In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

How useful is the echocardiogram to evaluate left ventricular remodelling in mitral valve regurgitation?

Echocardiography has turned out to be a tool par excellence for diagnosis and decision making in the management of mitral regurgitation. The aim of echocardiographic evaluation should include quantification of mitral valve regurgitation, analysing the mechanisms involved, as well as assessing the consequences on the function and geometry of the left ventricle (LV). Echocardiography is the imaging technique of choice in the follow-up of patients with mitral regurgitation who have undergone therapeutic interventions, both to assess the success of these and to evaluate their impact on the geometry and function of the LV.

Interventional Cardiology and Cardiovascular Surgery
Valvular Heart Disease


Mitral regurgitation (MR) is the most frequent clinically recognisable valvular heart disease in the western world [1]. MR can be caused by primary valve anatomical disorders (primary MR) or it can be secondary to cardiomyopathy (secondary MR, previously referred to as functional MR).

The pathophysiological key problem of MR is the magnitude of the regurgitation volume. Left ventricle (LV) response to this chronic volume overload is characterised by changes in LV structure and geometry as compensatory adaptation. Later, this compensatory mechanism is overwhelmed, leading to LV dysfunction.

Echocardiography is the main tool for assessing the severity and mechanism of the MR and its consequences on the LV as well as being a clinical standard for the evaluation of the mitral apparatus.

The present paper evaluates the echocardiographic parameters of LV remodelling in MR as well as the impact on them of surgical and endovascular interventions, such as cardiac resynchronisation therapy (CRT) and percutaneous endovascular mitral valve repair.

Left ventricular remodelling in mitral regurgitation: cause and consequence

LV remodelling is a complex and progressive set of structural and functional changes at the cellular and interstitial level which occur following volume and/or pressure overload and myocardial injury.

Primary mitral regurgitation

In MR, part of the stroke volume does not contribute to the peripheral circulation and therefore does not contribute to the cardiac output. The volume overload exerted on the LV due to mitral incompetence results in elevated stress on the LV walls during diastole. In response, LV compensates for it by eccentric hypertrophy and remodelling. At a molecular and cellular level, there is an increase in the length of the myocardial fibres with a disorganisation and remodelling of the extracellular matrix, resulting in a realignment of the myocardial fibres that leads to development of LV geometry abnormalities [2]. These changes in the LV geometry can be detected in the echocardiographic study:

  • Increase in LV end-diastolic and end-systolic volumes (LVEDV and LVESV).
  • Increase in the LV mass (LVM).

In the compensated stage of eccentric hypertrophy secondary to MR, the LV ejection fraction (LVEF) remains normal or increased, and the relative wall thickness (RWT) also remains normal. Because in eccentric hypertrophy the radius of the LV is increased, it requires an increase in the absolute thickness of the LV wall in order to maintain normal wall tension, i.e., to keep the relationship between radius and LV wall thickness normal. RWT typically remains ≤0.42.

The normal ellipsoidal shape of the LV in chronic mitral valve diseases is altered, becoming more spherical. This is detected in an echocardiographic study by measuring the sphericity index (calculated as LV short-to-long axis dimension ratio at end diastole in the apical four-chamber view), with a cut-off value of 0.7.

The shape of the LV is closely associated with the LVEF. When the geometrical alterations originating in an LV with eccentric hypertrophy secondary to chronic volume overload lead to loss in the normal orientation of the cardiomyocytes, LVEF finally decreases [3].

Secondary mitral regurgitation

The changes in LV geometry secondary to remodelling, whether the cause is ischaemic heart disease (IHD) or dilated cardiomyopathy (DCM), lead to a disruption in the normal relationships between the LV and the mitral apparatus. Secondary mitral regurgitation (SMR) entails not an affectation of the mitral valve per se, but a remodelling and an alteration of the normal geometry of the LV. This leads to a disruption of the normal spatial relationships of the valve apparatus and generates an imbalance between the closing and tethering forces [4].

Here echocardiography plays a crucial role not only in the diagnosis of the aetiology and determination of the degree of severity of the MR but also in the characterisation of LV remodelling when it comes to choosing an appropriate therapeutic approach. An echocardiography study must distinguish between functional MR produced by global ventricular dilation and that caused by localised abnormalities, and the effects of altered ventricular geometry on MR need to be specifically addressed.

