Katarina Steding-Ehrenborg

Cardiac output and cardiac index measured with cardiovascular magnetic resonance in healthy subjects, elite athletes and patients with congestive heart failure

BackgroundCardiovascular Magnetic Resonance (CMR) enables non-invasive quantification of cardiac output (CO) and thereby cardiac index (CI, CO indexed to body surface area). The aim of this study was to establish if CI decreases with age and compare the values to CI for athletes and for patients with congestive heart failure (CHF).MethodsCI was measured in 144 healthy volunteers (39 ± 16 years, range 21–81 years, 68 females), in 60 athletes (29 ± 6 years, 30 females) and in 157 CHF patients with ejection fraction (EF) below 40% (60 ± 13 years, 33 females). CI was calculated using aortic flow by velocity-encoded CMR and is presented as mean ± SD. Flow was validated in vitro using a flow phantom and in 25 subjects with aorta and pulmonary flow measurements.ResultsThere was a slight decrease of CI with age in healthy subjects (8 ml/min/m2 per year, r2 = 0.07, p = 0.001). CI in males (3.2 ± 0.5 l/min/m2) and females (3.1 ± 0.4 l/min/m2) did not differ (p = 0.64). The mean ± SD of CI in healthy subjects in the age range of 20–29 was 3.3 ± 0.4 l/min/m2, in 30–39 years 3.3 ± 0.5 l/min/m2, in 40–49 years 3.1 ± 0.5 l/min/m2, 50–59 years 3.0 ± 0.4 l/min/m2 and >60 years 3.0 ± 0.4 l/min/m2. There was no difference in CI between athletes and age-controlled healthy subjects but HR was lower and indexed SV higher in athletes. CI in CHF patients (2.3 ± 0.6 l/min/m2) was lower compared to the healthy population (p < 0.001). There was a weak correlation between CI and EF in CHF patients (r2 = 0.07, p < 0.001) but CI did not differ between patients with NYHA-classes I-II compared to III-IV (n = 97, p = 0.16) or patients with or without hospitalization in the previous year (n = 100, p = 0.72). In vitro phantom validation showed low bias (−0.8 ± 19.8 ml/s) and in vivo validation in 25 subjects also showed low bias (0.26 ± 0.61 l/min, QP/QS 1.04 ± 0.09) between pulmonary and aortic flow.ConclusionsCI decreases in healthy subjects with age but does not differ between males and females. We found no difference in CI between athletes and healthy subjects at rest but CI was lower in patients with congestive heart failure. The presented values can be used as reference values for flow velocity mapping CMR.

Atrial aspiration from pulmonary and caval veins is caused by ventricular contraction and secures 70% of the total stroke volume independent of resting heart rate and heart size

Whereas ventricular filling has been extensively studied and debated, atrial filling is less well characterized. Therefore, the aim of this study was to quantify atrial filling secured during ventricular diastole and systole, and to investigate whether atrial filling depends on heart rate (HR) and total heart volume (THV).

The relationship between longitudinal, lateral, and septal contribution to stroke volume in patients with pulmonary regurgitation and healthy volunteers.

Septal systolic motion is towards the left ventricle (LV) in healthy hearts. Patients with pulmonary regurgitation (PR) and right ventricular (RV) volume overload have systolic septal motion toward the RV. This may affect the longitudinal contribution from atrioventricular plane displacement (AVPD) and septal and lateral contribution to stroke volume (SV). The study aimed to quantify these contributions to SV in patients with PR. Cardiac magnetic resonance imaging was used for assessment of cardiac volumes. Patients (n = 30; age 9-59 yr) with PR due to surgically corrected tetralogy of Fallot and 54 healthy controls (age 10-66 yr) were studied. Longitudinal contribution to RVSV was 47 ± 2% (means ± SE) in patients with PR and 79 ± 1% in controls (P < 0.001). Lateral contribution to RVSV and LVSV was 40 ± 1 and 62 ± 2% in patients and 31 ± 1 and 36 ± 1% in controls (P < 0.001 for both). Septal motion contributed to RVSV by 8 ± 1% in patients and by 7 ± 1% to LVSV in controls (P < 0.001). PR patients have decreased longitudinal contribution to RVSV and increased lateral pumping, resulting in larger outer volume changes and septal motion towards the RV. The changes in RV pumping physiology may be explained by RV remodeling resulting in lower systolic inflow of blood into the right atrium in relation to SV. This avoids the development of pendulum volume between the caval veins and right atrium, which would occur in PR patients if longitudinal contribution to SV was preserved. Decreased AVPD suggests that tricuspid annular excursion, a marker of RV function, is less valid in these patients.

