6 Mitral Insufficiency
Goals of Echocardiography in Mitral Insufficiency
To establish that mitral insufficiency is present
To establish the severity of mitral insufficiency
To determine the hemodynamic consequences of mitral regurgitation (MR), pulmonary venous flow, cardiac index (CI), and right ventricular systolic pressure
To establish the underlying cause(s), when possible
To determine the reparability of the valve lesion
To verify adequacy of repair (intraoperative transesophageal echocardiography [TEE])
To identify complications of MR (e.g., pulmonary hypertension, left ventricle [LV] dysfunction)
To identify concurrent cardiac disturbances (e.g., other valve lesions, coronary artery disease)
Scanning Issues
Required Parameters to Obtain from Scanning
Valve apparatus details to explain the cause of the MR
MR severity—quantified if more than moderate MR (i.e., not if mild)
Stroke volume (SV; net forward, not total) and CI
Indirect volume/pressure overload descriptors
The height and weight for body surface area normalization
Scanning Notes
If sinus rhythm: measure three spectral profiles
If atrial fibrillation: measure five spectral profiles
Spectral profiles should be two-thirds the height of the display and wide enough to show two to three per display.
For Proximal Isovelocity Surface Area
Shift the color baseline down for MR (if transthoracic echocardiography [TTE]).
Measure at mid-systole to correspond to peak MR velocity. PISA is measured at mid-systole by convention, although this may be less accurate when the regurgitant orifice is dynamic and mid-systole does not characterize its mean size.
VAliasing to 35-45-52 cm/sec to optimize depiction of PISA hemisphere
The PISA method is unsuitable if there is frankly poor depiction of PISA.
Reporting Issues
Describe the severity of the MR.
If ≥2+, describe the hemodynamic effect of the MR:
Use of color Doppler flow mapping
Severe hemodynamic effect (pulmonary venous flow reversal)
PISA ≥ 1 cm at VAlias –40 cm/sec
Pulmonary venous systolic flow reversal (for TTE)
Describe the LV in detail: size, end-systolic diameter, end-systolic volume, ejection fraction, wall motion abnormality.
Describe the RV in some anatomic detail, beyond the right ventricular systolic pressure
Do not make assumptions about peak mitral velocity as it is quite variable.
Pay attention to the aortic root if severe mitral valve prolapse (MVP), because Marfan syndrome may underlie both.
Avoid the use of the term “trivial” in general and whenever the mitral valve is abnormal.
When the Grade of Mitral Regurgitation is Different on Serial Echocardiographic Studies
If the change is >1 grade, it probably is a true change.
None/mild/moderate/severe is the most logical grading system. The greater the number of grades, the greater the intraobserver, interobserver, and interstudy reclassification rates. Therefore, using fewer categories yields more consistent grading.
When serial studies suggest difference in grade, a careful review of the basis of grading of each study should be entertained. If the studies have different components (e.g., one without pulmonary venous flow) then true comparison is not possible.
When apparent changes have occurred, it is important to evaluate the likelihood of improvement. Some pathologies responsible for MR are unlikely to change: for example, a flail leaflet nearly always results in severe MR, and the associated degree of MR is unlikely to be altered by medical therapy. Conversely, peri-infarction MR often is evanescent, and “functional MR” associated with chronic ischemic cardiomyopathy and with dilated cardiomyopathy, may be significantly improved with load alteration on the LV via medical therapy or blood pressure changes.
TEE is able to record pulmonary venous flow patterns in all cases; TTE under-detects abnormalities of pulmonary venous flow because of less successful interrogation of the pulmonary veins. Since pulmonary venous systolic flow reversal is a criterion to establish severe MR, TEE will more often establish that MR is severe than will TTE.
TEE is more sensitive than TTE to record MR flow mapping, and, therefore, for any given MR jet, the MR generally looks worse by TEE.
Echocardiography–Catheterization Discordance of the Assessment of Mitral Regurgitation Severity
When Echocardiographic Assessment of Mitral Regurgitation Differs from the Contrast Ventriculographic Assessment of Mitral Regurgitation
Contrast ventriculography may underrepresent the severity of MR.
Contrast ventriculography may overrepresent the severity of MR:
Inter- and intraobserver agreement of the “middle” grades of MR are not consistent. Differentiation of 2+ from 3+ MR may influence management, as 3+ MR may be operated upon at some centers.
Echocardiographers who rely on color Doppler flow mapping, and who subscribe to 1985-derived color Doppler metrics of MR severity, will systematically describe the extent of MR as worse than it really is.
TEE is more likely to agree with contrast ventriculographic assessment, because it is less likely to misclassify severe MR. TEE remains superior to TTE in sampling pulmonary venous flow.
V-Waves on the Pulmonary Capillary Wedge Pressure Tracing and Mitral Regurgitation Grading
Notes on Specific Causes of Mitral Regurgitation
Altered LV geometry (regional or global cavitary dilation) causing mitral apparatus distortion often is referred to as “functional MR” (as the mitral apparatus components are not diseased themselves) and is the most common cause of MR in patients with coronary artery disease and dilated cardiomyopathy. Lateral and apical displacement of the papillary muscles exerts radial and longitudinal traction on the mitral leaflet tips, reducing and then resulting in loss of coaptation. The mitral apparatus appears “tented” in systole as the leaflet tips are apically displaced; the leaflets appear as structurally normal. The extent of tenting (which can be described as the area in the triangle formed by the mitral leaflets and a line across the mitral annulus) roughly correlates (r = 0.74; P < 0.0001) with the ERO.4 The same study established that there was a wide range of ERO, and that ERO was not related to EF% (P = 0.32). Papillary muscle tethering length has been shown in at least one study to be an independent cause of severe MR.5
Severe wall motion abnormality (e.g., infarction, stunning)
Papillary muscle rupture (PMR)*
Ischemia* alone may result in transient MR, although this is not nearly as common as the term “ischemic MR” would indicate. That term leads to confusion, as it implies that ischemia is the cause of the MR, but where the term is generally relevant is in CAD-related MR.
