Mitral regurgitation

1. Dr. Dharmraj Singh
SR, Intensive Care
CTVS

2.  Mitral leaflets
 Chodrae tendineae
 Papillary muscles
 Mitral annulus
Abnormalities of any of these structures
Causes MR

3.  Myxomatous degeneration (MVP & ruptured mitral chordae)
 Rheumatic heart disease
 Infective endocarditis
 HCM
 Annular calcification
 Dilated cardiomyopathy (DCM)
 Ischemic heart disease

4.  Collagen vascular diseases
 Trauma
 Hypereosinophilic syndrome
 Carcinoid

6.  In general, types II and IIIa usually are caused by primary disorders of the valve
leaflets.
 Whereas types I and IIIb have relatively normal leaflets, which are distorted by LV
and annular remodeling causing secondary MR.
 For clinical purposes, MR is classified as primary (or organic or degenerative) MR,
caused by intrinsic disease of the mitral leaflets, and secondary (or functional) MR,
caused by diseases of the left ventricle and/or mitral annulus.

7. (A) Severe annular dilation leading to type I
dysfunction.
(B) Severe myxomatous changes with redundant,
thick, and bulky segments in a patient with
Barlow disease and type II dysfunction.
(C) Rheumatic mitral valve disease with classic
“fish mouth” appearance and type IIIA
dysfunction.
(D) Ischemic mitral valve disease caused by
severe tethering of the P3 scallop leading to type
IIIB dysfunction.

8.  Developed world - Myxomatous degeneration
 MV is a dynamic structure with protein turnover and remodelling continuing throughout
life.
 MV is a thin (<3 mm) endothelium-lined bileaflet structure with-
 Fibrosa - dense collagen on the ventricular side
 Atrialis - less stiff layer of collagen and elastin on the atrial side
 Spongiosa - in b/w a loose connective tissue layer with abundant glycosaminoglycans
 Valvular interstitial cells (VICs) are Interspersed among the spongiosa- derived from
endocardial endothelium, which normally are inactive.

9. Schematic showing the mechanism of myxomatous degeneration, with activation of valve
interstitial cell to myofibroblasts that increase matrix production and turnover, secrete MMPs
that drive collagen and elastin fragmentation, and release transforming growth factor (TGF)-β,
which in turn promotes further cell proliferation and myofibroblast differentiation. GAGs,
Glycosaminoglycans; MMP, matrix metalloproteinase.
Mitral valve stained with hematoxylin and eosin to define
the lesion of MVP as disruption of the fibrosa by myxoid
extracellular matrix (*), which also infiltrates the
collagen core of the chordae tendineae, one of which
was ruptured (arrow). The elastin lamina beneath the
atrialis is also disrupted.

10.  Myxomatous disease - depends on the relative degree of leaflet thickening and redundancy
versus weakness in the chordae tendineae.
 On the extreme is Barlow syndrome, with gross leaflet thickening & redundancy,
multiscalloped deep prolapse, and severe regurgitation arising from multiple points along
the valve closure line.
 Developing world- chronic RHD remains a common cause of MR.
 In contrast with MS, rheumatic MR is more frequent in men than in women.
 It is a consequence of shortening, rigidity, deformity, and retraction of one or both mitral
valve cusps and is associated with shortening and fusion of the chordae tendineae and
papillary muscles.

11. (A) Prolapse of P2 owing to multiple ruptured chordae; the leaflet tissue is thickened compared with other segments. Note the translucency of the
anterior leaflet, and normal height and thickness of P1 and P3, in contrast to findings in Barlow’s disease.
(B) Prolapse of P3 with ruptured chord. Note that P3 is thickened, but P2 and P1 are thin and of normal height.
A B

12. (A) Large valve with redundant,
thick, bulky leaflets.
(B) Tall, posterior leaflet with tip
rising to anterior annulus.
(C) Calcified anterior papillary muscle
with fused, matted chords restricting
the P1/P2 junction.
(D) Atrialization of the base of the
posterior leaflet. Note the blurring of
the atrial-leaflet junction with
fissures and microthrombi (arrows).
A B
C D

13. DILATION-
 Normal 93 +/- 9 mm (10 cm)
 Annular constriction contributes to valve closure.
 Dilation of LV and/or atrium, especially DCM & longstanding AF, Myxomatous disease
CALCIFICATION-
 Idiopathic (degenerative) calcification
 Atherosclerosis, including systemic hypertension, hypercholesterolemia, and diabetes.
 Marfan and Hurler syndromes, chronic renal failure with secondary hyperparathyroidism, rheumatic
involvement.

