Each year, more than 40,000 people in the United States undergo mitral valve (MV) repair surgery to treat regurgitation caused by myocardial infarction (MI). Although continual strain-driven remodeling of the MV is believed to be a major cause of regurgitation recurrence following repair, the effects of MI and repair surgery on MV deformation patterns remain poorly understood. We thus cannot currently predict the remodeling of the MV in disease or post-surgery to facilitate functional assessment and surgical planning. As a necessary first step, the present study was undertaken to noninvasively quantify the e↵ects of MI on MV remodeling in terms of geometry and strains. MI was induced in eight adult Dorset sheep, and real-time three-dimensional echocardiographic (rt-3DE) scans were collected pre-MI as well as at 0, 4, and 8 weeks post-MI. A previously validated image-based morphing pipeline was used to register corresponding open- and closed-state scans and extract local in-plane strains throughout the leaflet surface at diastole and systole. We found that MI-induced overload yielded substantial and heterogeneous changes in both MV geometry and leaflet strain patterns, which manifested rapidly within 4 weeks, mostly stabilized by 8 weeks, and showed no evidence of reversal during the study period. Most notably, post-MI leaflet tethering caused permanent deformations that predominantly a↵ected the MV’s diastolic configuration, leading in turn to a significant decrease in the range of stretch experienced by most of the leaflet. This study demonstrated, through noninvasive methods, that the state of the MV leaflet tissue and the underlying collagen fiber network is substantially and irreversibly altered post-MI. Our findings elucidate the progression and extent of MV adaptation following MI and are thus highly relevant to the design of current and novel minimally invasive surgical repair strategies, which require accounting for realized and prospective MV remodeling phenomena on a patient-specific basis.
每年，美国有超过40,000人接受二尖瓣（MV）修复手术治疗由心肌梗死（MI）引起的反流。尽管持续的应变驱动重塑被认为是修复后反流复发的主要原因，但MI和修复手术对MV变形模式的影响仍然知之甚少。因此，我们目前无法预测疾病或手术后MV的重塑情况，以便进行功能评估和手术规划。作为必要的第一步，本研究旨在以非侵入性方式定量MI对MV几何形态和应变的影响。在八只成年多赛特绵羊中诱导了MI，并且在MI前以及MI后0、4和8周收集了实时三维超声心动图（rt-3DE）扫描。使用先前验证过的基于图像的形态学处理流程，对应的开放和闭合状态扫描进行了注册，并提取了舒张期和收缩期瓣叶表面的局部面内应变。我们发现，MI诱导的过载导致MV几何形态和瓣叶应变模式发生了显著且异质性的变化，这些变化在4周内迅速显现，大部分在8周内稳定下来，并且在研究期间没有证据表明会逆转。值得注意的是，MI后的瓣叶牵引导致了永久性变形，主要影响了MV的舒张配置，进而导致了大多数瓣叶所经历的伸展范围显著减少。这项研究通过非侵入性方法证明了MI后MV瓣叶组织和底层胶原纤维网络的状态发生了重大且不可逆转的改变。我们的研究阐明了MI后MV适应的进展和程度，因此对当前和新型微创手术修复策略的设计具有非常重要的意义，这需要根据患者具体情况考虑已实现和预期的MV重塑现象。