Mitral Valve Function | Mitral Valve Repair Center Skip to main content
Interactive 3D heart tour

The heart is a muscular structure with four chambers including two atria, which are the filling chambers and two ventricles, which are the pumping chambers. The venous blood is drained from the body to the right chambers of the heart, then oxygenated in the lungs and ejected to the entire body by the left chambers of the heart.

The human heart has four valves (flaps made of tissue) that control the direction of blood flow in the circulation. Normal valves act like a system of one-way doors, which assures unidirectional blood flow through the various chambers of the heart. The aortic and mitral valves are part of the "left" heart and control the flow of oxygen-rich blood from the lungs to the body, while the pulmonic and tricuspid valves are part of the "right" heart and control the flow of oxygen-depleted blood from the body to the lungs.

The aortic valve lies between the left ventricular chamber and aorta, preventing blood from leaking back into the left ventricle after it has been ejected into the circulation. The mitral valve lies between the left atrium and left ventricle preventing blood from leaking back into the left atrium during ejection (systole). Similarly on the right side, the pulmonic valve separates the right ventricle from the pulmonary artery, whereas the tricuspid valve separates the right ventricle from the right atrium.

The normal mitral valve opens when the left ventricle relaxes (diastole) allowing blood from the left atrium to fill the decompressed left ventricle. When the left ventricle contracts (systole), the increase in pressure within the ventricle causes the valve to close, preventing blood from leaking into the left atrium and assuring that all of the blood leaving the left ventricle (the stroke volume) is ejected through the aortic valve into the aorta and to the body. Proper function of the valve is dependent on a complex interplay between the annulus, leaflets and subvalvular apparatus.

Long-standing mitral regurgitation due to mitral valve prolapse is well established as a significant cause of cardiovascular morbidity and mortality1,2, with surgical intervention often required in patients with severe regurgitation to preserve life expectancy in affected patients. Mitral valve repair is now well established and is applicable in practically all patients with clinically significant mitral valve prolapse due to degenerative mitral-valve disease3,4. Valve repair offers a distinct event-free survival advantage compared with replacement with a bioprosthetic or mechanical valve5,6.7

  • 1. Naji P, Asfahan F, Barr T et al. Impact of duration of mitral regurgitation on outcomes in asymptomatic patients with myxomatous mitral valve undergoing exercise stress echocardiography. J Am Heart Assoc. 2015 Feb 11;4(2). pii: e001348.
  • 2. Topilsky Y1, Michelena H, Bichara V, et al. Mitral valve prolapse with mid-late systolic mitral regurgitation: pitfalls of evaluation and clinical outcome compared with holosystolic regurgitation. Circulation. 2012 Apr 3;125(13):1643-51.
  • 3. Adams DH, Anyanwu AC, Rahmanian PB, Filsoufi F. Current concepts in mitral valve repair for degenerative disease. Heart Fail Rev 2006; 11:241-257.
  • 4. Nishimura RA et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129:e521-e643.
  • 5. Castillo JG, Anyanwu AC, Fuster V, Adams DH, A Near 100% Repair Rate for Mitral Valve Prolapse is Achievable in a Reference Center: Implications for Future Guidelines. J Thorac Cardiovasc Surg. 2012; 144(2): 308-12.
  • 6. David TE. Outcomes of mitral valve repair for mitral regurgitation due to degenerative disease. Semin Thorac Cardiovasc Surg 2007; 19:116-120.
  • 7. Portions excerpted, with permission, Adams DH, Anyanwu AC. The cardiologist's role in increasing the rate of mitral valve repair in degenerative disease. Current Opinion in Cardiology 2008, 23:105-110.
Page Created: Dec. 19, 2017 Last Updated: Feb. 12, 2018