Extract

This editorial refers to ‘Left atrial function in heart failure with mid-range ejection fraction differs from that of heart failure with preserved ejection fraction: a 2D speckle-tracking echocardiographic study’, by L. Al Saikhan et al., pp. 279–290.

What is essential is invisible to the eye.1

Traditionally, the duration after left ventricular (LV) end-systole (ES) or mitral valve opening to before atrial contraction (Pre-A) is called ‘passive’ emptying phase (conduit phase) for the left atria (LA). But recently, there are several noteworthy publications suggested LA behaviour in the all three (reservoir, passive conduit, and active pumping) phase altered by LA property itself.2,3 That is, the LA behaves in the conduit phase not just as passively but as one of the important biomarkers, and the LA conduit function contributes the pathophysiological sequence in patients with heart failure (HF) with preserved LV ejection fraction (HFpEF; LVEF >50%); so-called ‘Atrial myopathy’.2 Al Saikhan et al.4 have further stepped forward the concept to HF patients with ‘mid-range’ LVEF (40–50%, HFmrEF) who had similar LV diastolic function as HFpEF patients.4 They found that the ‘intrinsic’ LA functions were more impaired in the all three phases in HFmrEF than HFpEF. Widely spread 2D echocardiographic speckle-tracking technique for functional assessment of LA5 obviously facilitates these investigations, and deepens our knowledge.

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Comments

2 Comments
Regarding Dr. Marino's important comment
30 March 2019
Yuichi Notomi
Keiyu hospital, Yokohama, Japan
Dear Dr. Paolo Marino
I appreciate very much and am pleased to have your comments, which surely corrects and deepens our knowledge regarding left atrial mechanics and flow dynamics. Dr. Marino’s comment contained 2 important issues; 1) accurate method to obtain conduit volume from pulmonary vein (CV-PV), and 2) usefulness of full volume 3D simultaneous datasets (volume profile through a cardiac cycle) of left atria and ventricle (LA and LV) also to obtain CV-PV. I totally agree both, obviously.
I think that we are in the same position: the change in total LA size is not equivalent to the volume entering to the LV during the diastole. That is when sinus rhythm is preserved, 1) during conduit phase, some flow enters into LV from PV directly (CV-PV) and some flow enters into LV from LA (CV-LA), and 2) while during pumping phase, LA contraction produces bi-directional flow; pumping forward flow into LV and pumping backward flow into PV (the dotted arrow of top of LA at ED in Figure 2 would indicate it).
Therefore; LV stroke volume (SV) = CV-LA + CV-PV + forward pumped volume.
And LASV = CV-LA + forward pumped volume + backward pumped volume.
I calculated CV-PV as LVSV-LASV, but to be accurate, LVSV-LASV=CV-PV – backward pumped volume. So the CV-PV I presented in the Figure 3 was overestimated by the backward pumped volume (especially in HFpEF/HFmrEF group, see below). To have an overview of LA mechanics and flow-dynamics in the athlete, controls, and HFpEF/HFmrEF in the both article (1, 2), it has been simply calculated by the often used method (3) (ie, CV-PV as LVSV-LASV), but this should be noted. I also understand LV volumes are sometimes underestimated by 2D echocardiography, and so Doppler SV would be preferred. But it was not available in the articles.

The backward pumped volume/flow (so called “reverse pulmonary venous flow”) has been detailed investigated by analyzing pulmonary venous flow velocity recorded with pulsed wave Doppler technique as known S wave (reservoir flow), D wave (conduit flow), and Ar (atrial reverse flow during the pumping phase). The ratio of Ar to (S+D) was 1.2% in the controls state (LA pressure at 6 mmHg), but 3.6% when LA pressure was elevated to 18 mmHg (4). Not only experimentally setting, aging itself affected increasing Ar (velocity time of integral was 1.6cm in young and 2.4cm in elderly) (5). Thus, relatively small but significant atrial reverse/backward flow dynamics would affect/overestimate the CV-PV in the Figure 3 especially in HFpEF/HFmrEF group but I believe overall message in the commentary is unaffected.
Current 3D echocardiography (3DE) that is able to visualize images with high spatio-time resolution and provides (no-assumption) cardiac volume dataset. This means that we can have true profile of LA and LV volume alteration through a cardiac cycle by 3DE data analysis. As noted by Dr. Marino, this clever method allows to calculate not only CV-PV but also rate change of CV-PV during conduit phase.
Yuichi Notomi, MD, FAHA, FJCC

