Nova Medical School, Lisboa, Portugal; Cardiology Department, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal; Cardiology Department, Hospital dos Lusíadas, Lisboa, Portugal.
Nova Medical School, Lisboa, Portugal; Pathology Department, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal.
Curr Probl Cardiol. 2021 May;46(5):100801. doi: 10.1016/j.cpcardiol.2021.100801. Epub 2021 Jan 24.
Aortic stenosis was once considered a pure isolated valve obstacle challenging left ventricle driving force of contraction and flow generation. Left ventricular (LV) adaptation was merely interpreted as a uniform hypertrophic response to increased afterload. However, in these last 2 decades cardiac imaging research and some histopathology correlation studies brought insight towards the complex interaction between the vasculature, the valve and the myocardium. Verily, LV remodeling in this setting is a complex multidetermined process that goes further beyond myocardial hypertrophy. Ultrastructural changes involving both diffuse and replacement fibrosis of the myocardium take part and might explain the transition of clinical phenotypes with distinct prognosis, from compensated hypertrophy to LV maladaptive dysfunction and heart failure. Presently, the combined appropriate use of echocardiography and cardiac magnetic resonance may better assess the global LV afterload, hypertrophy and geometric remodeling, global and regional LV function, beyond ejection fraction, and structural changes that include the fibrotic burden of the myocardium. As a whole these may not only better stratify individual risk of disease progression but also identify patients benefiting from earlier valve intervention. In this paper, we review the maladaptive response of the LV to chronic pressure overload, describing the different signaling pathways and mechanisms that underly both hypertrophy and remodeling. Histomorphology changes in this setting are described and we try to make sense of the use of new imaging tools for LV characterization.
主动脉瓣狭窄曾被认为是一种单纯的瓣膜病变,主要影响左心室的收缩力和射流。左心室(LV)的适应性改变通常被解释为对后负荷增加的均匀性肥厚反应。然而,在过去的 20 年里,心脏影像学研究和一些组织病理学相关性研究深入探讨了血管、瓣膜和心肌之间的复杂相互作用。实际上,在此背景下,LV 重构是一个复杂的多因素过程,远不止心肌肥厚那么简单。心肌的弥漫性和替代性纤维化等超微结构变化也参与其中,并可能解释了具有不同预后的临床表型的转变,从代偿性肥厚到 LV 适应性不良和心力衰竭。目前,超声心动图和心脏磁共振的联合适当应用可以更好地评估 LV 的整体后负荷、肥厚和几何重构、整体和局部 LV 功能(除射血分数外)以及包括心肌纤维化负担在内的结构变化。总的来说,这些不仅可以更好地分层疾病进展的个体风险,还可以确定哪些患者受益于早期瓣膜干预。本文综述了 LV 对慢性压力超负荷的适应性不良反应,描述了导致肥厚和重构的不同信号通路和机制。本文还描述了在此背景下的组织形态学变化,并尝试理解用于 LV 特征描述的新型影像学工具的应用。