15.1
二尖瓣脱垂 I: 介绍
介绍
二尖瓣是心脏四个瓣膜之一，负责调节血液流动。这些瓣膜具有瓣叶，瓣叶通过开启和关闭来引导血液正确流经心脏和全身。在每次心跳中，瓣叶会打开让血液通过，然后紧密闭合，防止血液回流。具体而言，二尖瓣打开时，允许血液从心脏的左心房流至左心室，然后当左心室收缩将血液泵送到全身时紧闭，防止任何血液逆流。
定…
二尖瓣脱垂（MVP）是一种心脏疾病，其特征是二尖瓣瓣叶、乳头肌或腱索出现异常，导致在收缩期瓣叶向左心房脱垂或翻转。
MVP 可能由多种因素引起。
由于黏液样变性导致的二尖瓣结构改变较为常见。
与马凡综合征等结缔组织疾病相关的遗传因素也有影响。
其他病因包括先天性畸形、与年龄相关的退行性改变，以及脊柱侧弯或肌营养不良等骨骼系统疾病。
二尖瓣脱垂（MVP）的发病机制始于瓣膜瓣叶因胶原蛋白和蛋白聚糖过多而增厚，导致瓣叶松弛，易于脱垂。
在心脏收缩期或收缩阶段，扩大的瓣膜瓣叶可能向后凸入左心房，导致瓣膜异常关闭。
连接瓣膜瓣叶与心脏乳头肌的腱索可能变弱，从而进一步损害瓣膜功能。
这会导致二尖瓣反流，即在收缩期血液倒流回左心房，从而引发心房颤动、肺动脉高压和心力衰竭等并发症。
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Q1: What happens to the mitral valve during mitral valve prolapse?
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.
Q2: What structural changes cause mitral valve prolapse?
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.
Q3: How does genetic predisposition contribute to mitral valve prolapse?
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.
Q4: What complications can result from mitral valve 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.
Q5: What non-genetic factors contribute to mitral valve prolapse development?
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.
Q6: How does the mitral valve normally function in the heart?
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.
Q7: What role do papillary muscles and chordae tendineae play in mitral valve function?
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.