Mitral RegurgitationR. Jay Widmer, MD/PhD

December 7, 2019

2

Mitral regurgitation (MR) is defined as retrograde flow from the left ventricle (LV) into the left atrium (LA) during ventricular systole

Although trivial to mild degrees of MR are commonly found incidentally by echocardiography, moderate to severe MR is one of the most common heart valve lesions in both the United States and Europe, despite a decreasing prevalence of rheumatic fever in these regions

Mitral Regurgitation

3

The mitral valve (MV) consists of four components– Mitral (anterior and posterior) leaflets

– Mitral annulus

– Subvalvular structure (including both chordae tendinae and papillary muscles)

– Left ventricular wall

Normal and integrated function of all four of these MV components is required for competency of the MV, and abnormal function of any one of the structures may result in MV regurgitation

The Mitral Valve

4

In the most common cause of primary MR, myxomatous degeneration, localized fibroelastic deficiency due to abnormalities in connective tissue results in chordal thinning and elongation and subsequent MV prolapse

– Chordal rupture may lead to flail leaflet and a sudden increase in MR volume

20-40% of MR cases are caused by a degenerative valve (over 60% in Europe)

15-35% are caused by ischemic heart disease

10-30% are caused by rheumatic disease

5-15% are caused by endocarditis

*Potential Acute Etiologies4

Primary Causes of Mitral Regurgitation

*

**

*

*

5

Caused by papillary muscle displacement and/or a dilated mitral annulus

– Can be associated with either ischemic or non-ischemic cardiomyopathy

– Stable hypertrophic cardiomyopathy

– Chronic pacing

Common in ischemic CVD

– In one study, up to 50% of patients with an acute ischemic syndrome experienced MR, with severe MR in 12%

Up to 20% of patients with a chronically dilated left ventricle can have significant MR

– Could be over 500,000 people in the US

5

Secondary Mitral Regurgitation

www.uptodate.com

6

Chronic MR More common than acute MR

Most commonly causes degenerative, ischemic, rheumatic, congenital, endocarditis, radiation, drugs

Results in volume overload of the LV, which prompts ventricular (and atrial) remodeling– Eccentric hypertrophy results in dilation of the LV without

increased wall thickness

– The increase in LV size is adaptive for increasing LV volume without an increase in diastolic filling pressure, increasing ventricular compliance and maintaining ventricular stroke volume and cardiac output via maintaining afterload

Progressive dilation may eventually lead to reduced contractility and systolic dysfunction– Increased pulmonary venous pressure and reduced stroke

volume and cardiac output

The elevation of LA pressure drives pulmonary hypertension and atrial fibrillation

Severe Acute MR Primary valve degeneration, non-ischemic

– Ruptured chordae tendineae (“flail”)

– Can be seen with myxomatous mitral prolapse, endocarditis, trauma, rheumatic disease, or spontaneous

– Reversible: dynamic LVOT obstruction (Stress or HCM)

Ischemic– Usually ischemic posterior papillary muscle (LCx)

Results in a sudden increase in LA and ventricular volume in the absence of LV or atrial dilation– However reduction in LV forward stroke volume (increased

aortic afterload and pulmonary “pop-off”)

Pulmonary venous pressure rises rapidly and leads to “flash” pulmonary edema

Physical examination findings (lots of extra noise):– Potentially S3 without apical displacement

– MR murmur may not be holosystolic or even audible due to rapid equalization of LV/LA pressures

Mitral Regurgitation – Timing is Everything

7

Holosystolic murmur generally best heard at the apical or left midclavicular region of the chest– May be accentuated by auscultation in a left lateral

decubitus position or by maneuvers that increase ventricular afterload (e.g., isometric handgrip)

Radiation may be highly variable depending on the direction of the MR jet– Anterior prolapse = posterior radiation and vice versa

In patients with MR due to MV prolapse, an early or mid-systolic click may be heard followed by a systolic murmur– Transient reduction in LV preload (by Valsalva maneuver or

change from squatting to standing position) will shorten the time interval between the first heart sound and systolic click, and prolong the duration of the heart murmur

In acute, severe MR or MR associated with LV systolic dysfunction, a third heart sound may be heard

In patients who develop pulmonary hypertension due to severe MR, the intensity of the pulmonic closure sound (P2) may be increased

Dilation of the LV may result in enlargement and displacement of the LV impulse.

