Brenner S, Ertl G
Department of Internal Medicine I/Comprehensive Heart Failure Center, University Hospital Würzburg, Oberdürrbacherstr. 6, 97080, Würzburg, Germany.
Herz. 2012 Sep;37(6):590-6. doi: 10.1007/s00059-012-3660-7.
Remodelling is the adaptive or maladaptive response to cardiac overload or injury resulting in changes of size and function of the heart. The final pathway of maladaptive or adverse cardiac remodelling is the evolution of heart failure or sudden cardiac death. In coronary artery disease, ischemic injury leads to changes in the cellular and extra-cellular architecture of the infarcted and non-infarcted region resulting in cavity enlargement and loss of contractility of the entire heart. During the last three decades, potential therapeutic concepts have been established and reversal of adverse remodelling could be demonstrated in up-to end-stage disease. A further understanding of the underlying cellular, extracellular, molecular and genetic alterations in ischemic remodelling should reveal other promising targets for prevention and reversal of remodelling.
重塑是心脏对负荷过重或损伤的适应性或适应不良性反应,会导致心脏大小和功能发生改变。适应不良或不良心脏重塑的最终途径是心力衰竭或心源性猝死的演变。在冠状动脉疾病中,缺血性损伤会导致梗死区和非梗死区的细胞及细胞外结构发生变化,从而导致心腔扩大和整个心脏收缩力丧失。在过去三十年中,已经确立了潜在的治疗理念,并且在直至终末期疾病中都可以证明不良重塑的逆转。对缺血性重塑中潜在的细胞、细胞外、分子和基因改变的进一步了解,应该会揭示出其他有希望的预防和逆转重塑的靶点。