Narrative review of fluid dynamics in the left ventricle: from the perspective of aortic regurgitation

Abstract

Background and Objective

From a fluid dynamics perspective, understanding intraventricular blood flow is essential for clarifying the mechanisms, progression, and potential therapeutic targets of various cardiac diseases. Recent advancements in imaging techniques have enabled the visualization of left ventricle (LV) blood flow, particularly the vortex formed during diastole. However, the inherently complex and dynamic nature of LV fluid motion makes the quantitative assessment of vortex function highly challenging. The impact of aortic regurgitation (AR) on LV fluid dynamics is equally critical for understanding the progression of cardiac dysfunction, yet its exact influence remains largely unclear. This manuscript is a narrative review of this novel perspective of AR in the context of fluid dynamics.

Methods

Articles from PubMed database and Google Scholar regarding LV blood flow and vortex assessment were reviewed. For the initial research, articles between 2010 and 2025 were prioritized, including original articles, case reports, and reviews. Following the initial search, additional articles were considered based on manual searches of references from the retrieved literature.

Key Content and Findings

AR jets have several interactions with LV blood flow depending on its direction, and the eccentric jet can be oriented in several directions based on the relationship to the mitral inflow location.

Conclusions

Various orientations of eccentric AR jet are possible and LV blood flow trajectory is modulated by the direction of AR jets. A reproducible classification of AR jet direction, combined with the quantification of vortex alterations according to jet direction, represents a vital step in elucidating the specific roles of these vortices in cardiac function.

Introduction

Background

The left ventricle (LV) is the site of major hemodynamic energy transformations: blood is drawn from the left atrium and undergoes a dynamic change in direction before it is forcefully ejected into systemic circulation (1). Recent advances data processing and in imaging, such as vector flow mapping (VFM) and four-dimensional flow magnetic resonance imaging (4D flow MRI), have enabled detailed assessment of LV blood flow and its fluid dynamics, providing researchers the opportunity to investigate the complex function and mechanisms of the LV diastolic vortex (2-6). Current assessments for various cardiac diseases do not account for alterations in flow dynamics. Our overarching hypothesis is that fluid dynamics is a significant factor of cardiovascular disease that is independent from pressure and volume. LV diastolic vortex may have a significant role for efficient blood transportation, and change in vortex may influence cardiac function. Proof of such hypothesis would transform present assessment of cardiac disease. However, elucidating the functional role of vortices and their impact on cardiac function remains a significant challenge. Largely due to the difficulty in quantifying their diverse three-dimensional structures and temporal variations. Although numerous studies have attempted to clarify vortex functions, establishing a causal relationship between vortex alterations and cardiac function hindered by these inherent complexities. Aortic regurgitation (AR) introduces an abnormal diastolic flow into the LV due to valve dysfunction, which leads to interacting with LV blood flow as well as volume and pressure loading of the LV (7,8). We hypothesize that AR flow, directed against LV vortex flow, increases myocardial workload independent from volume and pressure overload. Identifying the alterations in the diastolic vortex caused by AR represents a crucial first step in elucidating the impact of these vortices on overall cardiac function. Though our manuscript focused on AR given direct influence on the LV diastolic vortex flow, other valvular conditions, such as aortic stenosis and mitral stenosis/regurgitation, deserve similar attention (9-12).

Rationale and knowledge gap

AR interact with LV fluid dynamics by introducing an abnormal diastolic flow. This interaction may impose an additional workload on the myocardium, independent of traditional pressure and volume overload. Despite its significance, there are currently few reports that provide a detailed description of how AR jet specifically affects LV blood flow.

Objective

As a critical and foundational step toward elucidating how AR-induced vortex alterations impact myocardial workload, this review first synthesizes current evidence on diastolic vortex characteristics and LV fluid dynamics. Secondary, we offer novel perspectives on the under-recognized variability of AR jets and underscore the clinical significance of classifying the complex interactions between these jets and LV diastolic vortex. Moreover, we explore the potential implications of AR jet and vortex diversity for valvular and myocardial degeneration, highlighting the need for a comprehensive three-dimensional classification system for these flow patterns. We present this article in accordance with the Narrative Review reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1-2690/rc).

