Hydraulic force is a novel mechanism of diastolic function that may contribute to decreased diastolic filling in HFpEF and facilitate filling in HFrEF

Abstract

Background: A hydraulic force generated by blood moving the atrio-ventricular plane is a novel mechanism of diastolic function. The direction and magnitude of the force is dependent on the geometrical relationship between the left atrium and ventricle and is measured as the short-axis atrio-ventricular area difference (AVAD). In short, the net hydraulic force acts from a larger area towards a smaller. It is currently unknown how cardiac remodeling affects this mechanism. The aim of the study was therefore to investigate this diastolic mechanism in patients with pathological or physiological remodeling. Methods: 70 subjects (n=11 heart failure with preserved ejection fraction (HFpEF), n=10 heart failure with reduced ejection fraction (HFrEF), n=7 signs of isolated diastolic dysfunction, n=10 hypertrophic cardiomyopathy (HCM), n=10 cardiac amyloidosis, n=18 triathletes and n=14 controls) were included. Subjects underwent Cardiac MR and short-axis images of the left atrium and ventricle were delineated. AVAD was calculated as ventricular area minus atrial area and used as an indicator of net hydraulic force. Results: At the onset of diastole, AVAD in HFpEF was median -9.2 cm2 versus -4.4 cm2 in controls, p=0.02). The net hydraulic force was directed towards the ventricle for both, but larger in HFpEF. HFrEF was the only group with a positive median value 11.6 cm2 and net hydraulic force was throughout diastole directed towards the atrium. Conclusion: The net hydraulic force may impede cardiac filling throughout diastole in HFpEF, worsening diastolic dysfunction. In contrast, it may work favorably in patients with dilated ventricles and aid ventricular filling.

Decreased diastolic hydraulic forces incrementally associate with survival beyond conventional measures of diastolic dysfunction

“…In HFpEF, elevated LV filling pressures are propagated to the LA, resulting in remodelling and dilatation 24 , 29 , 31 . This may result in the LA cross-sectional area becoming equal to or larger than the LV cross-sectional area, orienting the net diastolic hydraulic force towards the apex of the heart and opposing LV filling 7 . Decreasing LA size in these patients may potentially restore the contribution of diastolic hydraulic forces to LV filling, possibly improving both diastolic function and survival.…”

“…This force is expected to contribute to the diastolic longitudinal motion of the atrioventricular plane, facilitating LV lengthening and accounting for between 10 and 60% of the peak driving force of LV filling in healthy subjects 4 . Applying these findings to a clinical population, a recent study investigating changes to diastolic hydraulic forces in patients with pathological cardiac remodelling found that patients with HFpEF had a smaller AVAD compared to healthy controls throughout diastole, possibly limiting LV filling and contributing to the diastolic dysfunction 7 .…”

Decreased diastolic hydraulic forces incrementally associate with survival beyond conventional measures of diastolic dysfunction

“…In HFpEF, elevated LV filling pressures are propagated to the LA, resulting in remodelling and dilatation in response to the increased pressure (22,27,29). This may result in the LA cross-sectional area becoming equal to or larger than the LV cross-sectional area during the cardiac cycle, thereby orienting the net diastolic hydraulic force towards the apex of the heart and opposing LV filling (7). Decreasing LA size in these patients may potentially restore the contribution of diastolic hydraulic forces to LV filling, possibly improving both diastolic function and survival.…”

“…This may result in the LA crosssectional area becoming equal to or larger than the LV cross-sectional area during the cardiac cycle. Consequently, the net diastolic hydraulic force under such conditions is oriented towards the apex of the heart and opposes LV filling (7). Decreasing LA size in these patients could restore the contribution of diastolic hydraulic forces to LV filling, potentially improving both diastolic function and survival.…”

“…This force is expected to contribute to the diastolic longitudinal motion of the atrioventricular plane, facilitating the lengthening of the LV and accounting for between 10% and 60% of the peak driving force of LV filling in healthy subjects (4). Applying these findings to a clinical population, a recent study investigating changes to diastolic hydraulic forces in patients with pathological cardiac remodelling found that patients with HFpEF had a smaller AVAD compared to healthy controls throughout diastole, possibly limiting LV filling and contributing to the diastolic dysfunction (7).…”