A Review on the Echocardiographic Estimation of Left Ventricular Filling Pressures: From Guideline to What is in the Pipeline

Abstract

Assessment of diastolic dysfunction is a cardiac anesthesiologist’ holy grail, considering the increasing recognition of diastolic dysfunction (DD) in cardiac surgical patient and its’ impact on the associated outcomes. Withstanding, there is a growing recent emphasis on the accurate, reliable, and reproducible echocardiographic measurement of left ventricular filling pressure (LVFP) for the quantification of DD; which essentially denotes an intrinsic relaxation abnormality. Despite a comprehensive 2016 American Society of Echocardiography and the European Association of Cardiovascular Imaging (ASE/EACVI) guideline for echocardiographic evaluation of the diastolic function, a definitive consensus on the echocardiographic parameters that correlate well with a wide range of intraoperative LVFP is lacking. The recent guidelines continue to focus mainly on the qualitative parameters. However, prompted by the limitation of the existing technique in predicting the quantitative diastolic function across diverse clinical scenario, a range of upcoming echocardiographic modalities are being evaluated with regards to their potential as surrogates of filling pressure in comparison to existing technique. These advanced echocardiographic techniques include speckle tracking echocardiography and pulmonary vein diastolic wave deceleration time, with the evolving role of former being categorically stated in the recent 2025 ASE documents outlining context-specific recommendations on LVDD. The index article, hence aims to review the existing and upcoming echocardiographic modalities as diastolic function assessment correlates particularly with regards to the technique, advantages, limitations, clinical application, and the relevant associated literature.

BACKGROUND

Diastolic function assessment features as an indispensable wedge of the comprehensive echocardiographic evaluation of the left ventricular (LV) function in the perioperative period.[1] LV diastolic dysfunction (DD) independently predicts difficult cardiopulmonary bypass (CPB) weaning, thereby prognosticating the subsequent outcomes.[2] LVDD may result either from an impaired relaxation or an increased ventricular chamber stiffness that is, a setting of elevated LV filling pressures (LVFP); largely resulting from intrinsic abnormalities at the level of the ventricle, itself.[3,4] Hence, the determination of the LVFP, as the surrogate of the LV enddiastolic pressure or the LVEDP, becomes pivotal for the quantification of LVDD. The assorted terminology extends to involve connotations such as the pulmonary capillary wedge pressure (PCWP), left trial pressure (LAP) or LVEDP, intricately linked to each other.

The pulmonary artery occlusion pressure (PAOC) or PCWP by pulmonary artery catheter (PAC), happened to be employed for the determination of LVFP. Meanwhile an accurate assessment of LV diastolic function is limited by the impediments in measuring the LV pressure, volume, or trans mitral flow directly,[5] the invasiveness and complexity attributable to PAC insertion-maintenance happens to have evoked a keen interest in non-invasive modalities. Accurate non-invasive estimation of LVFP indeed aids evaluation, quantification of LVDD, where the resultant risk stratification is a useful prognostic tool, independent of the LV systolic function.[1] Various echocardiographic parameters can potentially provide a non-invasive surrogate to LVFP, eliminating the adverse consequences of right-heart catheterization.

“Guide” line along the “Time” line: A critical appraisal

In 2009, American Society of Echocardiography (ASE) recommendations on echocardiographic evaluation of the LV diastolic function were published which included various parameters combined to frame a diagnostic algorithm. The series of parameters included were trans-mitral Doppler flow (TMDF, to compute the early diastolic filling i.e. the E and the atrial kick i.e. the A wave and the E/A ratio), the pulmonary venous doppler flow (PVDF) measurements, tissue Doppler imaging (TDI) for obtaining the early mitral annular diastolic velocities (e′) alongside the color m-mode propagation velocity (Vp), in reference to their clinical significance in subset with either depressed or normal ejection fractions (EF).[6]

An updated version, nonetheless, was published by the American Society of Echocardiography-European Association of Cardiovascular Imaging (ASE-EACVI) in the year 2016, suggesting a much simpler approach. The major parameters included are the average E/e′, septal as well as lateral e′ velocity, the tricuspid regurgitation (TR) velocity, LA volume index (LAV indexed or the LAVI), E/A ratio and, E velocity, by itself, to diagnose and grade the prevailing diastolic function.[3]