Methods

This narrative review was conducted to explore the role of LV diastolic vortex and interaction between AR jets and LV blood flow including diastolic vortex. Searches of the PubMed and Google Scholar databases were conducted to identify published literature on LV fluid dynamics and its association with AR. The search combined MeSH terms including: “Aortic Valve Insufficiency”, “Hydrodynamics”, “Heart Failure, Systolic”, “Piezo1 protein”, “KLF-1 protein”, “Transforming Growth Factor beta”, “Smad proteins” in PubMed, and free-text keywords, including: “Left ventricle blood flow”, “Diastolic vortex”, “Regurgitant jet”, “4D flow magnetic resonance imaging”, “vector flow mapping”, in PubMed and Google scholar. For the initial search, articles published between January 2010 and August 2025 were prioritized. Original articles, clinical trials, case reports, reviews, and expert consensus were included. Editorials were excluded. Additional sources were identified through a manual review of references in the retrieved literature was conducted. The overall search strategy is summarized in Table 1. Only studies published in English were considered. One reviewer (Y.K.) screened all titles and abstracts. Selected full-text articles were 73 then evaluated based on relevance to the LV fluid dynamics, interaction between AR jet and LV diastolic vortex, and molecular mechanobiology in the context of fluid dynamics. Finally, 46 studies were included for review. Since this is a narrative review and most existing reports consist of observational studies with small sample size, we reviewed literature based on their consistency with established concepts and the novelty of their findings without formal risk-of-bias evaluation or meta-analysis. Instead, this article aims to provide integrative interpretations to support clinical practice and research regarding LV fluid dynamics and associated cardiac functions along with novel perspectives for AR jets and LV blood flow as an educational framework.

Table 1. The search strategy summary.

Items	Specification
Date of search	October 1, 2025
Databases and other sources searched	PubMed, Google Scholar
Search terms used	MeSH: “Aortic Valve Insufficiency”, “Hydrodynamics”, “Heart Failure, Systolic”, “Piezo1 protein”, “KLF-1 protein”, “Transforming Growth Factor beta”, “Smad proteins”
	Free-text keywords: “Left ventricle blood flow”, “Diastolic vortex”, “Regurgitant jet”, “4D flow magnetic resonance imaging”, “vector flow mapping”
Timeframe	January 2010 to August 2025
Inclusion and exclusion criteria	Inclusion: original article, clinical trials, case reports, and reviews
	Exclusion: editorials, non-English articles
Selection process	Y.K. conducted the initial literature search. All authors reviewed the papers and contributed to the final selection of paper

Normal LV blood flow

Advanced imaging modalities such as VFM and 4D flow MRI have allowed high-resolution visualization of the complex blood flow in the LV and the dynamic behavior of interventricular vortices (2-6). LV flow patterns evolve in characteristic ways across the cardiac cycle, where the systolic phase and the diastolic phase can be divided into early, middle, and end phase each (13-20).

Early diastolic phase

The early diastolic phase corresponds to the combination of the isovolumetric relaxation phase and the early filling phase (13,14). During the isovolumetric relaxation, the LV flow is directed entirely toward the apex, and either no vortex or very few small transient vortices are observed (15). Once the mitral valve opens, the early filling phase starts, and mitral inflow directed towards the LV apex. Simultaneously, a vortex ring forms at the distal tips of the mitral valve leaflets (16). In a three-dimensional view, this structure appears as a compact quasi-torus-shaped vortex ring core that appears shortly after the onset of the early filling phase and reaches its full potential as the early filling approaches its peak (17). Concurrently, reversal flow, in contrast to the inflow, is observed toward the LV outflow track (LVOT) from the mid-ventricle (18).

