Regional contribution to ventricular stroke volume is affected on the left side, but not on the right in patients with pulmonary hypertension.

To develop more sensitive measures of impaired cardiac function in patients with pulmonary hypertension (PH), since detection of impaired right ventricular (RV) function is important in these patients. With the hypothesis that a change in septal function in patients with PH is associated with altered longitudinal and lateral function of both ventricles, as a compensatory mechanism, we quantified the contributions of these parameters to stroke volume (SV) in both ventricles using cardiac magnetic resonance (CMR). Seventeen patients (10 females) evaluated for PH underwent right heart catheterization (RHC) and CMR. CMR from 33 healthy adults (13 females) were used as controls. Left ventricular (LV) atrioventricular plane displacement (AVPD) and corresponding longitudinal contribution to LVSV was lower in patients (10.8 ± 3.2 mm and 51 ± 12 %) compared to controls (16.6 ± 1.9 mm and 59 ± 9 %, p < 0.0001 and p < 0.01, respectively). This decrease did not differ in patient with ejection fraction (EF) >50 % and <50 % (p = 0.5) and was compensated for by increased LV lateral contribution to LVSV in patients (49 ± 13 % vs. 37 ± 7 %, p = 0.001). Septal motion contributed less to LVSV in patients (5 ± 8 %) compared to controls (8 ± 4 %, p = 0.05). RV AVPD was lower in patients (12.0 ± 3.6 mm vs. 21.8 ± 2.2 mm, p < 0.0001) but longitudinal and lateral contribution to RVSV did not differ between patients (78 ± 17 % and 29 ± 16 %) and controls (79 ± 9 % and 31 ± 6 % p = 0.7 for both) explained by increased RV cross sectional area in patients. LV function is affected in patients with PH despite preserved global LV function. The decreased longitudinal contribution and increased lateral contribution to LVSV was not seen in the RV, contrary to previous findings in patients with volume loaded RVs.

Determinants of kinetic energy of blood flow in the four-chambered heart in athletes and sedentary controls.

The kinetic energy (KE) of intracardiac blood may play an important role in cardiac function. The aims of the present study were to 1) quantify and investigate the determinants of KE, 2) compare the KE expenditure of intracardiac blood between athletes and control subjects, and 3) quantify the amount of KE inside and outside the diastolic vortex. Fourteen athletes and fourteen volunteers underwent cardiac MRI, including four-dimensional phase-contrast sequences. KE was quantified in four chambers, and energy expenditure was calculated by determining the mean KE/cardiac index. Left ventricular (LV) mass was an independent predictor of diastolic LVKE (R(2) = 0.66, P < 0.001), whereas right ventricular (RV) end-diastolic volume was important for diastolic RVKE (R(2) = 0.76, P < 0.001). The mean KE/cardiac index did not differ between groups (control subjects: 0.53 ± 0.14 mJ·l(-1)·min·m(2) and athletes: 0.56 ± 0.21 mJ·l(-1)·min·m(2), P = 0.98). Mean LV diastolic vortex KE made up 70 ± 1% and 73 ± 2% of total LV diastolic KE in athletes and control subjects (P = 0.18). In conclusion, the characteristics of the LV as a pressure pump and the RV as a volume pump are demonstrated as an association between LVKE and LV mass and between RVKE and end-diastolic volume. This also suggests different filling mechanisms where the LV is dependent on diastolic suction, whereas the RV fills with a basal movement of the atrioventricular plane over "stationary" blood. Both groups had similar energy expenditure for intracardiac blood flow, indicating similar pumping efficiency, likely explained by the lower heart rate that cancels the higher KE per heart beat in athletes. The majority of LVKE is found within the LV diastolic vortex, in contrast to earlier findings.

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.

BACKGROUND: 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). METHODS: Thirty-two athletes (16 women) and 32 normal subjects (16 women) underwent cardiac magnetic resonance imaging. Cardiac volumes and atrioventricular plane displacement (AVPD) were determined. Longitudinal and radial contribution to stroke volume was calculated using planimetry and used to determine diastolic and systolic atrial filling. RESULTS: Atrial filling during ventricular diastole was 29 ± 10% of the total stroke volume, and during ventricular systole atrial filling was 68 ± 8% of the total stroke volume. There were no differences between groups of different HR (P = 0·70 and P = 0·41 for diastolic and systolic filling, respectively) or THV (P = 0·44 and P = 0·46 for diastolic and systolic filling, respectively). Systolic atrial filling was strongly correlated to longitudinal ventricular pumping (R = 0·76, P<0·001). CONCLUSION: This study demonstrated that in healthy humans at rest, approximately 30% of the total stroke volume enters the atria during ventricular diastole and approximately 70% during systole, independent of heart rate (HR) or heart size. The atria are filled through suction driven by ventricular longitudinal contraction which aspirates blood from the pulmonary and caval veins. As 70% of the atrial filling occurs during ventricular emptying, the heart volume remains relatively constant over the cardiac cycle, which minimizes pulling on surrounding tissues and therefore optimizes energy expenditure.