The 2016 recommendations were based mainly on expert consensus. It was within a year, in 2017, that a multicentric validation study was conducted to have revealed almost 87% sensitivity and 88% specificity for diagnosing elevated LVFP with echocardiographic guidelines, buttressing the incremental role of echocardiographic and clinical assessment, when used in close conjunction.[7] This partly “retrospective” validation actually featured some of the investigators involved in framing the current guidelines, as lauded in an Editorial by Flach Kampf and Baron as testing their own proposed concepts, however only acknowledging the reasonable utility, short of a perfectly accurate nature of the multiparametric recommended algorithms to characterize the resting LV diastolic pressures as proxy for the LV diastolic function.[8]

A head-on comparison of the 2009 and 2016 guidelines by Balaney et al.,[9] highlights the latter being more user-friendly that is unlikely to however compromise its’ contextual accuracy, or for that matter incorporation into the clinical decision-making. The recent algorithm resulted in an agreement of 75% between the assessed LVFP in relation to the invasive estimate, with 69% sensitivity and 81% specificity. Even the 2017 study by Cameron et al.,[10] on the echocardiographic prediction of LVEDP in a subset with pulmonary hypertension, delineated a dismal performance of the 2009 ASE/European Association of Echocardiography (EAE) prediction model (54% sensitivity and 66% specificity). The multi-centric Euro-Filling study also bespeaks of the diagnostic superiority of the 2016 guidelines over the 2009 version for LVDD assessment.[11]

The importance of other parameters, including PVDF, color M-mode and the implications of Valsalva maneuver (except in selected populations), in relation to LVFP, be equally emphasized. For instance, estimating the duration of atrial reversal (Ar) wave in PVDF has been shown to accurately predict LVEDP.[12] In addition, now E/A >2 is defined as a restrictive mitral flow with deceleration time (DT ≤160 msec) of E wave being described for the prediction of elevated LVFP with a reasonable accuracy in individuals with atrial fibrillation (AF).[3] E/e′ ratio as a dimensionless index, also, provides a useful echocardiographic estimate of LVFP, albeit with a considerable gray zone in predicting LVEDP across patients with varying degrees of preserved and depressed LVEFs.[13,14,15]

Alongside the 2016 recommendations offering the simplified approach for early determination of DD in routine practice, the important variables like LAV and peak TR velocity should be discussed.[3] Elevated LVFP tends to cause high pulmonary artery (PA) pressures resulting in TR > 2.8 m/s. Having said that, TR may be absent in a sizeable population and notably so, only 61% TR tracing be interpretable. In patients without TR, other modalities like echocardiographic assessment of PA pressure using pulmonary regurgitation (PR) jet; indirect measurement employing pulmonary artery acceleration time; or isovolumetric relaxation time (IVRT) on the tricuspid flow Doppler may prove helpful. The cohort with TR < 2.8 m/s might have pulmonary artery hypertension (PAH), like in patients with laminar TR velocity and prevailing right ventricle (RV) dysfunction where TR velocity is around 2 m/s and < 2.8 m/s, respectively. To that effect, the elderly, or the obese subset may have TR velocity more than 2.8 m/s, in striking absence of any pulmonary perturbation.[16] High LVFP results in increased LAV that is indexed as per patient’s body surface area. However, in overweight individuals, indexing trends to underestimate the LA enlargement. In this regard, lower threshold that is, 28 mL/m² has been proposed by some, instead of the widely guideline recommended threshold 34 mL/m².[3,17]

Off late, a 2025 ASE document on the recommendations for echocardiographic evaluation of LVDD for heart failure with preserved ejection fraction; underlines as to how ever since the publication of 2016 ASE/EACVI guidelines, novel modalities like strain imaging have featured into the arena of diastolic function assessment, as discussed in the article at a later stage.[18]

Echocardiographic modalities: Breaking it down to understand it better

• TMDF: The pulse of E and A waves

  Pulse wave Doppler technique is used to measure TMDF velocities that provide valuable insight into the diastolic function [Figure 1a]. TMDF depends on various parameters like pulse rate-rhythm, early diastolic filling pressure, atrial contractility, mitral-valve (MV) pathology, interventricular interaction, lusitropic state alongside the ventricular compliance.[19] Typically, diastolic dysfunction progress from impaired relaxation with a reduced E/A ratio (≤0.8), followed by pseudo normalization of the E/A ratio (>0.8 to <2), and finally to restrictive pathophysiology with an E/A ratio >2, as discussed above.[3]

