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Frank-Starling mechanism, fluid responsiveness, and length-dependent activation: Unravelling the multiscale behaviors with an in silico analysis.

ABSTRACT: The Frank-Starling mechanism is a fundamental regulatory property which underlies the cardiac output adaptation to venous filling. Length-dependent activation is generally assumed to be the cellular origin of this mechanism. At the heart scale, it is commonly admitted that an increase in preload (ventricular filling) leads to an increased cellular force and an increased volume of ejected blood. This explanation also forms the basis for vascular filling therapy. It is actually difficult to unravel the exact nature of the relationship between length-dependent activation and the Frank-Starling mechanism, as three different scales (cellular, ventricular and cardiovascular) are involved. Mathematical models are powerful tools to overcome these limitations. In this study, we use a multiscale model of the cardiovascular system to untangle the three concepts (length-dependent activation, Frank-Starling, and vascular filling). We first show that length-dependent activation is required to observe both the Frank-Starling mechanism and a positive response to high vascular fillings. Our results reveal a dynamical length dependent activation-driven response to changes in preload, which involves interactions between the cellular, ventricular and cardiovascular levels and thus highlights fundamentally multiscale behaviors. We show however that the cellular force increase is not enough to explain the cardiac response to rapid changes in preload. We also show that the absence of fluid responsiveness is not related to a saturating Frank-Starling effect. As it is challenging to study those multiscale phenomena experimentally, this computational approach contributes to a more comprehensive knowledge of the sophisticated length-dependent properties of cardiac muscle.

SUBMITTER: Kosta S

PROVIDER: S-EPMC8504729 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundWith larger blood volume flowing into a cardiac chamber, by stretching muscle fibers, increased contraction force could be detected. This phenomenon is called Frank-Starling mechanism, allowing the output of a cardiac chamber to be synchronized without external regulation. The purpose of the present study was to investigate the Frank-Starling mechanism in the right atrium (RA) represented by its volumes, volume-based functional properties and strains respecting the cardiac cycle in healthy adults by three-dimensional (3D) speckle-tracking echocardiography (3DSTE).MethodsThe present single center retrospective cohort study comprised 179 healthy adult volunteers (mean age: 33.2±12.0 years, 92 males), in whom complete two-dimensional Doppler echocardiography with 3DSTE was performed. Subjects were divided into 3 groups according to the mean value of maximum RA volume (Vmax) ± standard deviation: Vmax <30 mL, 30 mL ≤ Vmax <60 mL and Vmax ≥60 mL.ResultsAll RA volumes respecting the cardiac cycle of all subjects and calculated separately for females and males and their indexed equivalents increased with Vmax. RA stroke volumes increased with Vmax regardless of the phase it was measured in. While total atrial emptying fraction representing the reservoir phase remained unchanged with the increase of Vmax, a significant increase in passive atrial emptying fraction representing the conduit phase could be detected, in case of Vmax >60 mL (28.9%±15.1% vs. 32.5%±12.6%, P<0.05). Active atrial emptying fraction representing the booster pump function did not change with the increase of Vmax. Most global and mean segmental peak RA strains did not show significant changes with increasing RA volumes except for the RA area strain, it was the largest when Vmax was larger than 60 mL (64.7%±44.9% vs. 83.3%±49.4%, P<0.05). RA circumferential, longitudinal and area strains at atrial contraction decreased with increasing Vmax, RA radial and 3D strains did not change significantly with increasing Vmax.ConclusionsIncreasing RA volumes do not cause significant increase in RA contractility represented by strains, but reduction in strains in longitudinal and circumferential directions could be detected in end-diastolic booster pump function. In contrast to the left atrium, obvious signs of Frank-Starling mechanism could not be detected in case of the RA.

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Frank-Starling mechanism, fluid responsiveness, and length-dependent activation: Unravelling the multiscale behaviors with an in silico analysis.

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