UPMC Cardiovascular Magnetic Resonance Center, Pittsburgh, PA, USA; Heart and Vascular Institute, UPMC, Pittsburgh, PA, USA; Department of Medicine, University of Pittsburgh School of Medicine, 200 Lothrop Street, PUH E E354.2, Pittsburgh, PA 15101, USA; Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, PA, USA.
Heart Fail Clin. 2019 Apr;15(2):179-189. doi: 10.1016/j.hfc.2018.12.009. Epub 2019 Feb 2.
The cardiology community lacks a taxonomy to prioritize the origins of the complex myocardial pathology underlying heart failure. The key question, "Why does heart muscle fail?", remains unanswered. A large body of literature indicates that myocardial fibrosis represents a principal pathway mediating outcomes in heart failure. Cardiac amyloidosis illustrates how excess protein in the myocardial interstitium culminates in severe heart failure with a dismal prognosis. Robust methods now exist to quantify myocardial fibrosis. Investigators possess the tools to finally establish unequivocally that myocardial fibrosis represents one of the principal pathways mediating outcomes in heart failure that imparts vulnerability.
心脏病学领域缺乏一种分类法来确定心力衰竭潜在复杂心肌病理学的起源优先级。关键问题是“为什么心肌衰竭?”,这个问题仍然没有答案。大量文献表明,心肌纤维化代表了介导心力衰竭结局的主要途径。心脏淀粉样变性说明了心肌间质中过量的蛋白质如何导致严重心力衰竭和预后不良。目前已经存在量化心肌纤维化的可靠方法。研究人员拥有最终明确确定心肌纤维化代表介导心力衰竭结局的主要途径之一的工具,这使心力衰竭变得脆弱。