Kallergis Eleftherios M, Manios Emmanuel G, Kanoupakis Emmanuel M, Mavrakis Hercules E, Arfanakis Dimitris A, Maliaraki Niki E, Lathourakis Chrisovalantis E, Chlouverakis Gregory I, Vardas Panos E
Department of Cardiology, University Hospital of Heraklion, Crete, Greece.
J Am Coll Cardiol. 2008 Jul 15;52(3):211-5. doi: 10.1016/j.jacc.2008.03.045.
We investigated whether the serum markers of collagen turnover differed in various forms of atrial fibrillation (AF) and in sinus rhythm (SR) in humans.
Structural alterations and fibrosis have been implicated in the generation and perpetuation of AF.
Serum C-terminal propeptide of collagen type-I (CICP), C-terminal telopeptide of collagen type-I (CITP), matrix metalloproteinase-1, and tissue inhibitor of matrix metalloproteinases-1 were measured as markers of collagen synthesis and degradation in 70 patients with AF and 20 healthy control subjects in SR.
C-terminal propeptide of collagen type-I and CITP were significantly higher in AF patients than in control subjects (91 +/- 27 ng/ml vs. 67 +/- 11 ng/ml, p < 0.001 and 0.38 +/- 0.20 ng/ml vs. 0.25 +/- 0.08 ng/ml, p < 0.001, respectively). Persistent AF patients had higher levels of CICP (105 +/- 28 ng/ml vs. 80 +/- 21 ng/ml, p < 0.001), but not CITP, compared with those with paroxysmal AF. Patients with persistent AF had lower levels of matrix metalloproteinase-1 but increased levels of tissue inhibitor of matrix metalloproteinases-1 compared with patients with paroxysmal AF (11.90 +/- 4.79 ng/ml vs. 14.98 +/- 6.28 ng/ml, p = 0.03 and 155 +/- 45 ng/ml vs. 130 +/- 38 ng/ml, p < 0.001, respectively). Tissue inhibitor of matrix metalloproteinases-1 levels were significantly lower in control subjects compared with those in both paroxysmal and persistent AF patients (102 +/- 15 ng/ml vs. 130 +/- 38 ng/ml vs. 155 +/- 45 ng/ml, respectively, p < 0.001).
Serum markers of collagen type-I turnover differed significantly between patients with AF and SR. Furthermore, these markers also differed significantly between paroxysmal and persistent AF patients, suggesting that the intensity of the extracellular synthesis and degradation of collagen type-I may be related to the burden or type of AF.
我们研究了人类不同类型心房颤动(AF)和窦性心律(SR)患者的胶原代谢血清标志物是否存在差异。
结构改变和纤维化与房颤的发生及持续存在有关。
测量了70例房颤患者和20例窦性心律健康对照者的血清I型胶原C端前肽(CICP)、I型胶原C端肽(CITP)、基质金属蛋白酶-1和基质金属蛋白酶组织抑制剂-1,作为胶原合成和降解的标志物。
房颤患者的I型胶原C端前肽和CITP显著高于对照组(分别为91±27 ng/ml对67±11 ng/ml,p<0.001;0.38±0.20 ng/ml对0.25±0.08 ng/ml,p<0.001)。与阵发性房颤患者相比,持续性房颤患者的CICP水平更高(105±28 ng/ml对80±21 ng/ml,p<0.001),但CITP水平无差异。与阵发性房颤患者相比,持续性房颤患者的基质金属蛋白酶-1水平较低,但基质金属蛋白酶组织抑制剂-1水平升高(分别为11.90±4.79 ng/ml对14.98±6.28 ng/ml,p=0.03;155±45 ng/ml对130±38 ng/ml,p<0.001)。基质金属蛋白酶组织抑制剂-1水平在对照组显著低于阵发性和持续性房颤患者(分别为102±15 ng/ml对130±38 ng/ml对155±45 ng/ml,p<0.001)。
房颤患者和窦性心律患者的I型胶原代谢血清标志物存在显著差异。此外,这些标志物在阵发性和持续性房颤患者之间也存在显著差异,提示I型胶原细胞外合成和降解的强度可能与房颤的负荷或类型有关。