  With aging, there is delay in LV relaxation results in proportionally less early filling and higher atrial contribution up to 40% (lower E and higher A velocity). Comparatively, in young adults, more efficient elastic-recoil, and LV relaxation results in predominant early LV filling corresponding with a higher E and a lesser A wave velocity, depicting 15% atrial contribution.[20] Alternatively, rise in pressure gradient in reduced LV compliance is mainly because of progressive rise in LAP. Therefore, variation in LV relaxation and for the matter, compliance is accompanied by the consequential alterations of LAP accounting for the progressive patterns witnessed in the TMDF profiles.[5,19,20] Even more interestingly, the A wave transit time from the mitral valve to the LV outflow tract, has been revealed as a Doppler parameter of importance, to reflect diastolic stiffness.[21]

• Mitral annular TDI: As the wall velocities do not pseudo normalize

  LV diastolic function assessment by TDI, have been described as less vulnerable to immediate variations in loading conditions. Tissue velocity imaging catches low-velocity high-amplitude myocardial signals in place of the high-velocity low-amplitude blood signals [Figure 1b]. The e′ accurately reflects velocities due to LV volume alterations without any geometric distortion or any regional-wall motion abnormalities, hence assisting the differentiation of the normal versus pseudo normal filling pattern. It is mainly affected by elastic recoil and myocardial relaxation. The peak e′ velocity herein is not influenced significantly by preload alteration.[22] It is a proportionately preload-insensitive modality for LV diastolic function assessment and therefore, may prove particularly useful in the perioperative scenario where loading conditions tend to vary frequently. The recommended cut-off values are annular e′ velocity (lateral and septal e′ <10 and <7 cm/sec, respectively), lateral E/e′ >13, septal E/e′ >15 and average E/e′ ratio >14, considered as abnormal.[3]

• PVDF: The window to LA

  PVDF reflects LVFP in combination with the parameters of TMDF [Figure 2a]. If Ar velocity overshoots by >35 cm/s or Ar duration exceeds by >30 ms, the trans-mitral A-wave duration, it indicates an elevated LVFP.[3,20] Similarly, systolic blunting (S/D < 1) PVDF pattern is observed in the presence of pseudo normal LV filling on TMDF due to decreased LV compliance and elevated LAP. In this regard, a systolic fraction of less than 40% in setting of reduced LVEF denotes raised LAP, with high specificity.[20]

• LAVI: The HbA1c of LVDD

  Measurements of LAV reflects the sheer chronicity of elevated LVFP, pretty much akin to the glycated hemoglobin or the HbA1c levels in a long-standing diabetic patient. LA volume can be computed by the disk-summation algorithm or the linear measurements using an ellipsoid model [Figure 2b]. After various studies (including as many as 1,234 patients), the recommended normal upper limit of LAVI is 34 mL/m², in sharp contrast to the value of 28 mL/m² proposed previously.[23] This value seems to appropriately discriminate a normal from an otherwise enlarged LA and has been recommended by the ASE-EAE guideline on diastolic function evaluation.

• TR jet interrogation: Right heart has something to say

  TR jet velocity can very well be interrogated to estimate PA systolic pressure (PASP) as a surrogate of the RV systolic pressure (RVSP) when there does not exist any pulmonary valve stenosis or RVOT obstruction by the means of a simplified Bernoulli equation (RVSP or PASP = 4V_TR²+ right atrial pressure i.e. RAP)[24] [Figure 2c]. A close relation has been appreciated between the PASP and LVFP, in absence of pulmonary vascular-disease.

