LEFT-VENTRICULAR MYOCARDIAL STRUCTURE IN AORTIC-VALVE DISEASE BEFORE, INTERMEDIATE, AND LATE AFTER AORTIC-VALVE REPLACEMENT
LEFT-VENTRICULAR MYOCARDIAL STRUCTURE IN AORTIC-VALVE DISEASE BEFORE, INTERMEDIATE, AND LATE AFTER AORTIC-VALVE REPLACEMENT
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DOI：
10.1161/01.cir.79.4.744
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发表时间：
1989-04-01
期刊：
影响因子：
37.8
通讯作者：
TURINA, M
中科院分区：
文献类型：
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作者：
KRAYENBUEHL, HP;HESS, OM;TURINA, M
对27例主动脉瓣狭窄（AS）和17例主动脉瓣关闭不全（AI）患者进行了左心室双平面电影血管造影、微测压和心肌内膜活检。23例AS患者和15例AI患者在中间时间（成功瓣膜置换术后18个月）进行了再研究，9例AS患者和6例AI患者在晚期（手术后70个月和62个月）进行了再研究。对活检样本的肌纤维直径、间质纤维化百分比和肌原纤维体积分数进行评价。在移植时从5个供体心脏获得的对照活检样品中，这些形态测量变量分别平均为21.2 μ m、7.0%和57.2%。手术后，血管造影确定的AS患者的质量从186降至115和94 g/m2，AI患者的质量从201降至131和93 g/m2。在这三项研究中，AS患者的肌纤维直径为30.9、28.0和28.7 μ m，AI患者的肌纤维直径为31.4、27.6和26.4 μ m。AS患者间质纤维化百分比分别为18.2%、25.8%和13.7%，AI患者间质纤维化百分比分别为20.4%、23.7%和19.2%。左心室纤维含量在AS患者中从34.2降至29.8和12.7 g/m2，在AI患者中从42.1降至28.9和18.9 g/m2。AS患者肌原纤维体积分数为57.7%、56.8%和49.0%，AI患者为56.8%、56.6%和48.8%。因此，在瓣膜置换术后的中间时间通过血管造影术确定的肌肉质量的减少是由AS和AI患者的心肌细胞肥大的消退以及AI患者的纤维含量的减少介导的。术后晚期，AS患者左心室纤维含量也减少。这种晚期降低与舒张末期容积的微小变化相关，可能对改善舒张期心肌硬度增加很重要。即使在瓣膜置换术后6-7年，与正常心肌相比，左心室肥厚的结构异常仍然存在不完全消退。残余增加的相对间质纤维化和术后后期肌原纤维体积分数的小幅降低，与假体相关的轻微左心室压力增加相关，是肌原纤维水平持续收缩超负荷的起源。
Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 .mu.m, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 .mu.m in patients with AS and was 31.4, 27.6, and 26.4 .mu.m in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Later after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stiffness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.