Mitral Regurgitation – Physical Examination

8

ACC/AHA Class I recommendation to diagnose and assess MR– Transthoracic echocardiography (TTE) and transesophageal

echocardiography (TEE) provide both qualitative and quantitative analysis of MV pathology

Qualitatively – describe abnormalities of the mitral annulus, leaflets, subvalvular apparatus, or LV– Functional MR = central MR jet origin with normal valve structure

but restricted mobility and LV dilation– Should detail sequelae of MR, such as pulmonary hypertension,

tricuspid valve regurgitation, LA dilation, and ventricular dilation or systolic dysfunction

Quantitatively – provide severity of MR (effective regurgitant orifice, LA size, regurgitant jet depth/area, pulmonary vein flow,

TEE often provides incrementally more information regarding the mechanism of MR – May be utilized as the initial diagnostic test– Real-time three-dimensional echocardiography may provide

surgical views of the MV pathology for operative planning

Repeat echocardiography:– Every 6-12 months for severe MR– Every 1-2 years for moderate MR– Every 3-5 years for mild MR– Change in clinical status or physical examination findings

Diagnostic Testing - Echocardiography

Mitral Regurgitation, Treatment Recommend medical therapy for LV systolic dysfunction

(e.g., vasodilator agents) in patients with chronic, primary MR and left ventricular ejection fraction [LVEF] <60% in whom surgery is not planned (Class IIa recommendation).– Vasodilator therapy is not indicated for normotensive

asymptomatic patients with LVEF ≥60% and chronic, primary MR

In patients with acute, severe MR, afterload reduction may improve the hemodynamic status by reducing regurgitant volume and increasing LV forward stroke volume and cardiac output.– nitroprusside intravenously or mechanical support with intra-

aortic balloon

MV surgery is the only definitive treatment for symptomatic patients with signs of irreversible HF– Repair > replacement

In contrast to degenerative causes of MR, pharmacologic therapy has a primary role in the treatment of functional MR

In patients with severe LV dysfunction with mechanical dyssynchrony, cardiac resynchronization therapy by biventricular pacing may improve systolic function and reduce MR severity.

Management of Severe Chronic Mitral Regurgitation

AHA/ACC Valve Guidelines, 2017

©2012 MFMER | slide-15

Flail Width

Flail Gap

MitraClip

16

2D Long Axis/Grasping View 3D TEE Post-MitraClip

16

MitraClip

COAPT Study Results, TCT 2018

Mack, M et al, TCT 2019

COAPT vs MITRA-FR Trials

MITRA FR (n=304) COAPT (6=614)MR Entry Criteria EU Guidelines: EROA>20mm2 or RV>30 ml US Guidelines: EROA> 30 mm2 or

RV>45 ml

EROA 31 ± 10 mm2 41 ± 15 mm2

LVEDV 135 ± 35 ml/m2 101 ± 34 ml/m2

GDMT at baseline and follow up

Allowed variable adjustment as per “real world practice”

Maximal GDMT required for entry, and no changes within the trial

Procedural Failure 9% 5%

Procedural Complications 15% 9%

12-month >3+ MR 17% 5%

Industry Funded No Yes

19

Mitral Valve Regurgitation from Paravalvular Leak

20

21

Surgeon’s View, 3D TEE Watch for “Drop Out”

Mitral Valve Regurgitation from Paravalvular Leak

22

Post AVP-II Plug Fluoroscopy

22

Mitral Valve Regurgitation from Paravalvular Leak

Mitral Stenosis following Mitral Valve Replacement

23

2424

Mitral Valve in Valve following Mitral Valve Replacement

Mitral Valve-in-Valve N=344 Mitral V in V or V in Ring

procedures

STS PROM 11%

Outcomes:

Hospital mortality 7.2%

30d mortality 8.5%

Stroke 1%

Residual mod-severe MR 2.6%

©2012 MFMER | slide-25

Grover, JACC 2017

QUESTIONS?

Robert.Widmer@BSWHealth.org

@DrArgyle