• Doppler assessment: To profile the pulmonary flow

  Pulmonary artery diastolic pressure (PADP) can be corelated significantly with LAP derived either by invasively or noninvasively.[25] Amidst no pulmonary pathology, the elevated PADP corresponds to higher LVFP. However, recording of an adequate PR jet tracing is not possible most of the times albeit contrast is used. Accurate estimation mostly depends on the reliability in estimating mean RAP. If the mean pulmonary artery pressure is >40 mmHg or the pulmonary vascular resistance >200 dynes sec cm^–5, then PADP is considered to exceed by >5 mmHg over the mean PAOP.[3]

• Color M-mode, the trans-mitral propagation velocity

  Color M-mode propagation of the trans-mitral inflow displays color-coded mean blood column velocities traveling from LA to LV, providing for the estimation of the velocity of propagation (Vp). In healthy young adults, Vp ranges normally between 68 and 105 cm/s[26] [Figure 2d]. Vp is used to estimate PCWP using the formula PCWP = (5.27 × E/Vp) + 4.6.[27] Contrary to the standard indices, Vp is relatively independent of the preload and correlates well with the lusitropic changes as well as the systolic performance of LV. Altering preload by either intravenous nitroglycerin, Trendelenburg positioning, inferior vena cava occlusion, or partial CPB, is associated with transformation in trans-mitral peak E-wave and E/A-wave velocities but with a minimal effect on Vp.[28]

Figure 1.

Two-Dimensional Trans esophageal echocardiographic image showing (a) Trans mitral doppler flow velocity (TMDF) profile with early diastolic filling (e) wave, atrial contraction (a) wave, E/A ratio, isovolumetric relaxation time (IVRT) and deceleration time (DT) in midesophageal four-chamber view, (b) Mitral annular tissue doppler image demonstrating septal early diastolic filling (e') wave in midesophageal four-chamber view

Figure 2.

Two-Dimensional Trans esophageal echocardiographic image illustrating (a) Pulmonary venous doppler flow (PVDF) velocity with systolic (s), diastolic (d), atrial reversal (Ar) waves with Ar velocity and duration in midesophageal pulmonary vein focused view, (b) Estimation of left atrium (LA) volume index (LAVi) in the deep trans gastric LA focused view, (c) continuous wave doppler profile of Tricuspid regurgitation (TR) jet, TR jet velocity (TR Vmax), right ventricular systolic pressure (RVSP) in midesophageal modified bicaval view, and (d) Trans mitral color M mode propagation velocity (Vp) in midesophageal four-chamber view

Assessment of diastolic function in special scenario

LVDD causes LA dilatation, resulting in AF. In AF, Doppler guided diastolic function assessment is limited by variable heart rate and absent organized atrial activity. The recommended parameters are: DT ≤ 160 msec, IVRT (≤65 msec), and peak acceleration rate of the mitral E velocity ≥ 1,900 cm/sec², DT of the pulmonary venous diastolic velocity ≤220 msec, septal E/e′ and an E/Vp ratio greater than 11 and 1.4, respectively.[3] The recommended cut-off for sinus tachycardia with predominantly early LV filling in EF <50%, stand to be an IVRT ≤ 70 msec with 79% specificity, pulmonary venous systolic filling fraction higher than 40% depicting 88% specificity, with average E/e′ ratio accounting for the most specificity of 95% when compared to its’ corresponding sensitivity.[29] In E and A waves fusion, compensatory phase after each premature beat often leads to the separation of the E and A waves and used as surrogate of diastolic function.[30] Conduction abnormities because of aging, disease progression, any medications, or pacing can simultaneously affect adversely the atrioventricular synchrony. At the same time, chronic RV pacing causes LV desynchrony, resulting impaired LV filling and therefore lower LVEF, and higher occurrence of heart failure and AF.[31]

In face of a confounding effect of the MV disease on the conventional assessment, the duration from the onset of trans-mitral peak E to the peak e′ velocity (E-e′) has been related to the time-constant of LV relaxation or the tau. Diwan et al.[32] outline the IVRT to E-e′ ratio to correlate best with the PCWP (r = –0.92 and –0.88; for mitral regurgitation (MR) and mitral stenosis (MS), P < 0.001 alongside the correlation of the IVRT-tau ratio for MR, being –0.74 and –0.85 for those with MS. With IVRT/E-e′ <4.2, a shorter IVRT <60 msec has a high specificity, especially if the mitral A velocity is >1.5 m/sec, in cases of MS.[3] In MR however, IVRT/E-e′ <5.6 is recommended for the LVFP prediction in normal EF, where the importance of relatively unaffected association of LVFP with Ar-A duration cannot be undermined.[3,33] In severe aortic regurgitation (AR) on the other hand, trans-mitral tracing may be impeded, necessitating appropriate positioning of the sample volume. That said, an abbreviated LV filling, early MV closure, and presence of diastolic MR denote elevated LVFP in acute severe AR whereas predominantly early diastolic filling with shortened DT is more peculiar of chronic severe AR.