In IHD, an inferolateral scar and associated local remodelling distort the normal geometry of the LV and displace the posteromedial papillary muscle posteriorly and apically, producing an imbalance between closure forces and tethering forces that reduces the MV leaflet coaptation [5]. In this case, the displacement of papillary muscles is asymmetrical, resulting in a malapposition of the leaflets with an eccentric, posteriorly directed jet of MR.

In DCM, both papillary muscles are displaced symmetrically posteriorly and apically pushing to an apical displacement of the coaptation line. As the displacement of both leaflets is symmetrical, the regurgitant jet is central.

Reversal of left ventricular remodelling

LV reverse remodelling is associated with improved morbidity and mortality. The concept of reverse remodelling was introduced in the 1990s by Kass [6] and describes the regression of hypertrophy, size, shape and function of the LV. Both types of LV remodelling described above, the one caused by chronic volume overload in the primary valve lesion or the initial ventricular remodelling responsible for secondary MR, can be reversed after different types of therapeutic intervention.

Echocardiography is the imaging technique of choice in the follow-up of patients with MR who have undergone therapeutic interventions, both to assess the success of these and to evaluate their impact on the geometry and function of the LV.

Optimal medical treatment is the first line of treatment in MR and its use is recommended by the ESC guidelines [7]. In patients with secondary MR, medical treatment of the myocardiopathy from which it originates (DCM or IHD) is the most widely extended initial treatment. The effects of beta-blocker therapy in LV geometry in patients with heart failure (HF) with reduced ejection fraction have been widely studied. The beneficial effect of beta-blocker therapy on LV remodelling reversal has been linked to a decrease of LV volumes [8], a decrease in the LVM index [8,9] and an improvement of LV geometry as evidenced by a decrease of the sphericity index [9]. Long-term angiotensin-converting enzyme inhibition, angiotensin receptor blockade and aldosterone receptor antagonism affect LV remodelling through reducing the loading conditions and cardiac afterload, resulting in an improvement in LVM and LV geometry.

Cardiac resynchronisation therapy (CRT) is a well-established recommended therapy for patients with HF, depressed LVEF and intraventricular conduction disturbance. In responders, CRT may immediately reduce MR severity through increased closing force and resynchronisation of papillary muscles [10], which is directly related to the electric cardiac stimulation. Following CRT, there is less LV volume overload which, in addition to the increased LV contraction efficiency, participates in the restoration of the LV size. Echocardiographic follow-up of patients with DCM or IHD and MR treated with CRT is not only useful to confirm the reduction of the severity of it in responders, but also to assess the improvement of LV volumes [11].

The current ESC guidelines for the management of valvular heart disease recommend a surgical strategy for symptomatic patients and asymptomatic patients presenting with chronic primary MR and LVESD ≥45 mm, placing emphasis on the worse postoperative outcome of patients with LVESD of 40-44 mm compared to those with LVESD less than 40 mm [7]. After surgical intervention (both mitral valve repair and valve replacement), symptom and cardiac function improvement occur rapidly. Echocardiography is the most important imaging tool for assessing LV reverse remodelling by documenting the decrease in LV volumes that usually occurs between four and six months after the surgery [12].

After a successful percutaneous edge-to-edge mitral valve repair, MR severity and loading conditions decrease. The LV unload can explain the rapid decrease in LVEDV already seen 24 hours after the intervention [13]. After 12 months, further favourable changes are seen in the echocardiography follow-up consistent with a greater reduction in LVEDV and decreases in LVESV and LV mass [14].


Left ventricular remodelling may be the consequence of chronic volume overload in the case of primary MR or the cause of valvular insufficiency in the case of an LV with a distorted geometry resulting from IHD or DCM. Echocardiography is an invaluable tool able to differentiate between both aetiologies of MR (primary or secondary) and characterise the remodelling of the LV as well as reverse remodelling secondary to therapeutic interventions.