14.  Lengthening and rupture of the chordae tendineae are cardinal features of the MVP
syndrome.
 Chordae may be congenitally abnormal
 Rupture - spontaneous (primary), infective endocarditis, trauma, rheumatic fever, or
rarely, osteogenesis imperfecta or relapsing polychondritis.
 Secondary to trauma from percutaneous circulatory device

15.  The posterior papillary muscle (PD branch of the RCA)- ischemic and infarcted more
frequently
 Anterolateral papillary muscle (diagonal branches of the LAD & often by marginal
branches from the LCX artery as well)

16. (A) A dilated annulus with severe posterior leaflet tethering is characteristic of ischemic mitral regurgitation.
(B) Perforation (arrow) of the anterior leaflet of the mitral valve secondary to infective endocarditis.
A B

17.  Ischemic LV dysfunction and DCM
 LV dilation
 Obstructive HCM
 Hypereosinophilic syndrome
 endomyocardial fibrosis, trauma affecting the leaflets and papillary muscles,
Kawasaki disease, LA myxoma, and various congenital anomalies, including cleft
anterior leaflet and ostium secundum ASD

18.  Abnormal coaptation of mitral leaflets creates a regurgitant orifice during systole.
 Systolic pressure gradient b/w LA & LV is the driving force of regurgitant flow that
results in a regurgitant volume.
 Regurgitant volume represent a percentage of total ejection of the LV and may be
expressed as the regurgitant fraction.
 Regurgitant volume creates a volume overload by entering the LA in systole & the LV in
diastole, modifying LV loading & function.

19.  In MR Impedance to ventricular emptying is reduced.
 Significant proportion of the regurgitant volume is ejected into the LA before the
Aortic Valve opens and after it closes.
 volume of MR flow depends on a combination of the instantaneous size of the
regurgitant orifice and the (reverse) pressure gradient between the LV & LA
 LV-LA gradient depends on SVR

20. LV in Chronic MR

21.  LV initially compensates for the development of acute MR by emptying more
completely and by increasing preload (Frank-Starling principle).
 Acute MR reduces late systolic LV pressure and radius, LV wall tension declines
markedly (and proportionately to a greater extent than LV pressure), permitting a
reciprocal increase in the extent and velocity of myocardial fibre shortening and
leading to a reduced end-systolic volume (ESV)
 When MR, particularly severe MR, becomes chronic, the LV end-diastolic volume
(EDV) increases and the ESV returns to normal.

22.  ↑ LVEDV increases wall tension to normal or supra-normal levels in the “chronic
compensated stage” of severe MR.
 ↑ LVEDV and mitral annular diameter may create a vicious circle in which MR leads
to more MR.
 chronic MR, LVEDV and LV mass are increased; that is, typical volume overload
(eccentric) hypertrophy develops
 degree of hypertrophy is often not proportional to the degree of LV dilation, so the
ratio of LV mass/EDV may be less than normal, increasing wall stress.

23.  MR decreases impedence to LV – enhances LV emptying
 MR flow – instataneous Size of the orifice and LV-LA pressure gradient
 Torricelli principle –
 MRV = MROA x C x T x sq.root (LVP-LAP)
 LV-LA gradient – SVR
 MROA – Etiology of MR – variable response to drugs

24. ACUTE MR
CHRONIC
COMPENSATED
MR
CHRONIC
DECOMPENSATED
MR

25. ACUTE
FRANK-STARLING
PRINCIPLE
CHRONIC
LAW OF LAPLACE
MR begets more MR

28.  Increase in Pre-Load (Frank Starling principle)
 Decrease in After Load
 Increase in Ejection Fraction
 Increase in Total Stroke Volume
 Diminished Forward Stroke Volume

30. Acute Chronic
Symptoms Almost always present, usually
severe
May be present
Cardiac palpation Unremarkable Displaced dynamic apical
impulse
S1 Soft Soft or normal
Murmur Early systolic to holosystolic Holosystolic
ECG Normal LVH and AF common
CXR Normal cardiac silhouette;
pulmonary edema
Enlarged heart, normal lung
fields
ECHO Normal LA and LV Enlarged LA and LV

31. Ejection Fraction Indices
 Ejection Fraction (EF)
 Fractional Fibre Shortening (FS)
 Velocity of circumferential fibre shortening (VCF)
Inversely related to After load

32.  Elevated in early MR
 Chronic MR – diastolic overload – myocardial dysfunction
 Indices modestly affected
 Low to normal indices – impaired myocardial function
 LVEF - 40-45% (moderate dysfunction) - severe LV dysfunction