LVFP in individuals with hypertrophic cardiomyopathy, correlating with muscle mass, multiple phenotypes, myocardial-fiber disarray, and an obstructive pathology leads to varied amalgamations of altered relaxation-compliance. The recommended cut-offs applicable being: TR velocity >2.8 m/sec, average E/e′ >14, LAVI >34 mL/m² and Ar-A ≥ 30 msec.[3,34] Restrictive cardiomyopathy is characterized by dip and plateau waves in early diastolic pressure, E/A > 2.5, E wave DT < 140 msec, IVRT < 50 msec, reduced septal as well as lateral e′ (3–4 cm/sec) nonetheless with lateral e′ exceeding septal e′ (unlike annulus reverses of constrictive pericarditis), E/e′ ratio > 14, and a markedly higher LAVI > 50 mL/m².[3,35,36] Speaking of the pulmonary circulation, lateral E/e′ distinguishes PAH of cardiac versus that of non-cardiac etiology. Lateral E/e′ value >14 suggest PAH of cardiac origin, whereas value <8 suggest PAH due to a noncardiac etiology.[37] Table 1 summarizes the formulas described by independent researchers for the noninvasive estimation of LVFP, in specific enlisted scenarios.[27,29,38]

Table 1.

Formulas described by independent researchers for the estimation of LV filling pressures[27,29,38]

Normal Sinus Rhythm:

PCWP=1.9+1.24 (E/e′)

PCWP=5.27 (E/Vp) + 4.6

Sinus Tachycardia:

PCWP=1.55+1.47 (E/e′)

Atrial Fibrillation:

PCWP=6.49+0.82 (E/e′)

LV: left ventricular

Novel assessment modalities: Ongoing search for an ideal echocardiographic concur

Centralizing the focus on qualitative estimation of LVFP, in isolation, is a major impediment in the assessment of DD, especially when talking in terms of monitoring the therapeutic targets for lusitropic therapy. While the multipronged approach featuring a range of echocardiographic modalities has been at the cornerstone of DD assessment, there is an ongoing search of quantitative echocardiographic techniques which correlate well with the diastolic functional hemodynamics.

Echocardiographic innovations like novel speckle tracking imaging (STI), ensure quantification of LVDD indirectly by LV global longitudinal diastolic strain (Ds) and strain rate (DSr), avoiding the Doppler related angulation errors and tethering artifacts. Independent researchers have off late also proposed the utility of pulmonary venous flow morphology and velocity for its’ ability to predict the LAP.

Speckle tracking echocardiography

Strain is defined as the instantaneous deformation of the myocardium in relation to the pre-existing myocardial length with the strain rate being the corresponding rate of the deformation. With evolution of two-dimensional Speckle Tracking Imaging (2D-STI, Figure 3a-d), its’ feasibility for the estimation of LVDD, is being increasingly demonstrated. Albeit an indirect measurement, it has been described to correlate with the LV diastolic function, given the software happens to be well equipped to automatically track the myocardial motion through an entire the cardiac cycle, having carefully chosen the region of interest.[39,40,41,42,43,44,45]

Figure 3.

Speckle Tracking Echocardiography employed in a set of two-Dimensional Transesophageal echocardiographic midesophageal four-chamber (a) two-chamber, (b) aortic valve long-axis, (c) views, to obtain the myocardial strain values and the bull’s eye profile, and (d) Herein, utilizing the diastolic section of strain curves, values of the same obtained at the peak mitral filling and/or those during isovolumic relaxation period have been specifically focused by recent studies to formulate newer echocardiographic correlates of LV filling pressures. LV: left ventricular

Zhu et al.,[40] in their endeavor to characterize DD in peritoneal dialysis (PD) patients with a preserved LVEF, included thirty youngsters with EF ≥54% categorized as normal diastolic LV function by a conventional echocardiography and thirty age-, sex-matched healthy individuals as controls. The global longitudinal strain was considerably reduced in the PD subset in comparison to controls (P = 0.008). The average DSr during the late diastole that is, DSrA and the E/DSrE were increased (P = 0.006), the latter contributed by the reduction of the average DSr during late diastole or the DSrE (P < 0.001), where the DSr during the isovolumic relaxation (IVR) period or the DSrIVR and the E/DSrA simultaneously decreased (P = 0.017 and P < 0.001).

