Mitral valve anatomy Mitral Regurgitation Etiology Pathology Primary mitral regurgitation Secondary mitral regurgitation Functional Classification Pathophysiology Acute phase Chronic compensated phase Clinical Manifestations Physical examination Investigations classification of severity Indication for surgery MV operations for correction of MR

1. Cardiac Surgery
October / 2017

2. Mitral valve anatomy
 The mitral valve connects the left atrium (LA) and the
left ventricle (LV).
 The mitral valve opens during diastole to allow the
blood flow from the LA to the LV. During ventricular
systole, the mitral valve closes and prevents backflow
to the LA.

3. Mitral valve anatomy
 The normal function of the mitral valve depends on its 6
components, which are (1) the left atrial wall, (2) the annulus,
(3) the leaflets, (4) the chordae tendineae, (5) the papillary
muscles, (6) the left ventricular wall

4. Mitral valve anatomy

5. Mitral Regurgitation
 Mitral regurgitation (MR) is defined as an abnormal
reversal of blood flow from the left ventricle (LV) to the
left atrium (LA).
 It is caused by disruption in any part of the mitral valve
(MV) apparatus.

6. Etiology
 The most common etiologies of MR include mitral valve
prolapse (MVP), rheumatic heart disease, infective
endocarditis, annular calcification, cardiomyopathy and
ischemic heart disease.
 Less frequently, MR can be caused by collagen vascular
diseases, trauma, previous chest radiation, carcinoid
disease, the hypereosinophilic syndrome,and exposure to
certain drugs.

7. Pathology
 Mitral valve regurgitation is classified as primary and
secondary.
 Primary mitral valve regurgitation is caused by an
abnormality in the mitral valve.
 Secondary mitral valve regurgitation is caused by an
abnormality in the left ventricle of the heart.

8. Primary mitral regurgitation
 The most common cause of primary mitral regurgitation in the
United States (causing about 50% of primary MR) is
myxomatous degeneration of the valve.
 This causes a stretching out of the valve leaflets 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.

10.  Rheumatic disease, the chordae tendinae are thickened and
foreshortened, producing restrictive leaflet motion. Posterior
dilatation of the mitral annulus also usually is present.
 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.

11. Secondary mitral regurgitation
 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 .
 It is also called functional mitral regurgitation, because the
papillary muscles, chordae, and valve leaflets are usually
normal

12. Functional Classification
 Carpentier's functional classification of mitral valve disease
is used to describe the mechanism of valvular dysfunction.
 This classification is based on the opening and closing
motions of the mitral leaflets

13.  In Type I MR, valvular insufficiency occurs secondary to annular
dilatation or leaflet perforation, and normal leaflet motion is
maintained.
 Type II MR is seen in patients with mitral valve prolapse, and is
due to prolapse of often thickened excessive leaflet ,frequently in
addition to ruptured or elongated chordae tendineae causing
increased leaflet motion.
 Type III insufficiency, as seen in patients with rheumatic and
ischemic heart disease, occurs from restricted leaflet motion,
either during systole and diastole (Type IIIA) or during systole
alone (Type IIIB).

15. Pathophysiology
The pathophysiology of mitral regurgitation can
be classified into three phases of the disease
process:
• Acute phase .
• Chronic compensated phase .
 Chronic decompensated phase.

16. Acute phase :-
 Usually occurs with a spontaneous chordae tendineae or papillary
muscle rupture secondary to myocardial infarction.
 A sudden volume overload occurs on an unprepared left ventricle
and left atrium.
 The volume overload on the left ventricle increases left ventricular
stroke work.
 Increased left ventricular filling pressures, combined with the
transfer of blood from the left ventricle to the left atrium during
systole, results in elevated left atrial pressures. This increased
pressure is transmitted to the lungs resulting in acute pulmonary
edema and dyspnea

17. Chronic compensated phase :-

18. Chronic decompensated phase:-

21. Clinical Manifestations
Symptoms :-
 dependent on the phase of the disease .
 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.

22. chronic compensated mitral regurgitation may be
asymptomatic, with a normal exercise tolerance and no evidence of
heart failure.
 Patients may have normal exercise tolerance until systolic
dysfunction of the LV develops, at which point they may experience
symptoms of a reduced forward cardiac output (ie, fatigue, dyspnea
on exertion, or shortness of breath).
 With time, patients may feel chest palpitations if atrial fibrillation
develops as a result of chronic atrial dilatation.
 Patients with LV enlargement and more severe disease eventually
progress to symptomatic congestive heart failure with pulmonary
congestion and edema. At this stage of LV dilatation, the
myocardial dysfunction often becomes irreversible.

23. Physical examination
Ouscultaion --
 S1 is usually soft .
 laterally displaced apex beat, often with heave.
 high-pitched holosystolic murmur at the apex, radiating
to the axilla heard best when lying on the left side. The
loudness of the murmur does not correlate well with the
severity of regurgitation.
 S3 is commonly heard.
 Commonly, atrial fibrillation.

24. Investigations
CXR:-
 LVE
 LAE
 Pulmonary venous
congestion

25. ECG:-
 LA enlargement  p-mitral
 Atrial fibrillation
 LVH features

26. Echo:-
Diagnostic and 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, it may
detect a dilated left atrium and ventricle and decreased left
ventricular function

29. Treatment
Medical therapy includes the following:
 Afterload-reducing agents and diuretics in MR with
symptoms or LV dysfunction.
 Beta blockers for primary treatment of LV dysfunction in
functional MR.
 Consideration of intra-aortic balloon pump in acute MR with
hemodynamic compromise
 In the presence of AF, beta blockers, calcium channel
blockers, digitalis, or a combination

30.  Consideration of anticoagulation for patients who
develop AF or have had MV replacement surgery
 Prophylactic antibiotics before any dental procedure
involving manipulation of gingival tissue, the periapical
region of a tooth, or perforation of oral mucosa in
patients with a prosthetic heart valve, previous infectious
endocarditis, some forms of congenital heart disease, or
valvulopathy in a cardiac transplant recipient
 Consideration of inotropic agents in chronic severely
symptomatic MR; consultation with a cardiothoracic
surgeon

36. MV operations for correction of MR:-
1) MV replacement
2) Repair of leaflet perforation
3) Annuloplasty