Middle diastolic phase

The middle diastolic phase is called diastasis, which occurs between the end of early filling and the onset of late filling (13,14). During this phase, the vortex formed in the early phase combines and deforms into complex shapes which move towards the apex in parallel with the long-axis of the LV. Only a small remnant of the early vortex can be observed at the onset of atrial contraction, and this residual vortex dissipates completely by end-diastole (17,18) (Figure 1).

Figure 1.

Early and late filling diastolic vortex in the left ventricle.

End diastolic phase

This phase corresponds to the late filling phase caused by atrial contraction (13,14). In this phase, flow through the mitral valve increases again, and a new, isolated, and asymmetrically shaped vortex develops at the base of the ventricle with a dilated anterior side and more compressed posterior side. This structure reaches complete formation as the LV cycle approaches peak late filling phase and persists at the ventricular base without major dissipation until the end of diastole, while reversal flow is once again formed towards the LVOT (Figure 1) (17,18).

Early systolic phase

At the beginning of systole, limited flow is present at the LVOT, as the mitral valve has closed completely, while contraction of the LV has not yet occurred. A low intensity vortex, which was generated during the end-diastolic phase, is visible in the center of the LV (19). Forward flow vectors originate near the apex and shift anteriorly toward the aortic valve.

Middle systolic phase

As soon as contraction begins and the aortic valve opens, a complex vortex structure is defined along the lateral wall of the LV (19). Flow accelerates and becomes more linear, directed from the apex to the aorta.

Late systolic phase

In this phase, the flow vector is distributed unevenly in the anterior half area of the LV near the septum. The direction of the flow vector is nearly parallel to the septum from the LV’s apex to its base, but some parts in the outflow tract diverge the posteriorly. Then, about 1/3 to 1/6 of the ejected flow moves downward, and thereafter anteriorly, to the apex along the LV’s inner surface (20).

LV diastolic vortex and its role

Regarding the LV diastolic vortex, Elbaz et al. suggested that the two phase-specific vortices have different fluid dynamic characteristics (17). The early filling vortex (E-vortex) is located relatively far from the mitral valve and more circular, while the late filling vortex (A-vortex) is closer to the mitral valve and more elliptical (Figure 1). These differences stem from different functions, i.e., the E-vortex assists in LV filling, and the A-vortex ensures the efficient onward transport of LV blood toward the aorta (17). Furthermore, several studies suggested that “direct flow” (the fraction of blood that enters and exits the LV within a single cardiac cycle) retains measurable kinetic energy (KE) at the end of diastole, leading to efficient blood ejection (21,22). Though most existing research indicates that the diastolic vortex contributes to efficient LV blood transport, some studies argued opposite perspectives. Carlsson et al. measured healthy LV KE and reported the end-diastolic total KE as approximately 1 mJ, with the diastolic vortex KE measuring about 70% of the total LV KE (22,23). Considering the whole external energy of LV contraction is approximately 1 J, the energy contained in the end diastolic vortex has is relatively low, and its influence on the LV’s workload at the beginning of the systolic phase may be negligible (23). Watanabe et al. reported that heterogenous LV blood flow does not maintain momentum and suggested that the LV’s myocardial workload may not be different between healthy and abnormal LV blood flow (24). These findings imply a possibility that the diastolic vortex function is nominal and change in or abnormality of the vortex does not affect ventricular workload. However, existing reports focused solely on comparing vortex energy itself. To date, no study has been able to directly evaluate the myocardial workload in relation to those flow dynamics. To conclude the actual impact of the vortex on cardiac function, it is essential to quantify and compare the changes in vortex morphology with the corresponding myocardial workload. For this purpose, it is imperative to classify the morphological characteristics of the vortex contributing to ejection across various cardiac diseases. Only by comparing myocardial workload according to these classifications can we definitely conclude whether structural changes in the vortex influence myocardial performance. To clarify whether vortex flow alterations contribute to the decline of cardiac function in clinical practice, both a detailed disease-specific classification of the vortex and its direct impact on myocardial workload must be elucidated.