References;

1. McClean G, George K, Lord R, Utomi V, Jones N, Somauroo J, et al. Chronic adaptation of atrial structure and function in elite male athletes. Eur Heart J Cardiovasc Imaging. 2015 Apr;16(4):417-22. PubMed PMID: 25368211.
2. Al Saikhan L, Hughes AD, Chung WS, Alsharqi M, Nihoyannopoulos P. Left atrial function in heart failure with mid-range ejection fraction differs from that of heart failure with preserved ejection fraction: a 2D speckle-tracking echocardiographic study. Eur Heart J Cardiovasc Imaging. 2019 Mar 1;20(3):279-90. PubMed PMID: 30517648. Pubmed Central PMCID: PMC6383056.
3. Blume GG, McLeod CJ, Barnes ME, Seward JB, Pellikka PA, Bastiansen PM, et al. Left atrial function: physiology, assessment, and clinical implications. Eur J Echocardiogr. 2011 Jun;12(6):421-30. PubMed PMID: 21565866.
4. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity components: new insights from studies in lightly sedated normal dogs. J Am Coll Cardiol. 1997 Nov 15;30(6):1562-74. PubMed PMID: 9362417. Epub 1997/11/15. eng.
5. Bukachi F, Waldenstrom A, Morner S, Lindqvist P, Henein MY, Kazzam E. Pulmonary venous flow reversal and its relationship to atrial mechanical function in normal subjects--Umea General Population Heart Study. Eur J Echocardiogr. 2005 Mar;6(2):107-16. PubMed PMID: 15760687.
Submitted on 30/03/2019 8:48 AM GMT
Passing volumes in the shrinking conduit have to be carefully quantified
26 February 2019
Paolo Marino
Dept of Translational Medicine, Università del Piemonte Orientale, Novara, ITALY
This editorial is important because it clearly underlines the dissociation between deformation vs volume data when dealing with phasic cardiac function assessment. Author has to be congratulated also because, very clearly, he states that conduit function in the atrium is something that cannot be correctly assessed unless it is contextualized within the “atrio-ventricular” coupling concept (1). The editorial, however, is too simplistic when it suggests that conduit can be computed from the subtraction of the atrial stroke volume (minimum-maximum volume) from the ventricular stroke volume. During atrial contraction, in fact, part of the blood ejected with the atrial contraction flows back into the pulmonary veins, the amount being a function of the relative resistance between the ventricular diastolic condition and the pulmonary venous district. More correct is the author when he states that conduit can be derived as the difference between ventricular stroke volume, as obtained from the aortic systolic Doppler flow, and the atrial stroke volume. The best approach, however, should be the one that takes into account the simultaneous change in volume between the atrial and the ventricular cavities. This is something that can be relatively easily performed nowadays collecting full volume 3D atrio-ventricular datasets from the apex and analyzing dynamic atrial vs ventricular cavity volume changes as a function of time (2). If quantitation of the “shrinking conduit function” is physiologically important, given that it affects diastolic filling in normal and pathological conditions, I think that methodological boundaries have to be adequately modelled.
1) Marino P. Correct estimation of conduit function from left atrial volume curve assessment only is unlikely. J Am Soc Echocardiogr 2010;23:1333
2) Degiovanni A, Boggio E, Prenna E, Sartori C, De Vecchi F, Marino PN. Association between left atrial phasic conduit function and early atrial fibrillation recurrence in patients undergoing electrical cardioversion. Clin Res Cardiol. 2018;107:329-337.
Submitted on 26/02/2019 6:15 PM GMT