Mitral regurgitation - rheumatic heart disease is the commonest cause of MR. It coexists with MS and AR, particularly Ar

1. DR. KALPANA CHETIA
ASSOC. PROFESSOR
JMCH, JORHAT

2. INTRODUCTION
Mitral regurgitation (MR), mitral insufficiency or
mitral incompetence is a disorder of the heart
in which the mitral valve does not close
properly when the heart pumps out blood. It
is the abnormal leaking of blood from the left
ventricle, through the mitral valve, and into
the left atrium, when the left ventricle
contracts, i.e. there is regurgitation of blood
back into the left atrium.MR is the most
common form of valvular heart disease.

15. A dysfunction of any of these portions of the mitral
valve apparatus can cause mitral regurgitation.
The most common cause of mitral regurgitation
is mitral valve prolapse (MVP), which in turn is
caused by myxomatous
degeneration(pathological weakening of
connective tissue).
Myxomatous degeneration of the mitral valve is
more common in females, and is more common
in advancing age. This causes a stretching out of
the leaflets of the valve and the chordae
Tendineae. The elongation of the valve leaflets
and the chordae tendineae prevent the valve
leaflets from fully coapting when the valve is
closed, causing the valve leaflets to prolapse into
the left atrium, thereby causing mitral
Regurgitation.

16. Ischemic heart disease causes mitral
regurgitation by the combination of ischemic
dysfunction of the papillary muscles, and the
dilatation of the left ventricle that is present
in ischemic heart disease, with the
subsequent displacement of the papillary
muscles and the dilatation of the mitral valve
annulus.
Rheumatic fever and Marfan's syndrome (also
called Marfan's syndrome is a genetic
disorder of the connective tissue; People with
Marfan's tend to be unusually tall, with long
limbs and long, thin fingers). are other typical
causes of mitral regurgitation.

17. Secondary mitral regurgitation is due to the
dilatation of the left ventricle, causing stretching
of the mitral valve annulus and displacement of
the papillary muscles. This dilatation of the left
ventricle can be due to any cause of dilated
cardiomyopathy, including aortic insufficiency,
nonischemic dilated cardiomyopathy and
Noncompaction Cardiomyopathy. It is also called
functional mitral regurgitation, because the
papillary muscles, chordae, and valve leaflets are
usually normal.
Acute mitral regurgitation is most often caused by
endocarditis, mainly S. aureus. Papillary muscle
rupture or dysfunction, including mitral valve
prolapse, are also common causes in acute cases

18. PATHOPHYSIOLOGY
The pathophysiology of mitral regurgitation
can be broken into three phases of the
disease process:
 acute phase
 the chronic compensated phase
 the chronic decompensated phase

19. ACUTE PHASE
Acute mitral regurgitation (as may occur due to the
sudden rupture of a chorda tendinea or papillary
muscle) causes a sudden volume overload of both the
left atrium and the left ventricle. The left ventricle
develops volume overload because with every
contraction it now has to pump out not only the
volume of blood that goes into the aorta (the forward
cardiac output or forward stroke volume), but also
the blood that regurgitates into the left atrium (the
regurgitant volume). The combination of the forward
stroke volume and the regurgitant volume is known
as the total stroke volume of the left ventricle.

20. In the acute setting, the stroke volume of the left
ventricle is increased (increased ejection
fraction), this happens because of more complete
emptying of heart. However, as it progresses the
LV volume increases and the contractile function
deteriorates and thus leading to dysfunctional LV
and a decrease in ejection fraction. The increase
in stroke volume is explained by the Frank–
Starling mechanism, in which increased
ventricular pre-load stretches the myocardium
such that contractions are more forceful.
The regurgitant volume causes a volume overload
and a pressure overload of the left atrium. The
increased pressures in the left atrium inhibit
drainage of blood from the lungs via the
pulmonary veins. This causes pulmonary
congestion.

21. CHRONIC PHASE
Compensated:
If the mitral regurgitation develops slowly over months to
years or if the acute phase can be managed with medical
therapy, the individual will enter the chronic compensated
phase of the disease. In this phase, the left ventricle
develops eccentric hypertrophy in order to better manage
the larger than normal stroke volume. The eccentric
hypertrophy and the increased diastolic volume combine to
increase the stroke volume (to levels well above normal) so
that the forward stroke volume (forward cardiac output)
approaches the normal levels.

