

Oslo University Hospital

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Ola Gjesdal

Oslo University Hospital

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O S Andersen

Oslo University Hospital

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P Storsten

Oslo University Hospital

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