Atrioventricular plane displacement is the sole mechanism of atrial and ventricular refill

Arutunyan, Ara

doi:10.1152/ajpheart.00058.2015

Cited by 14 publications

(9 citation statements)

References 13 publications

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“…49,50 Recent studies have suggested that diastolic recoil of the aorta and left atrium, which are stretched during systole, facilitates LV filling and ejection. 12,[51][52][53][54][55] The association between increased aortic stiffness and worse GLS observed in our study may relate to both the systolic and diastolic components of direct mechanical ventricular-vascular coupling and requires further study. 48 Women tend to have greater aortic longitudinal strain, and better (more negative) GLS and LV ejection fraction than men even in older age.…”

Section: Discussionmentioning

confidence: 85%

“…The relation between aortic stiffness and diastolic function is often attributed to hemodynamic effects, while the relation between GLS and diastolic function has been attributed to recoil of contracted LV muscle fibers 49, 50. Recent studies have suggested that diastolic recoil of the aorta and left atrium, which are stretched during systole, facilitates LV filling and ejection 12, 51, 52, 53, 54, 55. The association between increased aortic stiffness and worse GLS observed in our study may relate to both the systolic and diastolic components of direct mechanical ventricular–vascular coupling and requires further study 48…”

Section: Discussionmentioning

confidence: 99%

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Relations Between Aortic Stiffness and Left Ventricular Mechanical Function in the Community

Bell

McCabe

Larson

et al. 2017

JAHA

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BackgroundAortic stiffness impairs optimal ventricular–vascular coupling and left ventricular systolic function, particularly in the long axis. Left ventricular global longitudinal strain (GLS) has recently emerged as a sensitive measure of early cardiac dysfunction. In this study, we investigated the relation between aortic stiffness and GLS in a large community‐based sample.Methods and ResultsIn 2495 participants (age 39–90 years, 57% women) of the Framingham Offspring and Omni cohorts, free of cardiovascular disease, we performed tonometry to measure arterial hemodynamics and echocardiography to assess cardiac function. Aortic stiffness was evaluated as carotid–femoral pulse wave velocity and as characteristic impedance, and GLS was calculated using speckle tracking–based measurements. In multivariable analyses adjusting for age, sex, height, systolic blood pressure, augmentation index, left ventricular structure, and additional cardiovascular risk factors, increased carotid–femoral pulse wave velocity (B±SE: 0.122±0.030% strain per SD, P<0.0001) and characteristic impedance (0.090±0.029, P=0.002) were both associated with worse GLS. We observed effect modification by sex on the relation between characteristic impedance and GLS (P=0.004); in sex‐stratified multivariable analyses, the relation between greater characteristic impedance and worse GLS persisted in women (0.145±0.039, P=0.0003) but not in men (P=0.73).ConclusionsMultiple measures of increased aortic stiffness were cross‐sectionally associated with worse GLS after adjusting for hemodynamic variables. Parallel reductions in left ventricular long axis shortening and proximal aortic longitudinal strain in individuals with a stiffened proximal aorta, from direct mechanical ventricular‐vascular coupling, offers an alternative explanation for the observed relations.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Relations Between Aortic Stiffness and Left Ventricular Mechanical Function in the Community

Bell

McCabe

Larson

et al. 2017

JAHA

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“…The mechanisms involved in left ventricular (LV) diastolic filling and their relative importance remain an area of active investigation12345678. Understanding the physiology of normal LV filling can advance characterization of the pathophysiology of diastolic dysfunction and consequently help in identifying optimal diagnostic metrics as well as targets for treatment.…”

