Background

Myocardial adaptation to severe aortic stenosis (AS) is a complex process that involves myocardial fibrosis (MF) beyond cardiomyocyte hypertrophy. Perfusion impairment is believed to be involved in myocardial remodeling in chronic pressure overload.

Aim

To describe morphological and ultrastructural myocardial changes at endomyocardial tissue sampling, possibly reflecting subendocardial ischemia, in a group of patients with severe AS referred to surgical aortic valve replacement (AVR), with no previous history of ischemic cardiomyopathy.

Methods

One-hundred-fifty-eight patients (73 [68-77] years, 50% women) referred for surgical AVR because of severe symptomatic AS with preoperative clinical and imaging study and no previous history of ischemic cardiomyopathy. Intra-operative septal endomyocardial sampling was obtained in 129 patients. Tissue sections were stained with Masson´s Trichrome for MF quantification and periodic acid-Schiff (PAS) staining was performed to assess the presence of intracellular glycogen. Ultrastructure was analyzed through Transmission electron microscopy (TEM).

Results

MF totalized a median fraction of 11.90% (6.54-19.97%) of EMB, with highly prevalent perivascular involvement (95.3%). None of the samples had histological evidence of myocardial infarction. In 58 patients (45%) we found subendocardial groups of cardiomyocytes with cytoplasmatic enlargement, vacuolization and myofiber derangement, surrounded by extensive interstitial fibrosis. These cardiomyocytes were PAS positive, PAS-diastase resistant and Alcian Blue/PAS indicative of the presence of neutral intracellular glyco-saccharides. At TEM there were signs of cardiomyocyte degeneration with sarcomere disorganization and reduction, organelle rarefaction but no signs of intracellular specific accumulation.

Conclusion

Almost half of the patients with severe AS referred for surgical AVR have histological and ultrastructural signs of subendocardial cardiomyocyte ischemic insult. It might be inferred that local perfusion imbalance contributes to myocardial remodeling and fibrosis in chronic pressure overload.

中文翻译：

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严重主动脉瓣狭窄患者的心内膜下“缺血样”状态：心肌组织病理学和超微结构的见解

背景

心肌对严重主动脉瓣狭窄（AS）的适应是一个复杂的过程，除了心肌细胞肥大之外还涉及心肌纤维化（MF）。据信，灌注损伤与慢性压力超负荷时的心肌重塑有关。

目的

描述一组接受外科主动脉瓣置换术 (AVR) 且既往无缺血性心肌病病史的严重 AS 患者心内膜心肌组织取样时的形态学和超微结构心肌变化，可能反映心内膜下缺血。

方法

158 名患者（73 [68-77] 岁，50% 女性）因严重症状性 AS 转诊接受外科 AVR，且具有术前临床和影像学检查且既往无缺血性心肌病病史。对 129 名患者进行了术中间隔心内膜心肌取样。组织切片用Masson Trichrome染色以进行 MF 定量，并进行高碘酸希夫 (PAS) 染色以评估细胞内糖原的存在。通过透射电子显微镜（TEM）分析超微结构。

结果

MF 的中位比例为 EMB 的 11.90% (6.54-19.97%)，血管周围受累非常普遍 (95.3%)。所有样品都没有心肌梗塞的组织学证据。在 58 名患者 (45%) 中，我们发现心内膜下心肌细胞群出现细胞质增大、空泡化和肌纤维紊乱，周围有广泛的间质纤维化。这些心肌细胞呈 PAS 阳性、PAS 淀粉酶抗性，并且阿尔新蓝/PAS 表明存在中性细胞内糖。TEM 观察到心肌细胞变性、肌节解体和减少、细胞器稀疏的迹象，但没有细胞内特异性积累的迹象。

结论

几乎一半转诊接受 AVR 手术的严重 AS 患者具有心内膜下心肌细胞缺血性损伤的组织学和超微结构体征。可以推断，局部灌注失衡有助于慢性压力超负荷时的心肌重塑和纤维化。