In 2004, Dokainish et al.,[41] involved 50 persons where Ds and the DSr were assessed during diastolic filling on transthoracic echocardiography (TTE) to be combined with peak E velocity, computing two indices: E/Ds and E/10DSr (DSr multiplied by a factor of 10 in the denominator). The parameters were hence compared with the LV preatrial (preA) contraction pressure and E/e′ ratio measured invasively. The E/Ds and E/10 DSr correlated better with the LV preA pressure, when compared to the E/e′ (r = 0.81, 0.80 versus 0.63, P < 0.001). The derived cut-off values were >8.5 for E/Ds, >11.5 for E/10DSr, and > 15 for E/e′, with regards to the prediction of LVFP > 15 mmHg. E/Ds > 8.5 displayed a higher sensitivity-specificity than E/e′ >15 to predict LV preA pressure of more than 15 mmHg. In those with EF > 50% and E/e′ values between 8 and 15 that is, the gray zone, the most noticeable finding was the stronger accuracy of E/Ds, E/10 DSr to determine LV preA pressure when compared to E/e′.[15,41]

In a study by Wang et al.,[42] the derived indices DSr during IVR were compared with LV diastolic function measured invasively. The authors enrolled 50 persons and found that mitral E/SrIVR ratio has a superior correlation with the mean PCWP (r = 0.79, P < 0.001). They also concluded the cut-off value for E/SrIVR to be more than 236 cm as to appropriately identify mean PCWP > 15 mmHg with 96% sensitivity and 82% specificity. E/SrIVR predicted LVFP accurately in individuals with a preserved LVEF or with regional wall motion abnormalities.[42]

As far as a strict perioperative setting with transesophageal echocardiography or TEE is concerned, Magoon et al.,[43] employed Ds and DSr, to reveal that E/Ds and E/DSr, as more accurate PCWP determinants as opposed to E/e′ in coronary artery bypass graft (CABG) patients with preserved EF. Strain based indices or the SBIs (as they called them) yielded a better sensitivity-specificity profile than the tissue Doppler indices (TDI or the E/e′) did for the detection of LVEDP in excess of 15 mmHg. They highlighted E/10DSr ≥ 12 to be the most closely related to LVEDP ≥ 15 mmHg, with area under the curve (AUC) of 0.99. Meanwhile the SBIs emerged as accurate LVEDP predictors in the gray zone of TDI (E/e′ values between 8 and 13), strain imaging during early filling can be load dependent, potentially influencing their results.[43,44] Addressing the limitation, 2D-STI on TEE was utilized by Ebrahimi et al.[45] to estimate the strain rate during IVR (SrIVR) and to derive E/SrIVR ratio. A strong enough correlation existed between SrIVR and E/SrIVR and PCWP (r = 0.80 and 0.73, P < 0.001). SrIVR better predicted high PCWP than the lateral E/e′ (AUC 0.94 versus 0.47). Also, SrIVR ≤ 0.2 per sec portrayed a 100% sensitivity and 81% specificity for PCWP ≥ 15 mmHg prediction.[45]

Pulmonary vein diastolic wave deceleration time

The diastolic flow of pulmonary veins has proposed to be well congruent with the invasive PCWP, regardless of the LV systolic function. Literature highlights as to how the analysis of the pulmonary venous diastolic wave profiles can prove to be useful for the prediction of LVFP.[46]

In a study by Reddy et al.,[47] DT of pulmonary venous diastolic wave, DT_D was compared with the LAP obtained noninvasively from the E/e′ ratio, to estimate the feasibility in candidates undergoing elective offpump CABG. Forty-five coronary artery disease patients with LVEF ≥ 50% were included. After analysis, a linear association was demonstrated between the DT_D and the LAP. With this background, they concluded that a DT_D ≤ 183 msec speculates a higher LAP. Furthermore, Kinnaird et al.[48] compared mean LAP obtained by pulmonary venous Doppler measurement, with predicted LAP using the PCWP during heart surgery and demonstrated DT_D is more precise in determining LAP than that estimated with PAOC.

