The rupture of an atherosclerotic plaque cap overlying a lipid pool and/or necrotic core can lead to thrombotic cardiovascular events. In essence, the rupture of the plaque cap is a mechanical event, which occurs when the local stress exceeds the local tissue strength. However, due to inter- and intra-cap heterogeneity, the resulting ultimate cap strength varies, causing proper assessment of the plaque at risk of rupture to be lacking. Important players involved in tissue strength include the load-bearing collagenous matrix, macrophages, as major promoters of extracellular matrix degradation, and microcalcifications, deposits that can exacerbate local stress, increasing tissue propensity for rupture. This review summarizes the role of these components individually in tissue mechanics, along with the interplay between them. We argue that to be able to improve risk assessment, a better understanding of the effect of these individual components, as well as their reciprocal relationships on cap mechanics, is required. Finally, we discuss potential future steps, including a holistic multidisciplinary approach, multifactorial 3D in vitro model systems, and advancements in imaging techniques. The obtained knowledge will ultimately serve as input to help diagnose, prevent, and treat atherosclerotic cap rupture.

覆盖脂质池和/或坏死核心的动脉粥样硬化斑块破裂可导致血栓性心血管事件。本质上，斑块帽的破裂是一种机械事件，当局部应力超过局部组织强度时就会发生。然而，由于帽间和帽内的异质性，最终帽强度各不相同，导致缺乏对破裂风险斑块的正确评估。参与组织强度的重要因素包括承载胶原基质、巨噬细胞（作为细胞外基质降解的主要促进者）和微钙化（可以加剧局部应力、增加组织破裂倾向的沉积物）。这篇综述总结了这些组件在组织力学中的作用以及它们之间的相互作用。我们认为，为了能够改进风险评估，需要更好地了解这些单独组成部分的影响以及它们对上限机制的相互关系。最后，我们讨论了未来可能采取的步骤，包括整体多学科方法、多因素 3D 体外模型系统以及成像技术的进步。获得的知识最终将作为帮助诊断、预防和治疗动脉粥样硬化帽破裂的输入。