Myxomatous disease of the mitral valve* includes MVP, MVP with flail, and flail leaflets. Myxomatous degeneration of the mitral valve is the leading cause for mitral valve surgery in North America, and the only common indication for valve repair at most centers.
Rheumatic MR is caused by rheumatic-incited scarring of the mitral leaflets that has left them so “frozen” that they cannot coapt. The ERO is fixed, and by virtue of the immobility of the leaflets, the S1 is muffled.
Mitral annular calcification (MAC) is unlikely to produce more than mild or moderate MR, as the leaflets are seldom involved enough to reduce coaptation. MAC, however, is a challenge for surgeons, because seating a prosthesis is more difficult, and prone to paraprosthesis insufficiency.
Annular dilation, by itself, does not usually cause severe MR.5
Endocarditis* is a necrotizing infection of valve leaflets, annuli, and chordae that will, in time, lead to leaflet perforation, chordal tearing, or annular disruption. Some cases are not associated with severe insufficiency, but most do have at least moderate insufficiency. Extensive involvement of the valve, as can be depicted by large or multiple vegetations, usually is associated with extensive necrosis and severe insufficiency. Some of what appears to be valve insufficiency is insufficiency through the annulus and is even more ominous.
Fibrosis of the medial half of the anterior leaflet is common with
Mitral Regurgitation and Progression
In the presence of “organic” causes, MR is a progressive lesion, but the rate of progression is highly variable. On average, the progression is as follows16:
New flail leaflets (P = 0.0001) and progressive annular dilation (P = 0.0001) were the best predictors of progression. Regression was possible (in 11% at 2 years apart), and was associated with decreased blood pressure (P = 0.008).16
Notes on the Pathophysiology of Mitral Regurgitation
Volume (over)load of the LA and LV
Leads to remodeling (increased compliance and dilation) of the LA and LV.
Sarcomeres replicate in series (wall thickness increases little, but overall LV mass increases—“eccentric hypertrophy”), therefore O2 demand increases. As LV mass is determined by wall thickness and cavitary size, generally, in chronic severe MR (where LV volumes are about twice normal but wall thickness is normal) myocardial mass is about twice normal (158 g/m2 vs 86 g/m2).17
Coronary (myocardial O2 supply) flow is seldom a problem (in the absence of CAD), as the aortic diastolic pressure is normal (unlike AI).
Systemic afterload dependence: increasing impedance to ejection increases the regurgitant volume. Factors that reduce afterload (e.g., pregnancy) are well tolerated, but hypertension is not.
MR may remain compensated for years, or may progress. Progression depends on many factors:
Notes on Mitral Repair and Mitral Replacement
Several issues render mitral repair conceptually attractive:
Pathologies that are amenable to repair include some complications of myxomatous disease:
Pathologies that are not well suited to repair include the following:
Chordal sparing is now the norm, with mitral replacement surgery, as long as the leaflets and chordae are not rheumatic. Chordal transsection is avoided when possible for the reasons listed in Table 6-318:
LVEF% falls with chordal severing because of
What is the Single Best Technique to Describe Mitral Regurgitation Severity?
In the ideal (most straightforward) case of severe MR, each of the following would be present:
Lesions that typically result in severe MR
Pulmonary venous flow reversal (often obtainable by TTE, but TEE is sometimes needed to establish that MR is severe)
LV dilation (if chronic—note that all of the above lesions are acute, and therefore generally without much LV dilation)
LA dilation (if chronic), and LA systolic bulging, unless there is an equal amount of tricuspid regurgitation
Pulmonary pressures elevated moderately or more (unless the LA is a huge reservoir)
In the end, no single isolated parameter should be used to establish the severity of MR. Multiple parameters, and a balance of Doppler, 2D, and clinical assessment should be used. Otto19 states that Doppler means alone should not be used.
Caveats Concerning Descriptors of Mitral Regurgitation
Color Doppler Flow Mapping
Color Doppler flow mapping of MR is a “low-tech” means to evaluate MR and is fraught with potential error. Unfortunately, color Doppler flow mapping is also the easiest and fastest technique, validated over a decade ago,20,21 and therefore is often used alone, or over–relied-upon to evaluate MR. Flow mapping with current equipment is prone to overestimating MR severity, especially as the now antiquated criteria are out of date for flow mapping by current equipment, which detects more flow, and therefore displays MR jets as larger than would older equipment. As well, color Doppler flow mapping is machine factor dependent (Va, color Doppler gain), chamber dependent (compliance), and jet dependent (best suited to central jets, and poorly suited to eccentric jets). TTE is notoriously insensitive to insufficiency of an MVR as the jet is shadowed by the prosthesis and its sewing ring.
The optimal use of color Doppler flow mapping is to
Alert the sonographer to the presence of MR, and roughly estimate its severity. If the MR appears by flow mapping and pulmonary venous flow to be moderate or more than moderate, then quantitative methods should be employed.