固定化间质性心脏纤维化。

IF 1.4 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Yuriy L Shevchenko, Alexey V Plotnitsky, Daniil S Ulbashev
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引用次数: 0

摘要

背景:肌内膜和肌周膜的改变可能引起心肌细胞的压实和逐渐的机械压迫,导致它们的固定。这一过程最终导致严重的硬化,因此单个心肌细胞及其簇周围新形成的框架阻碍了正常的舒张和随后的收缩。这种现象被称为固定化间质性心脏纤维化(IICF)。破译心肌变化的分子和结构因素是了解心力衰竭发展的病理基础的关键。方法:纳入69例患者。第一组(n = 32)包括IICF患者;第二组(n = 37)为对照组。我们评估了临床表现,疾病的记忆,体检结果,实验室和仪器检查的病人和尸检数据。结果:在记忆中,IICF患者比对照组患者更容易出现疾病:心律失常和电导率受损(88%对19%,优势比(OR): 30.0;95%可信区间(CI): 7.918 ~ 113.7, P < 0.001),系统性结缔组织疾病(78% vs. 5%, OR: 62.5;95% CI: 11.9 - 326.5, P < 0.001),病毒感染(包括严重急性呼吸综合征冠状病毒2 (SARS-CoV-2)) (53% vs. 19%, OR: 4.86;95% CI: 1.66 - 14.25, P = 0.003), 2型糖尿病(47%对8%,OR: 10.0;95% CI: 2.54 ~ 39.34, P < 0.001),纵隔淋巴瘤等肿瘤疾病(19% vs. 0%, P = 0.008), 12个月内局灶性感染(鼻窦炎、骨髓炎、牙周炎、肾炎、膀胱炎、肾盂肾炎、胸膜炎等)(31% vs. 11%, P = 0.069),慢性肾脏疾病(25% vs. 8%, P = 0.097),结核病(9% vs. 0%, P = 0.095)。我们发现两组之间存在统计学上的显著差异:纤维化区域的体积(17.5±9.2%和4.9±2.3%,P = 0.001), I型胶原蛋白的表达(5182±1301和2189±754年1平方毫米,P = 0.0001), III型胶原蛋白(7562±1405和2320±541年1平方毫米,P = 0.0001),基质金属蛋白酶(MMP) 2(12850±6200和9501±7145年1平方毫米,P = 0.005), MMP-9(15745±5695和6920±3125年1平方毫米,P = 0.0001), connexin-43(25689±14871和37523±12561年1平方毫米,P = 0.001),纤维连接蛋白(3,448±720比1,544±610,1 mm2, P = 0.0001)和转化生长因子β (TGF-β)(5,121±1,243比2,531±1,489,P = 0.001)。结论:IICF是一种独立的病理状态,是慢性心力衰竭的主要原因之一。它是由心肌结缔组织的变化引起的,这种变化阻止了心肌的正常功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Immobilizing Interstitial Cardiac Fibrosis.

Immobilizing Interstitial Cardiac Fibrosis.

Immobilizing Interstitial Cardiac Fibrosis.

Immobilizing Interstitial Cardiac Fibrosis.

Background: The alterations in the endomysium and perimysium might cause compaction and gradual mechanical compression of cardiomyocytes resulting in their immobilization. This process finally leads to severe stiffening, so that the newly formed frame around individual cardiomyocytes and their clusters hinders normal diastole, and later systole. This phenomenon is referred to as immobilizing interstitial cardiac fibrosis (IICF). Deciphering the molecular and structural elements of myocardial changes is the key to understanding the pathogenetic foundations of heart failure development.

Methods: The study included 69 patients. Group I (n = 32) included patients with IICF; group II (n = 37) was comparison group. We evaluated the clinical picture, anamnesis of the disease, the results of physical examination, laboratory and instrumental examination of patients and autopsy data.

Results: In the anamnesis, patients with IICF were more likely to have diseases than patients in the control group: arrhythmia and impaired conductivity (88% vs. 19%, odds ratio (OR): 30.0; 95% confidence interval (CI): 7.918 - 113.7, P < 0.001), systemic connective tissue diseases (78% vs. 5%, OR: 62.5; 95% CI: 11.9 - 326.5, P < 0.001), viral infections (including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)) (53% vs. 19%, OR: 4.86; 95% CI: 1.66 - 14.25, P = 0.003), type 2 diabetes mellitus (47% vs. 8%, OR: 10.0; 95% CI: 2.54 - 39.34, P < 0.001), radiation therapy for mediastinal lymphoma and other oncological diseases (19% vs. 0%, P = 0.008), focal infections (sinusitis, osteomyelitis, periodontitis, nephritis, cystitis, pyelonephritis, pleurisy, etc.) within 12 months (31% vs. 11%, P = 0.069), chronic kidney disease (25% vs. 8%, P = 0.097), and tuberculosis (9% vs. 0%, P = 0.095). We have identified a statistically significant difference between the groups: the volume of the fibrosis zone (17.5±9.2% vs. 4.9±2.3%, P = 0.001), the expression of type I collagen (5,182 ± 1,301 vs. 2,189 ± 754 in 1 mm2, P = 0.0001), type III collagen (7,562 ± 1,405 vs. 2,320 ± 541 in 1 mm2, P = 0.0001), matrix metalloproteinase (MMP)-2 (12,850 ± 6,200 vs. 9,501 ± 7,145 in 1 mm2, P = 0.005), MMP-9 (15,745 ± 5,695 vs. 6,920 ± 3,125 in 1 mm2, P = 0.0001), connexin-43 (25,689 ± 14,871 vs. 37,523 ± 12,561 in 1 mm2, P = 0.001), fibronectin (3,448 ± 720 vs. 1,544 ± 610 in 1 mm2, P = 0.0001), and transforming growth factor β (TGF-β) (5,121 ± 1,243 vs. 2,531 ± 1,489 in 1 mm2, P = 0.001).

Conclusion: IICF is a separate pathological condition and one of the main causes of chronic heart failure. It is induced by changes in the myocardial connective tissue that prevent normal functioning of the myocardium.

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来源期刊
Cardiology Research
Cardiology Research CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
2.50
自引率
0.00%
发文量
42
期刊介绍: Cardiology Research is an open access, peer-reviewed, international journal. All submissions relating to basic research and clinical practice of cardiology and cardiovascular medicine are in this journal''s scope. This journal focuses on publishing original research and observations in all cardiovascular medicine aspects. Manuscript types include original article, review, case report, short communication, book review, letter to the editor.
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