Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis 38163, USA.
Am J Med Sci. 2011 Aug;342(2):129-34. doi: 10.1097/MAJ.0b013e3182231ee3.
The progressive nature of heart failure is linked to multiple factors, including an ongoing loss of cardiomyocytes and necrosis. Necrotic cardiomyocytes leave behind several footprints: the spillage of their contents leading to elevations in serum troponins; and morphologic evidence of tissue repair with scarring. The pathophysiologic origins of cardiomyocyte necrosis relates to neurohormonal activation, including the adrenergic nervous system. Catecholamine-initiated excessive intracellular Ca accumulation and mitochondria Ca overloading in particular initiate a mitochondriocentric signal-transducer-effector pathway to necrosis and which includes the induction of oxidative stress and opening of their inner membrane permeability transition pore. Hypokalemia, ionized hypocalcemia and hypomagnesemia, where consequent elevations in parathyroid hormone further account for excessive intracellular Ca accumulation, hypozincemia and hyposelenemia each compromise metalloenzyme-based antioxidant defenses. The necrotic loss of cardiomyocytes and adverse structural remodeling of myocardium is related to the central role played by a mitochondriocentric pathway initiated by neurohormonal activation.
心力衰竭的进行性与多种因素有关，包括心肌细胞的持续丢失和坏死。坏死的心肌细胞会留下几个痕迹：其内容物的溢出导致血清肌钙蛋白升高；以及组织修复的形态学证据，伴有瘢痕形成。心肌细胞坏死的病理生理起源与神经激素激活有关，包括肾上腺素能神经系统。儿茶酚胺引发的细胞内 Ca 积累过多和线粒体 Ca 超载，特别是启动了以线粒体为中心的信号转导效应器途径导致坏死，其中包括诱导氧化应激和开放其内膜通透性转换孔。低钾血症、离子钙降低和低镁血症，随后甲状旁腺激素的升高进一步导致细胞内 Ca 积累过多，低锌血症和低硒血症都损害基于金属酶的抗氧化防御。心肌细胞的坏死性丧失和心肌的不利结构重塑与神经激素激活引发的以线粒体为中心的途径所起的核心作用有关。