22. In the left atrium, the volume overload causes
enlargement of the chamber of the left
atrium, allowing the filling pressure in the left
atrium to decrease. This improves the
drainage from the pulmonary veins, and signs
and symptoms of pulmonary congestion will
decrease.
These changes in the left ventricle and left
atrium improve the low forward cardiac
output state and the pulmonary congestion
that occur in the acute phase of the disease.
Individuals in the chronic compensated phase
may be asymptomatic and have normal
exercise tolerances.

23. CHRONIC PHASE
Decompensated:
An individual may be in the compensated
phase of mitral regurgitation for years, but
will eventually develop left ventricular
dysfunction, the hallmark for the chronic
decompensated phase of mitral regurgitation.
It is currently unclear what causes an
individual to enter the decompensated phase
of this disease. However, the decompensated
phase is characterized by calcium overload
within the cardiac myocyte.

24. In this phase, the ventricular myocardium is no
longer able to contract adequately to
compensate for the volume overload of mitral
regurgitation, and the stroke volume of the
left ventricle will decrease. The decreased
stroke volume causes a decreased forward
cardiac output and an increase in the endsystolic
volume. The increased end-systolic
volume translates to increased filling
pressures of the left ventricle and increased
pulmonary venous congestion. The individual
may again have symptoms of congestive
heart failure.

25. The left ventricle begins to dilate during this
phase. This causes a dilatation of the mitral valve
annulus, which may worsen the degree of mitral
regurgitation. The dilated left ventricle causes an
increase in the wall stress of the cardiac chamber
as well.
While the ejection fraction is less in the chronic
decompensated phase than in the acute phase or
the chronic compensated phase of mitral
regurgitation, it may still be in the normal range
(i.e.: > 50 percent), and may not decrease until
late in the disease course. A decreased ejection
fraction in an individual with mitral regurgitation
and no other cardiac abnormality should alert the
physician that the disease may be in its
decompensated phase.

26. SYMPTOMS AND SIGNS
 The symptoms associated with mitral regurgitation
are dependent on which phase of the disease
process the individual is in. Individuals with acute
mitral regurgitation will have the signs and
symptoms of decompensated congestive heart
failure (i.e. shortness of breath, pulmonary
edema, orthopnea, and paroxysmal nocturnal
dyspnea), as well as symptoms suggestive of a
low cardiac output state (i.e. decreased exercise
tolerance). Palpitations are also common.
Cardiovascular collapse with shock (cardiogenic
shock) may be seen in individuals with acute
mitral regurgitation due to papillary muscle
rupture or rupture of a chorda tendinae.

27. Individuals with chronic compensated mitral
regurgitation may be asymptomatic, with a
normal exercise tolerance and no evidence of
heart failure. These individuals may be
sensitive to small shifts in their intravascular
volume status, and are prone to develop
volume overload (congestive heart failure).

28. CLINICAL S/S
 Findings on clinical examination depend on the
severity and duration of mitral regurgitation. The
mitral component of the first heart sound is
usually soft and with a laterally displaced apex.
beat, often with heave. The first heart sound is
followed by a high-pitched holosystolic murmur
at the apex, radiating to the back or clavicular
area.
The loudness of the murmur
does not correlate well with the severity of
regurgitation. It may be followed by a loud,
palpable P2, heard best when lying on the left
side. A third heart sound is commonly heard.
Commonly, atrial fibrillation is found.

29. CHEST X-RAY
1. The chest x-ray in individuals with chronic
mitral regurgitation is characterized by
enlargement of the left atrium and the left ventricle.
2. The pulmonary vascular markings
are typically normal, since pulmonary venous
pressures are usually not significantly
elevated.

30. ECHOCARDIOGRAPHY
 The echocardiogram is commonly used to
confirm the diagnosis of mitral regurgitation.
 Color Doppler flow on the transthoracic
echocardiogram (TTE) will reveal a jet of
blood flowing from the left ventricle into the
left atrium during ventricular systole.
 Also detect a dilated left atrium and ventricle
and decreased left ventricular function.

31. ELECTROCARDIOGRAPHY
 P mitrale is broad, notched P waves in several
or many leads with a prominent late negative
component to the P wave in lead V1, and may
be seen in mitral regurgitation, but also in
mitral stenosis.

32. TREATMENT
 The treatment of mitral regurgitation depends on
the acuteness of the disease and whether there
are associated signs of hemodynamic
compromise.
 In acute mitral regurgitation secondary to a
mechanical defect in the heart (i.e.: rupture of a
papillary muscle or chordae tendineae), the
treatment of choice is urgent mitral valve
REPLACEMENT.

