Mitral Valve Regurgitation and Prolapse

Mitral regurgitation (MR) is a multifaceted condition with several etiologies. The leading cause is mitral valve prolapse, which is predominantly a consequence of myxomatous degeneration—a pathologic deterioration of the connective tissue. While this degeneration can prompt chordae tendinae rupture, other causes, including acute papillary muscle rupture following an MI, can also trigger acute MR. Furthermore, infectious agents can exacerbate the condition; infective endocarditis may damage the chordae tendinae leading to rupture or result in vegetations forming on the mitral valve, both causing MR. Notably, acute rheumatic fever can instigate valvulitis, which subsequently gives rise to MR.

The repercussions of MR, especially in its acute form, are profound on cardiac hemodynamics. An acute onset leads to a swift decline in forward stroke volume and cardiac output, with grave outcomes such as acute hypotension and cardiogenic shock. It profoundly alters the ventricular dynamics, increasing LEDV & preload, which can cause pulmonary venous hypertension and flash pulmonary edema. Acute MR is associated with the creation of a second low-resistance outlet for the ventricle, resulting in diminished afterload but a paradoxical increase in ejection fraction. When severe, acute MR can cause severe hypotension & cardiogenic shock. Additionally, dilated cardiomyopathy can stretch the mitral annulus and cause mitral regurgitation

Chronic mitral regurgitation provides an adaptive phase where the left atrium undergoes dilation and hypertrophy, effectively diminishing the pressure transmission to the pulmonary circuit, thereby preventing significant pulmonary edema. This chronic condition maintains cardiac output due to an elevated ejection fraction. The pathophysiological hallmark of chronic mitral regurgitation is the chronically elevated preload in the left ventricle, setting the stage for eccentric hypertrophy of the ventricle. However, a lurking threat is its potential progression to decompensated congestive heart failure. On auscultation, chronic mitral regurgitation is characterized by a blowing, holosystolic murmur which is most audible over the cardiac apex, and it radiates to the axilla. Additionally, the dilation of the left ventricle in this condition can evoke an S3 heart sound. It's interesting to note that functional mitral regurgitation due to acute left ventricular volume overload can witness a decreased intensity of the murmur upon diuresis.

Mitral valve prolapse (MVP), a significant causative factor behind mitral regurgitation, presents with a distinctive mid-systolic click. The click is indicative of the sudden tensing of chordae as the valve leaflets prolapse, lies between the S1 and S2 heart sounds. When preload decreases, such as during Valsalva maneuver or tachycardia, the click moves closer to the S1 heart sound. Conversely, maneuvers that increase preload (straight leg raise or squatting), or increase afterload (sustained hand grip), push the click closer to the S2 sound. MVP can also be instigated by connective tissue diseases, notably Marfan syndrome, osteogenesis imperfecta, and Ehlers-Danlos, primarily due to myxomatous degeneration of the mitral valve.