Impact of ventricular function on LV diastolic vortex

LV morphology strongly affects diastolic vortex structure (11,25,26). Apart from acute reduction of LV ejection fraction (EF), lower LV function correlates to LV dilation for compensatory mechanism (27). As the results of LV dilation, the diastolic vortex becomes larger and more spherically shaped, and is located more apical (25,26). Chan et al. reported that reduced EF was associated with more fragmented vortices and higher diastolic energy loss (EL), while Bermejo et al. reported that, in nonischemic dilated cardiomyopathy, diastolic vortex became stronger and keep the first vortex throughout diastolic phase compared to healthy ones (28,29). While these reports consistently show that LV dilation leads to an enlarged diastolic vortex and its apical displacement, the true impact of LV dilation on the vortex remains controversial: whether the vortex becomes unstable and disrupts intraventricular transport following LV dilation or LV dilation strengthen and stabilize the vortex, potentially functioning as a compensatory mechanism against declining cardiac function. This indicates that LV dilation due to cardiac dysfunction does not necessarily affect the vortex in a uniform manner. Nonetheless, considering LV morphology is essential when observing and evaluating vortices in valvular diseases, including AR.

AR and regurgitant jet variability

Our hypothesis is that alteration of LV vortex induced by AR jets trigger augments LV workload. To validate this hypothesis, we first need to address the interaction between AR jet and vortex flow. AR jets are generally classified as a central versus eccentric jet (Figure 2) (30,31). While a central jet directs toward the apex, an eccentric jet deviates toward one of the LV structures or walls (31,32). It is questionable whether such distinctly different AR jet directions could influence LV blood flow in a uniform manner or exert equivalent myocardial workload. While the current classification of AR jet direction, typically simplified into central and eccentric jets, is defined by anatomical positioning, this binary categorization may be insufficient for a comprehensive understanding of complex LV fluid dynamics. In evaluating the relationship between LV blood flow and myocardial workload, it is essential to categorize them based on their dynamic interactions with the global LV flow field. However, the detailed characterization of AR jet direction based on LV blood flow remains limited. Prior studies indicated substantial directional variability in eccentric jet profiles, though most of their directionality still depends on only anatomical landmarks (9,10,30-38). Bertrand et al. stratified the eccentric jets as posteriorly directed versus others, while Cesarovic et al. described some eccentric jets as septal-directed (36,37). Further, a report from Galea et al. indicated the presence of mitral valve-directed eccentric AR jets (10). Consistent with these reports, our group’s 4D flow MRI data from bicuspid aortic valve (BAV) patients demonstrated the presence of an anteriorly directed AR jet (Figure 3A), an AR jet directed towards the mitral inflow (Figure 3B), posteriorly directed jet (Figure 3C), and a septal-directed jet (Figure 3D) based on mitral inflow. We defined the mitral-directed jet as the jet which overlapped with mitral inflow at the level of basal LV. In other words, posterior and anterior-directed jet was defined as the jet does not overlap with mitral inflow at the basal LV. In addition, septal-directed jet was defined as a jet located medial to the most anterior portion of the LVOT. This wide variation highlights that “eccentric AR” is not a single entity but a spectrum of anatomical and fluid-dynamic patterns. Furthermore, regarding the interaction with LV flow, it remains uncertain whether even a ‘central jet’ can be adequately represented by a single category. The frequent use of a binary “central vs. eccentric” classification system leads to differing perspectives and their influence on surgical outcomes. To investigate the interaction between AR jet and LV blood flow, and its subsequent impact on myocardial workload, stratification by AR volume alone is insufficient. We believe it is essential to observe vortex alterations relative to the AR jet direction and to classify vortex morphology before evaluating its impact on myocardial workload.

Figure 2.

Aortic regurgitant jet. (A) Central jet. (B) Eccentric jet.

Figure 3.

Variation of eccentric AR jet direction. (A) Anterior direction. (B) Mitral valve direction. (C) Posterior direction. (D) Septal direction. AR, aortic regurgitation; LA, left atrium.

