本文選題：冠狀動脈粥樣硬化 + 竇房結　； 參考：《青島大學》2017年碩士論文

【摘要】：目的探討竇房結(sinoatrial node,SAN)間質(zhì)增生和超極化激活環(huán)核苷酸門控陽離子通道基因4(hyperpolarization activated cyclic nucleotide gated cation channel 4,HCN4)的表達與心肌梗死(myocardial infarction,MI)的關系,及其與左右冠狀動脈粥樣硬化管腔狹窄程度、年齡、性別等臨床病理學特征的關系,以分析心肌梗死是否影響竇房結間質(zhì)增生和HCN4的表達,并進一步研究心肌梗死透壁程度、竇房結間質(zhì)增生和HCN4表達的相關性。方法收集35例非心肌梗死和13例心肌梗死尸體解剖心臟標本,記錄死者死亡原因、年齡、性別。肉眼觀察左右冠狀動脈狹窄和心肌梗死情況,分別對竇房結和左右冠狀動脈(狹窄最嚴重處)進行取材;對于心肌梗死者,一并在其左心室各壁(包括室間隔和心尖)梗死透壁程度最嚴重處取材。常規(guī)制片。左右冠狀動脈進行HE染色;各心室壁進行HE染色、苦味酸染色;竇房結進行HE染色、Masson染色。從35例非心肌梗死案例中選取13例與13例心肌梗死者的竇房結進行HCN4免疫組織化學染色(由HE染色、Masson染色后選定位置)。北京Tissue Gnostics China Division公司組織圖像分析系統(tǒng)、Image pro plus 6.0圖像分析系統(tǒng)和本中心法醫(yī)病理醫(yī)師肉眼及鏡下觀察分析相結合統(tǒng)計竇房結間質(zhì)增生程度、HCN4表達情況、左右冠狀動脈相對狹窄程度和心肌梗死透壁程度。采用等級logistic回歸、多元線性回歸、Spearman相關和Mann-Whitney U秩和檢驗進行統(tǒng)計學分析。結果本實驗發(fā)現(xiàn)竇房結主要病理形態(tài)學改變?yōu)殚g質(zhì)增生,即纖維化和脂肪浸潤,心肌梗死患者竇房結間質(zhì)增生程度絕大部分達Ⅱ~Ⅲ級,其內(nèi)P細胞數(shù)量減少。竇房結間質(zhì)增生與左右冠狀動脈粥樣硬化管腔狹窄程度和年齡有關(P0.05),而與性別和心肌梗死可能無直接相關性(P0.05)。HCN4在竇房結內(nèi)非均質(zhì)的表達在細胞質(zhì)及細胞膜上,但主要表達在細胞膜;HCN4的表達與右冠狀動脈供血減少有關(P0.05)。心肌梗死者左右冠狀動脈粥樣硬化與竇房結間質(zhì)增生的多元線性回歸方程:Y=3.885+0.462X1+0.380X2,決定系數(shù)R2=0.688,P=0.003。針對每一個體而言,心肌梗死透壁程度與竇房結間質(zhì)增生呈正相關(rs=0.608,P=0.028),與HCN4的表達無直接相關性(P=0.871);竇房結間質(zhì)增生與HCN4的表達也無直接相關性(P=0.808)。MI組與非MI組竇房結HCN4的表達無統(tǒng)計學差異(P=0.724)。結論左右冠狀動脈粥樣硬化管腔狹窄、年齡均可影響竇房結間質(zhì)增生,右冠狀動脈粥樣硬化管腔狹窄可以影響竇房結HCN4的表達。對心肌梗死患者,竇房結間質(zhì)增生與血供減少密切相關。尸檢心肌梗死透壁程度與竇房結間質(zhì)增生呈同向發(fā)展,但與HCN4的表達并不相關。竇房結間質(zhì)增生可能是心肌梗死引起心源性猝死的一個重要原因。
[Abstract]:Objective to investigate the relationship between interstitial hyperplasia and hyperpolarization-activated cyclic nucleotide-gated cationic channel gene 4(hyperpolarization activated cyclic nucleotide gated cation channel _ 4 (HCN4) and myocardial infarction (myocardial infarction) in sinoatrial node (San), and its relationship with stenosis degree and age of left and right coronary atherosclerotic arteries. The relationship between sex and other clinicopathological features in order to analyze whether myocardial infarction affects sinoatrial node interstitial hyperplasia and HCN4 expression, and to further study the correlation between myocardial infarction transmural degree, sinus node interstitial hyperplasia and HCN4 expression. Methods 35 non-myocardial infarction and 13 myocardial infarction cadaveric heart specimens were collected to record the cause of death, age and sex. The left and right coronary artery stenosis and myocardial infarction were observed with the naked eye. The sinus node and the left and right coronary arteries (where the stenosis was most serious) were taken, respectively. At the same time, the most severe transmural infarction of the left ventricular wall (including septum and apical) was obtained. Conventional production. The left and right coronary arteries were stained with HE, each ventricular wall was stained with HE, picric acid was stained, and sinoatrial node was stained by HE staining and Masson staining. The sinoatrial node of 13 cases and 13 cases of myocardial infarction were selected from 35 cases of non-myocardial infarction. The sinoatrial node was stained by HCN4 immunohistochemical staining (selected location by HE staining and Masson staining). The image pro plus 6.0 image analysis system of Beijing Tissue Gnostics China Division Company combined with the naked eye and microscopic observation and analysis of the forensic pathologist of our center analyzed the expression of HCN4 in sinoatrial node stromal hyperplasia. Relative stenosis of left and right coronary artery and transmural myocardial infarction. Grade logistic regression, multivariate linear regression and Mann-Whitney U rank sum test were used to analyze statistical data. Results the main pathomorphological changes of sinoatrial node were interstitial hyperplasia, I. E. fibrosis and fat infiltration. The degree of interstitial hyperplasia of sinoatrial node in patients with myocardial infarction was mostly grade 鈪，

本文編號：1871822