Mitral valve prolapse (MVP) occurs when the leaflets of the mitral valve, which normally open and close tightly to regulate blood flow between the left atrium and left ventricle of the heart, become abnormally loose or floppy. Instead of closing firmly during each heartbeat, these leaflets bulge backward into the left atrium like a sailboat’s sail caught in wind. This improper closure can cause blood to leak backward, a condition called mitral regurgitation.
The causes behind this abnormal leaflet behavior are varied but generally fall into two broad categories: structural abnormalities present from birth (congenital) and changes that develop over time (acquired).
One common underlying factor is **myxomatous degeneration**, a process where connective tissue within the valve becomes thickened and redundant due to excessive accumulation of mucopolysaccharides. This weakens the valve structure, making it more flexible but less able to maintain proper shape during contraction. Myxomatous changes often lead to MVP by causing leaflet enlargement and elongation as well as stretching or rupture of supporting chordae tendineae—the string-like structures anchoring leaflets to papillary muscles inside the ventricle.
Another important anatomical contributor is **mitral annular disjunction (MAD)**—a condition where there is an abnormal separation between parts of the mitral valve annulus (the ring-like base that anchors leaflets) and adjacent heart muscle tissue. MAD disrupts normal mechanical function by allowing excessive motion or displacement during heartbeats, increasing stress on both leaflets and chordae. This added strain can worsen prolapse severity over time and may also promote electrical instability in surrounding cardiac tissue, potentially leading to arrhythmias.
Aging plays a significant role as well; with advancing years, valves undergo wear-and-tear changes including calcification—calcium deposits stiffen tissues—and fibrosis—scarring that reduces elasticity. These degenerative processes reduce leaflet flexibility necessary for tight closure and contribute substantially to acquired forms of MVP especially in older adults.
Certain diseases also predispose individuals to MVP:
– **Connective tissue disorders** such as Marfan syndrome or Ehlers-Danlos syndrome affect collagen synthesis throughout the body including heart valves; this results in weakened valvular structures prone to prolapse.
– **Rheumatic heart disease**, once a major cause worldwide before widespread antibiotic use for strep throat infections, leads to inflammation followed by scarring that distorts normal valve anatomy.
– Damage from **heart attacks** can impair papillary muscles responsible for holding chords taut; if these muscles weaken or die due to ischemia, they fail mechanically causing sudden onset severe leakage associated with acute MVP symptoms.
Genetic factors are increasingly recognized too; familial clustering suggests inherited mutations affecting extracellular matrix proteins may underlie some cases.
In summary:
– The primary mechanism involves weakening or redundancy of mitral valve components—leaflets themselves plus supporting chords—that prevents full closure.
– Structural abnormalities like myxomatous degeneration enlarge/floppy leaflets.
– Mitral annular disjunction adds mechanical instability worsening prolapse.
– Aging-related calcification/fibrosis stiffen valves reducing function.
– Connective tissue diseases genetically predispose fragile valves.
– Inflammatory damage from rheumatic fever scars valves long-term.
– Heart attack-induced papillary muscle dysfunction causes acute failure.
Together these factors explain why some people develop mitral valve prolapse while others do not—even though mild forms are quite common in general populations without symptoms. Understanding these causes helps guide monitoring strategies since only certain patients progress toward serious complications requiring intervention such as surgery or catheter-based treatments targeting arrhythmias linked with complex MVP anatomy.