Impact of aortic regurgitant jet on LV fluid dynamics

Chronic AR causes recurrent volume overload in the LV, which subsequently leads to long-term LV dysfunction (1,37). Several studies investigated the effect of direct regurgitant jet flow on the LV diastolic vortex or mitral inflow through the lens of fluid dynamics (9,10,24,30-38). Okafor et al. reported that AR jets prevent the mitral inflow from generating a vortical structure in vivo (9). Galea et al. demonstrated that posteriorly directed AR jets cause deflection of trans-mitral streamlines, shifting them away from their normal apex-directed trajectory (10). They also reported that the systolic myocardial strain rate and strain velocity were not significantly different between a posteriorly directed AR jet group and another-directed jet group, while diastolic strain rate and velocity were significantly reduced in the posterior AR jet group (9,10). Bertrand et al. published a similar case report regarding the interaction of eccentric AR jets and anterior mitral leaflet opening (36). Regarding the diastolic vortex, Cesarovic et al. reported on the interactions between the septal AR jet and the diastolic vortex (37). They concluded that even with mild AR, a septal oriented regurgitant jet collides with the diastolic vortex, reducing its size, and increases residence time of blood in the apical region. In terms of EL, Yoshida et al. suggested that AR jet severity was not associated with the value of EL, while AR jet direction (central vs. eccentric) was significantly associated with EL (30). We summarize the key fluid dynamics studies related to AR and LV blood flow interactions in Table 2. Though it is difficult to conclude that high EL or LV filling delay due to reduced mitral inflow truly contributes to cardiac dysfunction, there is a possibility that the diastolic vortex changes caused by the AR jet contribute to inefficient blood flow movement in the LV, leading to heart failure progression. It is crucial to note that existing reports have evaluated the interaction between eccentric AR and LV blood flow by focusing on specific jet directions, rather than encompassing the full spectrum of AR directionality. Furthermore, even within these specific categories, the classifications are subjective, raising concerns regarding reproducibility. For instance, even if a jet is anatomically classified as “posterior”, individual variations in the spatial relationship between the aortic and mitral valves, as well as LV morphology, mean that posterior jets in two different cases do not necessarily interact with LV blood flow in the same manner. According to our preliminary observations, the interaction between LV blood flow and a variety of AR directions resulted in different vortex behaviors. This suggests a need of more granular description of AR jet direction.

Table 2. Overview of key fluid dynamics studies investigating AR and LV blood flow interactions.

First author	Methodology	Described AR jet direction	Key findings
Okafor et al., 2017 (9)	Heart simulator experience	Inferolateral wall of the LV	Kinematic obstruction between mitral valve and LV apex
Cesarovic et al., 2021 (37)	Pig model, 4D flow MRI, 12 models with mild AR	Anterior mitral leaflet-oriented jet and septal-oriented jet	Septal-oriented jet reduce diastolic vortex size
Galea et al., 2022 (10)	4D flow MRI, 50 BAV patients with mild AR	Posterior jet and other directions jet	Posterior AR jet may hamper mitral valve opening, disturbing transmitral flow and slowing LV diastolic filling
Yoshida et al., 2025 (30)	VFM, 40 patients with severe AR	Eccentric jet with flow direction towards mitral valve and central jet with flow direction towards apex	Energy loss is higher in eccentric jet than central jet

4D flow MRI, four-dimension flow magnetic resonance imaging; AR, aortic regurgitation; BAV, bicuspid aortic valve; LV, left ventricle; VFM, vector flow mapping.

