Mitralklappenprolaps I: Einführung

During mitral valve prolapse, the mitral valve leaflets abnormally bulge backward into the left atrium during systole, the heart's contraction phase. This occurs when the valve leaflets become thickened and enlarged due to myxomatous degeneration, making them floppy and prone to prolapse. The weakened chordae tendineae, which anchor the leaflets to papillary muscles, further impair proper valve closure.

Mitral valve prolapse results from thickening of valve leaflets due to excess collagen and proteoglycans, a process called myxomatous degeneration. This abnormal tissue accumulation makes the leaflets spongy and enlarged. Additionally, alterations in the chordae tendineae weaken the cords anchoring the valve to the heart muscle, compromising the valve's ability to close properly during systole.

Genetic factors play a significant role in mitral valve prolapse development. The condition is often inherited and commonly associated with connective tissue disorders like Marfan syndrome, Ehlers-Danlos syndrome, and osteogenesis imperfecta. These inherited disorders affect the body's connective tissues, leading to structural abnormalities in the mitral valve that predispose individuals to prolapse.

Mitral valve prolapse can lead to mitral regurgitation, where blood rushes backward into the left atrium during systole. This causes volume overload in the left atrium and may result in left atrial and left ventricular enlargement. Significant mitral regurgitation can trigger serious complications including atrial fibrillation, pulmonary hypertension, and heart failure.

Beyond genetic factors, mitral valve prolapse can develop from congenital malformations, age-related degenerative changes in valve leaflets, and skeletal conditions like scoliosis, chest wall deformities, and muscular dystrophies. Developmental abnormalities occurring during the fetal stage may also predispose individuals to MVP. Additionally, evidence suggests higher prevalence in women, though the reasons remain unclear.

The mitral valve regulates blood flow from the heart's upper left chamber (left atrium) to the lower left chamber (left ventricle). During each heartbeat, the valve opens to allow blood passage and closes securely as the ventricle contracts to pump blood to the body. This prevents backflow and ensures unidirectional blood circulation through the heart.

The chordae tendineae are cords that anchor the mitral valve leaflets to the papillary muscles, specialized heart muscle structures. Together, they stabilize the valve leaflets and ensure proper closure during systole. When these structures weaken or become altered, the valve leaflets cannot close smoothly, increasing the likelihood of prolapse and valve dysfunction.