Nishimura et al.,[49] correlated variation in velocities of the pulmonary venous flow with trans-mitral flow under diverse loading conditions in 19 patients undergoing CABG. They found a direct correlation of trans-mitral E velocity with the pulmonary venous early diastolic flow velocity as well as between the DT of the mitral and the pulmonary venous early diastolic velocities. Olariu, et al.,[50] evaluated the pulmonary venous diastolic DT to determine the enddiastolic pressure and grade patients according to the degree of elevated LVEDP. One hundred and seventy four patients were embodied in the study. LVEDP was obtained noninvasively by pulmonary venous flow diastolic DT (determined by TTE) and invasively by cardiac catheterization. The study result showed a fair correlation between LVEDP with pulmonary venous diastolic DT (r = 0.74). A value of diastolic DT < 220 msec suggested elevated LVEDP, value < 190 msec predicted elevated and <165 msec predicted severely elevated LVEDP.

Future directions

The role of LA is governed by an intricate balance between its’ reservoir, the conduit, and the contractile functions. LA demonstrates adaptive structural alterations in the setting of abnormal LV filling pattern, signifying the consequences of DD. Recently, strain analysis is being utilized for estimation of the various functions of LA.[51] As discussed earlier, strain examines the myocardial deformation whereas strain rate captures the rate of the change in deformation. It is also monitored in entire cardiac cycle, hence enabling the assessment of LA reservoir function during systole and then the conduit as well as the contractile domain during diastole. LA strain is angle-independent, eliminating the limitations of Doppler echocardiographic parameters [Figure 4].

Figure 4.

2-Dimensional Transthoracic echocardiographic image showing left atrial strain parameters including reservoir strain (S_R), conduit strain (S_CD), and contraction strain (S_CT) in apical four chamber view

During reservoir period, LA filling and stretching, causes a positive strain which reaches its’ peak before the opening of the MV in systole. Then, with opening of the MV, passive LA emptying results in a reduced LA strain with manifestation of a negative deflection till a plateau phase suggesting diastasis. Atrial systole ensues, leading to a second deflection in the strain curve. LA systolic strain which is also called peak atrial longitudinal strain (PALS) is estimated at the culmination of the reservoir-phase whereas, the late diastolic strain otherwise called peak atrial contraction strain (PACS) is evaluated after P-wave and corroborates with the atrial contraction. Moreover, strain rate in the ventricular systole, the early diastole and the late diastole correspond to the reservoir, the conduit, and the contractile pump function, respectively.[52] Morris et al.,[53] conducted a multicentric study of 329 healthy individuals and concluded the LA strain values that is, LA reservoir function to be 45.5 ± 11.4% in healthy and 27.8 ± 10.6 in DD with the allied LA strain rate being –2.11 ± 0.61 per sec and –1.68 ± 0.64, respectively. As for the practical utility of the LA strain analyses, it detected subtle LA dysfunction, in backdrop of normal LA volumetric measurement where the functional clinical class related inversely to LA deformation parameters. Kurt et al.,[54] revealed the peak LA strain at the end of ventricular systole to correlate well with the LVEDP and N-terminal pro-brain natriuretic peptide (NT pro-BNP).

In the 2025 ASE guidelines and standards,[18] PALS is referred to as left atrial reservoir strain (LARS). LARS declines with worsening DD and demonstrates an inverse relationship with LVFP. Similarly, the late diastolic parameter, PACS is inversely associated with LVEDP. Furthermore, according to the 2025 ASE recommendations,[18] a LARS value of <18% is indicative of elevated LAP.

CONCLUSION

Echocardiographic estimation of LVFP happens to be an ever-evolving subject where it is for its’ sheer clinical relevance that the cardiac anesthesiologist needs to stay abreast with the recent developments in the complex field of diastology, only when we are inching closer to multimodal machine-learning approaches in the modern era of artificial intelligence.[55]

Conflict of interest

There are no conflicts of interest.

Funding Statement

Nil.