Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.
Etiology and Mechanisms:
Primary Mitral Regurgitation: This type arises from direct problems with the mitral valve leaflets themselves, such as:
Secondary Mitral Regurgitation: This type results from conditions affecting the left ventricle or papillary muscles indirectly, such as:
Pathophysiological Changes:
Regardless of the cause, the pathophysiology of MR involves the dysfunction of the mitral valve or its supporting structures (leaflets, chordae tendineae, annulus, papillary muscles). Damage or deformation in these areas leads to incomplete valve closure and blood regurgitation during Systole.
Volume Overload: MR significantly increases the volume the left atrium and ventricle must handle, as the regurgitated blood adds to the normal blood flow from the pulmonary veins.
Mitral regurgitation, or MR, is a heart condition where the mitral valve fails to close entirely during systole, causing blood to leak backward from the left ventricle into the left atrium.
Its etiology is classified into two types.
Primary MR originates from direct mitral valve abnormalities, including mitral valve prolapse, rheumatic fever, and degenerative changes.
Secondary MR results from indirect factors like ischemic heart disease and infective endocarditis.
The pathophysiology of MR involves dysfunction in the mitral valve or its supporting structures, including the leaflets, chordae tendineae, annulus, or papillary muscles, which leads to backward blood flow and volume overload.
This overload causes left atrial enlargement and left ventricular hypertrophy and dilation.
These compensatory changes can eventually result in systolic dysfunction.
Increased pressure in the left atrium may cause pulmonary congestion and hypertension, straining the right ventricle and leading to reduced cardiac output and heart failure symptoms.