Cardiovascular Center, Miyazaki Medical Association Hospital, Miyazaki, Japan; Department of Cardiology, Hokkaido Cardiovascular Hospital, Sapporo, Japan.
Cardiovascular Center, Miyazaki Medical Association Hospital, Miyazaki, Japan; Division of Cardiovascular Physiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
J Cardiol. 2021 Nov;78(5):423-430. doi: 10.1016/j.jjcc.2021.05.014. Epub 2021 Jun 12.
Previous studies have proposed that osteogenic and apoptotic processes of valve interstitial cells contribute to the mineralization and then calcification of the aortic valve. Osteoblast-like cells subsequently mediate calcification of the aortic valve as part of a highly regulated process analogous to skeletal bone formation. The objective of this study was to evaluate the pathogenesis of the sclerotic/calcific changes in the aortic valve from histological and biological findings, and investigate the role of osteoblasts in the calcified pathway of aortic stenosis.
Preoperative echocardiography in 550 consecutive patients with osteoporotic hip fracture were retrospectively examined (475 females, mean 25th-75th, 89 [85-93] years). One hundred sixteen patients were under medical treatment with anti-osteoporosis drugs. We evaluated the prevalence and degree of degenerative changes in the aortic valve and examined the associations of bone turnover biomarkers N-terminal pro-peptide of type 1 collagen (P1NP) and serum tartrate-resistant acid phosphatase (TRACP-5b) with degenerative calcific changes in the aortic valve.
Of 550 patients, 112 patients (20.9%) showed no leaflet calcification; 296 (53.8%), 1 leaflet calcification; and 142 (25.8%), 2 ≥ leaflets calcification. Significant (peak velocity ≥ 3.0m/s) Aortic stenosis was found in 43 patients (7.8%). In patients who were not taking anti-osteoporotic drugs, P1NP was higher in the 2 ≥ leaflets calcification group than in the other groups (p < 0.01). TRACP-5b was not significantly different among the three groups (p = 0.15).
Degenerative changes in the aortic valve were related to bone biomarker activation in osteoporotic hip fracture patients.
先前的研究表明，瓣膜间质细胞的成骨和凋亡过程有助于主动脉瓣的矿化，然后是钙化。成骨细胞样细胞随后作为高度调节过程的一部分介导主动脉瓣的钙化，类似于骨骼形成。本研究的目的是从组织学和生物学发现评估主动脉瓣硬化/钙化变化的发病机制，并研究成骨细胞在主动脉瓣狭窄钙化途径中的作用。
回顾性检查了 550 例骨质疏松性髋部骨折连续患者的术前超声心动图（475 名女性，平均 25-75 岁，89 [85-93] 岁）。116 例患者接受抗骨质疏松药物治疗。我们评估了主动脉瓣退行性变化的发生率和程度，并检查了骨转换生物标志物 1 型胶原 N 端前肽（P1NP）和血清耐酒石酸酸性磷酸酶 5b（TRACP-5b）与主动脉瓣退行性钙化变化的相关性。
在 550 例患者中，112 例（20.9%）无瓣叶钙化；296 例（53.8%），1 叶瓣钙化；142 例（25.8%），2 ≥叶瓣钙化。43 例（7.8%）发现有明显的（峰值速度≥3.0m/s）主动脉瓣狭窄。在未服用抗骨质疏松药物的患者中，2≥叶瓣钙化组的 P1NP 高于其他两组（p<0.01）。三组间 TRACP-5b 无显著差异（p=0.15）。
骨质疏松性髋部骨折患者主动脉瓣退行性改变与骨生物标志物激活有关。
