Liu S K, Magid N R, Fox P R, Goldfine S M, Borer J S
Division of Cardiovascular Pathophysiology, Cornell University Medical College, New York Hospital- Cornell Medical Center, New York, NY 10021, USA.
Cardiology. 1998 Oct;90(2):101-9. doi: 10.1159/000006827.
Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 +/- 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 +/- 0.8 years (range 0.6-2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 +/- 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.
据报道，慢性主动脉瓣反流（AR）患者存在心肌纤维化和心肌细胞变性，这可能与该疾病中充血性心力衰竭（CHF）的病理生理学有关。为了明确慢性AR中心肌组织病理学变化与CHF之间的关系，我们对慢性AR兔模型的尸检组织进行了大体和显微镜评估，该模型表现出与人类相似的左心室（LV）对AR的反应。通过开胸主动脉瓣穿孔术在11只新西兰白兔中诱导出中度至重度慢性AR（超声心动图反流分数=52±13%）；5只对照兔接受假手术。11只AR兔中有6只在AR诱导后1.5±0.8年（范围0.6 - 2.8年）死亡；所有6只在尸检时均有CHF的大体和组织学解剖学证据。其余5只AR兔存活至AR诱导后2.9±0.1年处死；均无CHF的病理证据。6只AR CHF兔的心脏肥大、LV纤维化程度和心肌细胞坏死程度均最为严重。所有动物均未出现明显的炎症反应。中度至重度慢性实验性AR常导致CHF，CHF与心肌纤维化和坏死密切相关，无炎症证据。这些组织病理学变化可能在病理生理上与CHF的发展有关。