Longitudinal strain from velocity encoded cardiovascular magnetic resonance: a validation study

BackgroundRegional myocardial function is typically evaluated by visual assessment by experienced users, or by methods requiring substantial post processing time. Visual assessment is subjective and not quantitative. Therefore, the purpose of this study is to develop and validate a simple method to derive quantitative measures of regional wall function from velocity encoded Cardiovascular Magnetic Resonance (CMR), and provide associated normal values for longitudinal strain.MethodBoth fast field echo (FFE) and turbo field echo (TFE) velocity encoded CMR images were acquired in three long axis planes in 36 healthy volunteers (13 women, 23 men), age 35±12 years. Strain was also quantified in 10 patients within one week after myocardial infarction. The user manually delineated myocardium in one time frame and strain was calculated as the myocardium was tracked throughout the cardiac cycle using an optimization formulation and mechanical a priori assumptions. A phantom experiment was performed to validate the method with optical tracking of deformation as an independent gold standard.ResultsThere was an excellent agreement between longitudinal strain measured by optical tracking and longitudinal strain measured with TFE velocity encoding. Difference between the two methods was 0.0025 ± 0.085 (ns). Mean global longitudinal strain in the 36 healthy volunteers was −0.18 ± 0.10 (TFE imaging). Intra-observer variability for all segments was 0.00 ± 0.06. Inter-observer variability was −0.02 ± 0.07 (TFE imaging). The intra-observer variability for radial strain was high limiting the applicability of radial strain. Mean longitudinal strain in patients was significantly lower (−0.15± 0.12) compared to healthy volunteers (p<0.05). Strain (expressed as percentage of normal strain) in infarcted regions was lower compared to remote areas (p<0.01).ConclusionIn conclusion, we have developed and validated a robust and clinically applicable technique that can quantify longitudinal strain and regional myocardial wall function and present the associated normal values for longitudinal strain.

Left ventricular atrioventricular plane displacement is preserved with lifelong endurance training and is the main determinant of maximal cardiac output.

Ageing has negative effects on cardiac function. Endurance training in young subjects is known to improve cardiac function and the ability to deliver blood to exercising tissue. This study shows that lifelong endurance training maintains cardiac pumping function at a level similar to sedentary young subjects and by the same mechanisms. Healthy untrained elderly subjects have maintained cardiac pumping function but use compensatory mechanisms similar to what is seen in patients with heart failure. Healthy ageing should include regular physical activity to maintain cardiac function.

A new method for vessel segmentation based on a priori input from medical expertise in cine phase-contrast Magnetic Resonance Imaging.

Background Phase contrast magnetic resonance imaging (PC-MRI) is the current gold standard for blood flow quantification. Using this technique it is possible to quantify cardiac output, stroke volume, shunts and valve insufficiencies. The accuracy of flow quantification is highly dependent on the manual delineation of the vessels of interest. Therefore, the purpose of this study is to develop an automatic method for vessel segmentation in PC-MRI sequences.