  1. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M. Burden of valvular heart diseases: a population-based study. Lancet. 2006;368:1005-11. 
  2. Ho SY. Anatomy and myoarchitecture of the left ventricular wall in normal and in disease. Eur J Echocardiogr. 2009;10:iii3-7.
  3. Triposkiadis F, Giamouzis G, Boudoulas KD, Karagiannis G, Skoularigis J, Boudoulas H, Parissis J. Left ventricular geometry as a major determinant of left ventricular ejection fraction: physiological considerations and clinical implications. Eur J Heart Fail. 2018;20:436–44. 
  4. Piérard LA, Carabello BA. Ischaemic mitral regurgitation: pathophysiology, outcomes and the conundrum of treatment. Eur Heart J. 2010;31:2996‑3005. 
  5. He S, Fontaine AA, Schwammenthal E, Yoganathan AP, Levine RA. Integrated mechanism for functional mitral regurgitation: leaflet restriction versus coapting force: in vitro studies. Circulation. 1997;96:1826-34. 
  6. Kass DA, Baughman KL, Pak PH, Cho PW, Levin HR, Gardner TJ, Halperin HR, Tsitlik JE, Acker MA. Reverse remodeling from cardiomyoplasty in human heart failure. External constraint versus active assist. Circulation. 1995;91:2314-8. 
  7. Baumgartner H, Falk V, Bax JJ, De Bonis M, Hamm C, Holm PJ, Iung B, Lancellotti P, Lansac E, Rodriguez Muñoz D, Rosenhek R, Sjögren J, Tornos Mas P, Vahanian A, Walther T, Wendler O, Windecker S, Zamorano JL; ESC Scientific Document Group. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2017;38:2739-91. 
  8. Groenning BA, Nilsson JC, Sondergaard L, Fritz-Hansen T, Larsson HB, Hildebrandt PR. Antiremodeling effects on the left ventricle during beta-blockade with metoprolol in the treatment of chronic heart failure. J Am Coll Cardiol. 2000;36:2072-80. 
  9. Lowes BD, Gill EA, Abraham WT, Larrain JR, Robertson AD, Bristow MR, Gilbert EM. Effects of carvedilol on left ventricular mass, chamber geometry, and mitral regurgitation in chronic heart failure. Am J Cardiol. 1999;83:1201-5. 
  10. van Bommel RJ, Marsan NA, Delgado V, Borleffs CJ, van Rijnsoever EP, Schalij MJ, Bax JJ. Cardiac resynchronization therapy as a therapeutic option in patients with moderate-severe functional mitral regurgitation and high operative risk. Circulation. 2011;124:912-9. 
  11. Linde C, Gold MR, Abraham WT, St John Sutton M, Ghio S, Cerkvenik J, Daubert C; REsynchronization reVErses Remodeling in Systolic left vEntricular dysfunction Study Group. Long-term impact of cardiac resynchronization therapy in mild heart failure: 5-year results from the REsynchronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study. Eur Heart J. 2013;34:2592-9. 
  12. Pandis D, Grapsa J, Athanasiou T, Punjabi P, Nihoyannopoulos P. Left ventricular remodeling and mitral valve surgery: prospective study with real-time 3-dimensional echocardiography and speckle tracking. J Thorac Cardiovasc Surg. 2011;142:641-9. 
  13. Siegel RJ, Biner S, Rafique AM, Rinaldi M, Lim S, Fail P, Hermiller J, Smalling R, Whitlow PL, Herrmann HC, Foster E, Feldman T, Glower D, Kar S; EVEREST Investigators. The acute hemodynamic effects of MitraClip therapy. J Am Coll Cardiol. 2011;57:1658-65. 
  14. Foster E, Kwan D, Feldman T,Weissman NJ, Grayburn PA, Schwartz A, Rogers JH, Kar S, Rinaldi MJ, Fail PS, Hermiller J, Whitlow PL, Herrmann HC, Lim DS, Glower DD; EVEREST Investigators. Percutaneous mitral valve repair in the initial EVEREST cohort: evidence of reverse left ventricular remodeling. Circ Cardiovasc Imaging. 2013;6:522-30. 

Notes to editor


Ivan Keituqwa Yañez1, MD; Silvestre  Nicolas-Franco2, MD, PhD

  1. Consultant Intensive Care Medicine, Intensive Care/Coronary Care and Cardiac Pacing Unit, Hospital General Universitario Rafael Mendez, Lorca (Murcia), Spain. Member of the Spanish Society of Cardiology (SEC); Member of the European Society of Cardiology (ESC). European Association of Cardiovascular Imaging (EACVI) member. Member of Acute Cardiovascular Care Association.
  2. Intensive Care Medicine, Chairman of the Intensive Care/Coronary Care and Cardiac Pacing Unit, Hospital General Universitario Rafael Mendez, Lorca (Murcia), Spain. Member of the Spanish Society of Cardiology (SEC). Member of the European Society of Cardiology (ESC). Member of the European Heart Rhythm Association (EHRA).


Address for correspondence:

Ivan Keituqwa Yañez, C/ Martin Morata, Nº4, 4º D, 30800 Lorca (Murcia), Spain.


Tel: +34 606408350; +34 968428039


Author disclosures:

The authors have no conflicts of interest to declare.




The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.