Significance of AR flow dynamics on valve and ventricular biology

In recent years, it has been known that laminar flow in vascular cells maintains the pathway for suppressing inflammatory responses in vascular tissues (38-40). Piezo 1 and 2 are critical mechanosensitive ion channels in endothelial cells, transducing mechanical signals, especially shear stress, to exert different cellular processes (41,42). Through finely tuned calcium influx, they orchestrate endothelial inflammatory tone, barrier integrity, and communication with underlying interstitial cells. Krüppel-like factor 2/4 (KLF2/4) is a transcription factor in endothelial cells which is induced by mechanosensitive channels including Piezo1 regulates immune response and maintain endothelial homeostasis through regulating the expression of multiple anti-inflammatory genes, such as transforming growth factor-beta (TGF-β) and Smad (43,44). TGF-β and Smad signaling pathway plays an important role in the pathogenesis of fibrotic and hypertrophic remodeling (45,46). In myocardial endothelial cells and myofibroblasts, the molecular biological mechanism of LV remodeling driven by the progression of fibrosis due to pressure or volume overload have been elucidated similarly (47,48). In contrast to normal laminal flow, disturbed or oscillatory shear reduces endothelial KLF2/4 expression and promotes endothelial-to-mesenchymal transition, proteoglycan accumulation, and fibrosis or leaflet thickening (47,48). Similar mechanisms likely occur along the LV endocardium or aortic valve, where altered AR jet or diastolic vortex structure expose the LV wall or valve surface to irregular shear stress, fostering regional fibrosis and diastolic dysfunction. Thus, the AR direction and coherence of LV bloodflow change may determine not only hemodynamic efficiency but also transcriptional and structural adaptation within the valve-ventricle continuum. It is crucial to recognize that variations exist in the direction of the AR jet, which can lead to differing patterns of the diastolic vortex and subsequent influence on LV fluid dynamics in the entire LV structure. The three-dimensional classification of AR direction and its resulting vortex alterations will not only clarify the impact of LV blood flow on myocardial workload but also catalyze future investigation into the mechanistic links between fluid dynamic stress and molecular biological remodeling of the valves and myocardium.

Future directions

The possibility that diastolic flow abnormalities within the LV caused by AR influence both diastolic and systolic myocardial workload cannot be ruled out. Further disease-specific research is necessary, utilizing flow analysis tools such as 4D flow MRI and VFM to evaluate abnormalities in the diastolic vortex. Going forward, the combination of AR jet and diastolic vortex evaluation using advanced imaging analysis and molecular biological analysis is likely to play a crucial role in clarifying the mechanisms of LV myocardial remodeling and valve degeneration in AR. It is anticipated that, in the future, recognizing the difference in the AR direction and the subsequent patterns of diastolic vortex changes will form the basis for elucidating their impact on LV workload, LV remodeling, and valve degeneration. Other valvular diseases, such as aortic stenosis, mitral regurgitation, and mitral stenosis, also interact with the diastolic vortex flow. As the initial step in evaluating the relationship between vortex and cardiac function, we chose to discuss the interaction between the AR jet and the vortex, along with its subsequent effects on cardiac function.

Limitations

Major limitations are centered around the narrative nature of this review. Due to the heterogeneity of the published studies, including their differing patient populations and imaging modalities, a comparative analysis was not feasible. The review was not systematic in nature and is therefore subject to selection bias. Current understanding of the morphological changes in LV diastolic vortex associated with the varying LV geometries, as well as the relationship between AR and LV diastolic vortex, may be subject to biased interpretations derived from studies limited to specific disease groups or particular AR jet directions. Future research has to categorize the characteristics of LV vortices based on specific pathologies and AR jet direction to facilitate a truly comprehensive evaluation. Finally, the scope of application in fluid dynamics is wide-ranging, and a search focused only on the medical field may not include the latest findings concerning vortices in general fluid dynamics.

Conclusions

Normal LV diastolic vortex has been well documented and may play an important role in efficient blood movement in the LV Several specific AR jet directions were observed in patients with BAV. The correlation between AR-induced alterations in LV diastolic vortex and myocardial workload has the potential to be a game-changer in redefining existing severity assessments and the timing of therapeutic interventions. To elucidate the novel hypothesis that diastolic vortex alteration induced by specific-directed AR jet is associated with increased LV myocardial workload, the detailed observation and classification of AR jet orientation and its interaction with the diastolic vortex serve as the fundamental basis.

Supplementary

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