A longitudinal study on cardiac effects of deconditioning and physical reconditioning using the anterior cruciate ligament injury as a model

Studies of cardiovascular deconditioning are primarily carried out after experimental bed rest. No previous study has followed the cardiovascular effects of decreased and resumed physical activity in athletes after acute physical injury and convalescence. Anterior cruciate ligament (ACL) injury causes a significantly decreased activity level over a long period, making it an ideal model for studying effects of deconditioning and reconditioning. Therefore, the aim of this study was to investigate how cardiac dimensions and maximal exercise capacity change after an ACL‐injury.

Changes in blood volume shunting in patients with atrial septal defects: assessment of heart function with cardiovascular magnetic resonance during dobutamine stress.

Abstract Background The purpose of this study was to determine the effect of stress on left-to-right shunting in patients with atrial septal defect (ASD) and to investigate if the degree of shunting, cardiac output (CO), and right ventricular (RV) volumes are related to exercise capacity. Methods Twenty-six patients with a secundum ASD and 16 healthy volunteers were studied with rest/stress cardiac magnetic resonance using 20 µg/kg/min dobutamine and 0.25–0.75 mg atropine to quantify CO, pulmonary to systemic flow ratio (QP/QS), and left ventricular (LV) and RV volumes. Peak oxygen uptake (VO2peak) was determined on ergospirometry. Results In patients with ASD the QP/QS decreased from 2.0 ± 0.2 at rest to 1.5 ± 0.1 (P < 0.001) during dobutamine stress (n = 20) and shunt volume per heartbeat decreased from 70 ± 9 to 38 ± 9 mL (P < 0.001). However, absolute shunt volume per minute was unchanged (5.1 ± 0.8 vs. 4.5 ± 1.0 L/min, P = 0.32) explained by a higher increase in systemic CO during stress (90 ± 11%) compared with pulmonary CO (43 ± 7%, P < 0.001). In ASD patients, VO2peak correlated with aortic CO during stress (r = 0.77) and QP/QS at rest (r = −0.48) but not during stress (P = 0.09). VO2peak did not correlate with RV volumes in patients. Conclusion Pulmonary to systemic flow ratio and shunt volume per heartbeat decrease during stress in ASD patients. This may be explained by an enhanced LV diastolic function during stress and may have implications to detect disturbances in LV compliance in ASD patients. A high systemic CO during stress is a strong predictor of exercise capacity.

Whole-heart 4D flow can be acquired with preserved quality without respiratory gating facilitating clinical use

Results Stroke volume from 4D flow was lower compared to 2D flow (5ch Resp(+) 86.9±17.0 vs 97.1±22.7, p=0.001; 5ch Resp(-) 83.9±16.0 vs 97.1±22.7, p<0.001), with no difference in bias (-10.3±11.0% vs -13.8±11.9%, p=0.16) (Figure 1). There was a good correlation between Resp(+) and Resp(-) for particle-trace derived volumes (R=0.82, 1.6±12.4%), mean kinetic energy (R=0.86, -4.3±12.4%), peak kinetic energy (R=0.88, 0.7±16.9%), and vortexring volume (R=0.70, -3.7±13.2%). Average scan duration for Resp(-) was shorter compared to Resp(+) (27±9 min vs 61±19 min, p<0.05). Conclusions Whole-heart 4D flow can be acquired with preserved quality without respiratory gating, facilitating clinical use.

Intracardiac hemodynamic forces using 4D flow: a new reproducible method applied to healthy controls, elite athletes and heart failure patients

Background Blood flow in the left ventricle (LV) is closely linked to the function of valves, great vessels and the myocardium. Previous studies have used the Pressure Poisson Equation (PPE) to compute relative pressure fields from 4D flow data. However, the PPE may be numerically sensitive to errors in velocities and delineations. Hemodynamic forces is a quantitative measure similar to relative pressure maps, which may be less sensitive to errors. Therefore, the aim of this study was to investigate the reproducibility of hemodynamic force quantification, and to present initial observations in controls, elite endurance athletes and patients with heart failure.