Mitral regurgitation

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. Mitral Regurgitation ( Insufficiency ) 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.

9. 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.

10. Secondary mitral regurgitation D ilatation 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

11. 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

12. 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).

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

14. Acute phase :- U sually 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

15. Chronic compensated phase :-

16. Chronic decompensated phase:-

17. 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.

18. 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.

19. 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. 

20. Investigations CXR :- LVE LAE Pulmonary venous congestion

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

22. 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

23. 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

24. 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

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