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confidence: 99%

Hydraulic forces contribute to left ventricular diastolic filling

Maksuti

Carlsson

Arheden

et al. 2017

Sci Rep

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Myocardial active relaxation and restoring forces are known determinants of left ventricular (LV) diastolic function. We hypothesize the existence of an additional mechanism involved in LV filling, namely, a hydraulic force contributing to the longitudinal motion of the atrioventricular (AV) plane. A prerequisite for the presence of a net hydraulic force during diastole is that the atrial short-axis area (ASA) is smaller than the ventricular short-axis area (VSA). We aimed (a) to illustrate this mechanism in an analogous physical model, (b) to measure the ASA and VSA throughout the cardiac cycle in healthy volunteers using cardiovascular magnetic resonance imaging, and (c) to calculate the magnitude of the hydraulic force. The physical model illustrated that the anatomical difference between ASA and VSA provides the basis for generating a hydraulic force during diastole. In volunteers, VSA was greater than ASA during 75–100% of diastole. The hydraulic force was estimated to be 10–60% of the peak driving force of LV filling (1–3 N vs 5–10 N). Hydraulic forces are a consequence of left heart anatomy and aid LV diastolic filling. These findings suggest that the relationship between ASA and VSA, and the associated hydraulic force, should be considered when characterizing diastolic function and dysfunction.

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“…If mitral annular displacement solely accounted for LV filling, there would be no need for the D-wave. Thus mitral annular displacement cannot be the sole determinant of filling, as recently claimed (2). Constant-volume physiology also clarifies that, although atrial size (best measured at diastasis) is an atrial anatomic feature, "left atrial reservoir volume" and "left atrial conduit volume" are dynamic quantities and are both directly generated by the LV, while the atrium remains passive.…”

Section: Left Atriummentioning

confidence: 85%

What global diastolic function is, what it is not, and how to measure it

Chung

Shmuylovich

Kovács

2015

American Journal of Physiology-Heart and Circulatory Physiology

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Leonardo da Vinci's observation (circa 1511) that "the atria or filling chambers contract together while the pumping chambers or ventricles are relaxing and vice versa," the dynamics of four-chamber heart function, and of diastolic function (DF) in particular, are not generally appreciated. We view DF from a global perspective, while characterizing it in terms of causality and clinical relevance. Our models derive from the insight that global DF is ultimately a result of forces generated by elastic recoil, modulated by cross-bridge relaxation, and load. The interaction between recoil and relaxation results in physical wall motion that generates pressure gradients that drive fluid flow, while epicardial wall motion is constrained by the pericardial sac. Traditional DF indexes (, E/E=, etc.) are not derived from causal mechanisms and are interpreted as approximating either stiffness or relaxation, but not both, thereby limiting the accuracy of DF quantification. Our derived kinematic models of isovolumic relaxation and suction-initiated filling are extensively validated, quantify the balance between stiffness and relaxation, and provide novel mechanistic physiological insight. For example, causality-based modeling provides load-independent indexes of DF and reveals that both stiffness and relaxation modify traditional DF indexes. The method has revealed that the in vivo left ventricular equilibrium volume occurs at diastasis, predicted novel relationships between filling and wall motion, and quantified causal relationships between ventricular and atrial function. In summary, by using governing physiological principles as a guide, we define what global DF is, what it is not, and how to measure it. diastolic function; echocardiography; hemodynamics; mathematical modeling; suction pump LEFT VENTRICULAR (LV) DIASTOLIC dysfunction is typically reported and indexed as either an increase in myocardial stiffness or a slowing of relaxation (i.e., cross-bridge dissociation). In actuality, diastolic function (DF) is the result of the continuous interaction between the restoring force of elastic recoil and the opposing force generated by cross bridges that have yet to uncouple from the previous systole. The restoring forces seek to lengthen the muscle, while the cross-bridge forces previously acted to shorten the muscle. The simultaneous action of these two opposing forces during both isovolumic relaxation (IVR) and filling result in wall motion, constrained by pericardial sac volume, and simultaneous generation of pressure gradients. This review discusses the governing physical laws and the constraints of DF, as well as which indexes of DF are consistent with diastolic physiology. Deriving and evaluating indexes of DF using this conceptual framework both clarifies and advances our understanding of DF and diastolic dysfunction in health and disease. Physiology of DiastoleCardiovascular physiology is taught using the Wiggers diagram, which segments the cardiac cycle into systole and diastole ( Fig. 1) (49, 124). Systole begins...

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Atrioventricular plane displacement is the sole mechanism of atrial and ventricular refill

Cited by 14 publications

References 13 publications

Relations Between Aortic Stiffness and Left Ventricular Mechanical Function in the Community

Relations Between Aortic Stiffness and Left Ventricular Mechanical Function in the Community

Hydraulic forces contribute to left ventricular diastolic filling

What global diastolic function is, what it is not, and how to measure it

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