33.  Independent of pre-load
 Varies linearly with afterload
 Reduced – Acute MR
 Normal – Compensated Chronic MR
 Increased – Decompensated Chronic MR
 Pre-op value >40mm – impaired lv function post op
 Index for evaluating LV function
 Predictor of function and survival following MV surgery

34.  Better index of after load
 Accounts for ventricular geometry
 High end systolic wall volume for given end systolic wall stress – depressed
contractility
 Predicts the prognosis for valve replacement

37.  Normal or Reduced Compliance
 In acute MR, marked increase in LA pressure
 LA thick walled
 Symptoms of pulmonary congestion

38.  Markedly Increased Compliance
 Thin walled, large LA
 Normal or slightly elevated LA pressure
 AF and low CO
 Moderately increased compliance
 Most common
 Variable sized LA/LA pressure -> AF

39.  Mostly asymptomatic
 Chronic weakness & fatigue –most common
 Dyspnea/orthopnea/PND
 Palpitations
 Atypical chest pain
 Hemoptysis & systemic embolization- less common
 Acute MR -> Right sided heart failure
 Chronic MR -> Left sided heart failure

40.  Small volume brisk/jerky pulse – DEC FSV
 JVP
 a - Decreased RV compliance
 a, v - Right heart failure
 v - Severe TR/LAP In acute MR
 Hyperdynamic Apical impulse – LV Vol overload and dilatation
 Parasternal lift (dilated LA,RVH)
 Palpable S2 - severe PHTN

41.  S1, Loud S1 in MVP (Ejection click)
 S2 –Wide split, loud P2, S3+
 Holosystolic murmur
 Severity inflicted by murmur intensity
 Radiates to axiila/back/base

42. MVP Organic MR Functional MR
Symptoms Chest pain Fatigue CHF
Physical examination Mid-systolic click,
End-systolic murmur
Loud holosystolic
murmur, S3
Soft early systolic
murmur S4, S3
ECG ST-T changes Atrial fibrillation Q wave, LBBB
CXR Pectus excavatum Cardiomegaly, LA
enlargement
Cardiomegaly,
pulmonary edema

43.  Cardiomegaly with LA and left atrial
appendages dilatation
 Giant left atria
 Annular calcification
 Interstitial edema with Kerley B lines

44. Mitral valve prolapse. A, Parasternal long-axis view showing deep prolapse of the posterior mitral leaflet.
B, Anteriorly directed mitral regurgitation. AML, anterior mitral leaflet; PML, posterior mitral leaflet.

45. Mild Moderate Severe
Specific Signs of
Severity
Small central jet <4 cm2 or <20% of LA area*
Vena contracta width <0.3 cm
No or minimal flow convergence†
Signs of MR > mild present, but
no criteria for severe MR
Vena contracta width ≥0.7 cm
with large central MR jet (area
>40% of LA) or with a wall-
impinging jet of any size, swirling
in LA*
Large flow convergence†
Systolic reversal in pulmonary
veins Prominent flail MV leaflet
or ruptured
papillary muscle
Supportive Signs of
Severity
Systolic dominant flow in pulmonary veins
A-wave dominant mitral inflow‡
Soft density, parabolic CW Doppler
MR signal
Normal LV size§
Intermediate signs and findings Dense, triangular CW Doppler MR
jet E-wave dominant mitral
inflow
(E>1.2 m/sec)‡
Enlarged LV and LA size‖
(particularly
when LV function is normal)
Quantitative
Parameters
R Vol (mL/beat)
RF (%)
EROA (cm2)
<30
<30
<0.20
30-44 45-59
30-39 40-49
0.20-0.29 0.30-0.39
≥60
≥50
≥0.40

46. Mild central MR Severe central MR Severe eccentric MR

47. Functional mitral regurgitation. A, Apical long-axis view showing a large posterior myocardial
infarction, which is tethering the posterior leaflet preventing the anterior leaflet from closing.
B, This causes a posteriorly directed jet of mitral regurgitation. AML, anterior mitral leaflet; PML,
posterior mitral leaflet; arrow indicates tenting of the AML caused by tethering of the secondary
chordae.

48. Severe mitral regurgitation caused by prolapse of the mitral valve with quantitative determination of effective
regurgitant orifice area (ERO) on echocardiography. A, B, Severe prolapse of the mitral valve with severe MR.
C, D, ERO was calculated with the proximal isovelocity surface area (PISA) radius and peak velocity of the MR jet.