Pathophysiology of chronic mitral regurgitation
- William H Gaasch, MD
William H Gaasch, MD
- Section Editor — Valvular Disease
- Professor of Medicine
- University of Massachusetts Medical School
- Tufts University School of Medicine
- Senior Consultant in Cardiology
- Lahey Clinic
Chronic mitral regurgitation (MR) is a relatively common valvular disorder that can progress to ventricular decompensation and the need for mitral valve surgery. The pathophysiology and phases of chronic MR will be reviewed here. The etiology, clinical features, natural history, and overview of management are discussed separately. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation" and "Natural history of chronic mitral regurgitation caused by mitral valve prolapse and flail mitral leaflet" and "Management of chronic primary mitral regurgitation".)
Causes and mechanisms — Mitral regurgitation (MR) may be due to a primary abnormality (often referred to as organic MR) of one or more components of the valve apparatus (leaflets, chordae tendineae, papillary muscles, and/or annulus) or may be secondary (often referred to as functional MR) to left ventricular (LV) dysfunction (such as coronary heart disease or a cardiomyopathy) (table 1). In the developed world, the most common etiologies of MR are degenerative disease with mitral valve prolapse (a primary cause) and coronary heart disease (a secondary cause).
Primary MR — Several disease processes cause abnormalities of the mitral valve complex leading to primary MR.
●Degenerative mitral valve disease (mitral valve prolapse, partial flail, and flail leaflet) includes a range of disorders ranging from myxomatous mitral valve disease (also known as myxomatous degeneration, with redundancy of anterior and posterior mitral leaflets and the chordae), seen primarily in younger populations, and fibroelastic deficiency disease, seen primarily in older populations. It is not clear if these are two distinct disease processes or manifestations of a single disease. In mitral valve prolapse, excessive mitral leaflet tissues lead to folding and hooding effecting one or more segments of one or both leaflets. Chordae are elongated and may rupture, and the annulus is typically dilated and frequently disjuncted from its normal myocardial support. The alterations yield insufficient apposition of the rough zones of the mitral leaflets so they no longer support each other during systole and fall into the left atrium. (See "Definition and diagnosis of mitral valve prolapse", section on 'Pathology'.)
●Among patients with acute rheumatic carditis, the intensity and time course of the inflammatory process may impact the course of mitral valve disease. Severe inflammation of the chordal structures and mitral valve leaflets can lead to isolated MR, seen predominantly in children and young adults. Moderate chordal and leaflet inflammation, which may be exacerbated by repeated acute rheumatic carditis, may lead to mixed MR and mitral stenosis. Chronic chordal and leaflet inflammation may be exacerbated by repeated acute rheumatic carditis, which may lead to mitral stenosis (algorithm 1). (See "Natural history, screening, and management of rheumatic heart disease", section on 'Natural history'.)
Subscribers log in hereLiterature review current through: Jul 2017. | This topic last updated: Mar 09, 2017.References
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- Causes and mechanisms
- - Primary MR
- Flail leaflet
- - Secondary MR
- Cardiac response to MR
- - Acute MR
- - Chronic compensated MR
- - Chronic decompensated MR
- Afterload and MR
- - Definitions
- - Afterload in chronic MR
- - Impedance in chronic MR
- - Afterload following corrective surgery
- Functional status of the ventricle
- Mitral valve replacement versus repair
- NATURAL HISTORY
- Factors affecting the natural history
- Phases of MR
- Transition to heart failure
- Markers of a decompensated ventricle