33. MEDICAL TREATMENT
If the individual with acute mitral regurgitation
is normotensive, vasodilators may be of use
to decrease the afterload . The vasodilator most
commonly used is nitroprusside.
Individuals with chronic mitral regurgitation
can be treated with vasodilators as well to
decrease afterload. In the chronic state, the
most commonly used agents are ACE
inhibitors and hydralazine. Studies have
shown that the use of ACE inhibitors and
hydralazine can delay surgical treatment of
mitral regurgitation.

34. SURGICAL TREATMENT
There are two surgical options for the
treatment of mitral regurgitation: mitral valve
replacement and mitral valve repair.

35. INTRODUCTION
 Rheumatic heart disease is the commonest cause of
MR .
 It usually coexists with MS and aortic valve disease ,
particularly AR .

36. PATHOPHYSIOLOGY
 Due to incompetent MV , during LV contraction , a
proportion of left ventricular blood regurgitates into
LA producing pansystolic murmur at mitral area.
 There is rising of left atrial and pulmonary venous
pressure and in late stages pulmonary arterial
pressure.
 During diastole there is inflow of extra blood back into
left ventricle producing mid diastolic flow murmur.

37. ETIOLOGY
 Rheumatic fever
 Infective endocarditis
 Dilated cardio myopathy
 Congenital mitral valve prolapse
 Endocardial cushion defect
 Ischemic ( papillary muscle dysfunction and rupture )
 Connective tissue disorders
 Traumatic
 Myocarditis
 Prosthetic valve mechanical failure.

38. CLINICAL FEATURES
 SYMPTOMS : palpitation
 Dyspnea
SIGNS :
Normal bp, good volume pulse, ankle edema , enlarged
tender lever , basal crepitations in the lungs
CVS SIGNS : hyperdynamic apex beat, systolic thrill,
pansystolic murmur , loud P2, S3, mid diastolic flow
murmur.

39. INVESTIGATIONS
 Electrocardiogram – normal in mild cases, in severe
cases LVH , LAH, biventricular hypertrophy are seen
in later stages.
 Chest x-ray – in mild cases it may be normal. In
advanced cases there is cardiomegaly . Mitralisation of
left cardiac border . Enlarged LA may be seen as
double density between two bronchi causing incease
in carinal angle

40. INVESTIGATIONS
 2D ECHO – 2D echo assesses severety of mitral
incompetence and rules out other causes of MR, e.g.
MVP, ruptured chordae tendineae , primary CMP and
IE.
 CARDIAC CATHETARISATION AND LEFT
VENTRICULAR CINE ANGIOGRAPHY – it is done to
assess MR , and in elderly patients coronary
angiography is done to rule out CAD before valve
surgery.

41. COMPLICATIONS
 LVF
 IE
 AF
 LAT AND SE

42. D/D
 MVP
 CMP
 FUNCTIONAL TR
 IE
 MARFAN’S SYNDROME
 PAPILLARY MUSCLE DYSFUNTION OR RUPTURE IN
AMI
 CONNECTIVE TISSUE DISORDER
 RUPTURED CHORDAE TENDINEAE
 SEPTUM PRIMUM DEFECT (ASD)
 MITRAL ANNULUS CALCIFICATION
 TRAUMATIC (POST VALVOPLASTY )

43. MEDICAL MANAGEMENT
 Rheumatic fever prophylexis
 Infective endocarditis prophylexis
 Treatment of heart failure
 Treatment of AF
 Anticoagulation in presence of left atrial clot.

44. SURGICAL MANAGEMENT
 Valve replacement or repair- acute MR needs
emergency valve repair or replacement.
 If due to IHD patient may need coronary
revascularization.

45. INDICATIONS FOR SURGERY
 Severe MR
 Left ventricular failure
 Infective endocarditis.

46. Q- how do you judge severity of
MR ?
 Systolic thrill plus pan systolic murmur over mitral
area
 Presence of S3 and mid diastolic flow murmur over
mitral area.
 Degree of LVH as seen clinically and on ECG and chest
x-ray.

47. Q- What is the D/D of pansystolic
murmur of MR ?
 TR
 VSD
 PAPILLARY MUSCLE DYSFUNCTION
 MITRAL VAVE PROLAPSE : 1. most common cause of
isolated MR.
2. Myxomatous degeneration of mitral leaflets
3. posterior leaflet commonly involved , aneriore leaflet
rarely
4. common in young females
5. mid or late – systolic click followed by late high pitched
systolic murmur which decreases with sitting posture.

48. THANK YOU