Correlating Aortic Valve Structure to Heart Sound Characteristic

摘要/摘要： 当主动脉瓣叶因纤维化而变厚和僵硬时，就会发生主动脉瓣膜病。 钙化结节的重塑和形成。因此，当血液分配到动脉时，就会发生主动脉狭窄。 由于阀门不能正确打开，阀体受损。患者诊断不足仍然是一种 问题是--即使是严重的--AVD也可能是无症状的。没有症状的患者不会被提及 可以诊断AVD的高级成像程序的专家。主动脉狭窄的延迟介入治疗 会导致心脏重塑，最终导致心力衰竭。为了解决与以下内容相关的问题 诊断不足，需要可以在常规体检中实施的筛查策略 检测无症状患者的AVD。关闭瓣膜时，主动脉瓣叶的振动会产生 通过医生的听诊器听到的可听频率(S2声音)。我们假设微观结构 主动脉瓣重塑和相关生物力学改变的差异可以通过以下变化来确定 早期AVD的瓣膜声学特征(S2音)。结构和组成的变化 细胞外基质(ECM)导致AVD的生物力学改变。建议的目标是 这项研究通过两个目的进行测试，目的是确定主动脉瓣生物力学的变化如何影响心音。 特点。目标1将确定ECM结构改变是否会导致S2声音频率和 小鼠主动脉狭窄模型的时间特征。目标2将进一步开发一种新的分析技术 小鼠主动脉瓣的生物力学，为微结构和功能叶的改变提供了新的视角 在不同的AVD阶段。建议的研究成果可以为未来的发展做出贡献 一种非侵入性诊断工具，用于识别有发展风险或有严重但无症状的患者 AVD。这项工作可能在两个方面对AVD管理产生重大影响：1)使患者能够识别 在早期、可逆的疾病阶段，使人们有机会探索新的非侵入性治疗方法，以及2) 诊断无症状的晚期AVD患者，从而进行挽救生命的瓣膜置换手术。

Summary/Abstract: Aortic valve disease (AVD) occurs when aortic valve leaflets become thickened and stiff due to fibrotic remodeling and formation of calcific nodules. Consequently, aortic stenosis develops when blood distribution to the body is compromised due to the valve not being able open properly. Underdiagnosis of patients remains a problem because—even when severe—AVD can be asymptomatic. Asymptomatic patients are not referred to specialists for advanced imaging procedures that can diagnose AVD. Delayed intervention of aortic stenosis leads to cardiac remodeling and eventually cardiac failure. In order to address problems associated with underdiagnosis, screening strategies that can be implemented into routine physical examinations are needed to detect AVD in asymptomatic patients. The vibrations of aortic valve leaflets during valve closure produce the audible frequencies (S2 sound) heard through a doctor's stethoscope. We hypothesize that microstructural differences in aortic valve remodeling and related alterations in biomechanics can be identified by changes in the valvular acoustic characteristics (S2 sound) in early AVD. Structural and composition changes in the extracellular matrix (ECM) lead to the biomechanical alterations that cause AVD. The goals of the proposed study, tested through two aims, is to identify how changes in aortic valve biomechanics influence heart sound characteristics. Aim 1 will identify whether ECM structural alterations induce changes in S2 sound frequency and time characteristics in a mouse model of aortic stenosis. Aim 2 will further develop a new technique to analyze mouse aortic valve biomechanics, providing new insight into the microstructural and functional leaflet alterations during various AVD stages. The outcomes of the proposed research can contribute to the future development of a non-invasive diagnostic tool to identify patients who are at risk of developing or have severe but asymptomatic AVD. This work could have a major impact in AVD management in two ways: 1) enable identification of patients in early, reversible disease stages, enabling opportunities to explore new non-invasive treatments, and 2) diagnose asymptomatic patients with late-stage AVD, leading to lifesaving valve replacement surgery.