Sigurdur S Stephensen

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.

Agreement of left ventricular mass in steady state free precession and delayed enhancement MR images: implications for quantification of fibrosis in congenital and ischemic heart disease

BackgroundLeft ventricular mass (LVM) is used when expressing infarct or fibrosis as a percentage of the left ventricle (LV). Quantification of LVM is interchangeably carried out in cine steady state free precession (SSFP) and delayed enhancement (DE) magnetic resonance imaging (MRI). However, these techniques may yield different LVM. Therefore, the aim of the study was to compare LVM determined by SSFP and DE MRI in patients and determine the agreement with these sequences with ex vivo data in an experimental animal model.MethodsEthics committees approved human and animal studies. Informed written consent was obtained from all patients. SSFP and DE images were acquired in 60 patients (20 with infarction, 20 without infarction and 20 pediatric patients). Ex vivo MRI was used as reference method for LVM in 19 pigs and compared to in vivo SSFP and DE.ResultsLVM was greater in SSFP than in DE (p < 0.001) with a bias of 5.0 ± 6.7% in humans (r2 = 0.98), and a bias of 7.3 ± 6.7% (p < 0.001) in pigs (r2 = 0.83). Bias for SSFP and DE images compared to ex vivo LVM was -0.2 ± 9.0% and -7.7 ± 8.5% respectively.ConclusionsLVM was higher when measured with SSFP compared to DE. Thus, the percentage infarction of the LV will differ if SSFP or DE is used to determine LVM. There was no significant difference between SSFP and ex vivo LVM suggesting that SSFP is more accurate for LVM quantification. To avoid intrinsic error due to the differences between the sequences, we suggest using DE when expressing infarct as a percentage of LVM.

Isolated pulmonary regurgitation causes decreased right ventricular longitudinal function and compensatory increased septal pumping in a porcine model

Longitudinal ventricular contraction is a parameter of cardiac performance with predictive power. Right ventricular (RV) longitudinal function is impaired in patients with free pulmonary regurgitation (PR) following corrective surgery for Tetralogy of Fallot (TOF). It remains unclear whether this is a consequence of the surgical repair, or whether it is inherent to PR. The aim of this study was to assess the relationship between longitudinal, lateral and septal pumping in a porcine model of isolated PR.

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.

Alterations in ventricular pumping in patients with atrial septal defect at rest, during dobutamine stress and after defect closure

Regional ventricular pumping mechanisms in patients with volume‐loaded right ventricles (RV) are altered, but the cause is unknown. The aim was to determine whether these changes in ventricular pumping mechanisms are influenced by the RV dilatation itself or the aetiology behind it.

Regional contributions to ventricular stroke volumes are affected on the left side, and not on the right in patients with pulmonary hypertension

Background Right ventricular (RV) function is of prognostic value in patients with pulmonary hypertension (PH). Eighty percent of RV stroke volume (SV) comes from longitudinal ventricular function in a normal population, while longitudinal function accounts for 60 % of left ventricular (LV) SV. Radial function, consisting of septal and lateral function, accounts for the remaining contribution to SV. Longitudinal, septal and lateral changes in regional function has been seen as pressure is elevated on the right side. The aim of this study was quantify the longitudinal, septal and lateral contributions to SV in patients with PH using cardiac magnetic resonance (CMR), and demonstrate if there is a relationship between pulmonary pressure and these contributors to SV.

Factors determining exercise capacity in patients with atrial septal defect: assessment of heart function with CMR during dobutamine stress

Background Patients with left to right shunting of blood through an atrial septal defect (ASD) have decreased exercise capacity. This study hypothesized that central factors influence exercise capacity, namely systemic and pulmonary cardiac output and right ventricular (RV) function during stress as well as left atrial pressure (LAP) and pulmonary artery pressure (PAP). Previous studies have found varying effects of stress and increased heart rate on the degree of shunting. The purpose of the study was therefore to determine if atrial shunting ratio changes during stress and examine if central factors can explain decreased exercise capacity in ASD patients. Methods Eighteen patients with ASD and 16 healthy volunteers underwent cardiac magnetic resonance at rest and during 20 µg/kg/min dobutamine infusion and 0.25-0.75 mg atropine injection, aiming for an increase in heart rate to at least 70% of age-predicted maximal pulse. Two patients could not undergo stress CMR. Cine ssfp images were used for LV and RV volumes. Flow velocity mapping of the aorta and pulmonary trunk quantified cardiac output and shunt ratio (QP/QS) at rest and during stress. Ergospirometry was used to determine peak oxygen uptake (VO2peak). LAP and PAP were invasively measured at rest at the time of transcutaneous closure of the ASD.

Alterations in right ventricular pumping in patients with atrial septal defect at rest and during dobutamine stress

Background CMR can provide details on ventricular pumping by subdividing the contribution to stroke volume (SV) into longitudinal shortening and radial inward motion of the ventricular borders. Previous studies have shown that patients with volume loaded dilated right ventricles (RV) due to pulmonary regurgitation (PR) have decreased longitudinal contribution to RVSV. Patients with atrial septal defects (ASD) also have volume loaded dilated RVs but it is not known if this affects longitudinal shortening.

Quantification of the contribution of septal movement to stroke volume in healthy subjects, athletes, patients with pulmonary insufficiency and patients with pulmonary hypertension

Background In theory, movement of the septum contributes to left ventricular stroke volume (LVSV) if the movement is toward the left ventricle (LV) in systole. If the septum movement is toward the right ventricle (RV), as in dyssynchrony, the septal contribution to LVSV decreases. In patients with increased volume load of the RV the septum may move towards the RV and contribute to right ventricular stroke volume RVSV) at the expense of LVSV. The amount of contribution to stroke volume from septal movement is not kown. The aim of the study was to quantify the percentage of the left ventricular stroke volume, that is derived by the septal movement during systole, in healthy volunteers and patients with volume or pressure load of the RV. Methods Cardiac MRI was used for three-dimensional assessment of cardiac volumes and septal movement. Four groups were examined; healthy subjects (n=29), athletes with high aerobic capacity (n=12), patients with an increased right ventricular volume load from moderate or severe pulmonary insufficiency (PI) in surgically corrected tetralogy of Fallot (n=20) and surgically corrected pulmonary stenosis (PS) (n=2) and patients with an increased right ventricular pressure overload secondary to pulmonary hypertension (n=11). LVSV was calculated by delineation of the endocardium of the LV in diastole and systole. The border between the LV and RV, i.e. the epicardial contour of the septum was delineated in diastole and systole from the apex to the base. Thereby the three-dimensional volume, derived from septal movement, was quantified. Results Septal movement contributed to 8.7±0.7% of stroke volume in healthy subjects and 7.5±0.6% in athletes (p=ns). However, in patients with PI because of surgically corrected tetralogy of Fallot or PS, the septum contributes to right ventricular stroke volume by 14.1±1.7% (p<0.001 compared to healthy subjects). In patients with pulmonary hypertension the contribution to LVSV was 2.5±2.5% (p<0.001 compared to healthy subjects) with a wide range (19% to -9%) of left ventricular stroke volume.