Russian Heart Failure Journal 2011year Arterial wall structure and functions in patients with chronic heart failure of ischemic etiology depending on level of left ventricular ejection fraction
Arterial wall structure and functions in patients with chronic heart failure of ischemic etiology depending on level of left ventricular ejection fraction
Koziolova N. A., Cherniavina A. I., Surovtseva M. V., Eltsova M. A.
Keywords: arterial stiffness, left ventricle, EF, CHF
DOI: 10.18087/ rhfj.2011.6.1602
Relevance. Processes of revascularization include proliferation of artery smooth muscle cells with the further increase of their rigidity, as well as the change of intercellular matrix with the increase of media collagen content and the subsequent development of fibrosis. In this connection, studying of arterial wall fibrosis markers in patients with CHF became of higher interest. Purpose. The study of structure and functional features of arterial wall in patients with CHF of ischemic etiology. Materials and methods. 90 patients with stable II–III class CHF of ischemic etiology were enrolled to the study. Clinical symptoms were estimated by V. Yu. Mareev SHOKS scale (assessment scale of the clinical status), LV systolic function by Doppler EchoCG, artery conduction and damping functions by means of volume sphygmoplethysmography. Assays of NT-proBNP, c-terminal telopeptide of type 1 collagen and tissue inhibitor of matrix metalloproteinase-1 was determined. Results. Abnormal structure and functions of arterial wall was registered both in patients with preserved and decreased LVEF, and it was characterized by increased vascular wall stiffness, decreased elasticity and extensibility, one of its development factors was damage of the artery collagen intercellular matrix structure. Change of arterial wall depended on CHF severity (first of all, NT-proBNP level) and functional class of stable angina.
- Dzau V. The cardiovascular continuum and renin-angiotensin-aldosterone system blockade. J Hypertens Suppl. 2005;23 (1):S9–17.
- Tartière JM, Logeart D, Safar ME, Cohen-Solal A. Interaction between pulse wave velocity, augmentation index, pulse pressure and left ventricular function in chronic heart failure. J Hum Hypertens. 2006;20 (3):213–219.
- Deschamps AM, Spinale FG. Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation. Cardiovasc Res. 2006;69 (3):666–676.
- Vorovich EE, Chuai S, Li M et al. Comparison of matrix metalloproteinase 9 and brain natriuretic peptide as clinical biomarkers in chronic heart failure. Am Heart J. 2008;155 (6):992–997.
- Капелько В. И. Ремоделирование миокарда: роль матриксных металлопротеиназ. Кардиология. 2001;41 (6):49–55.
- Chatzikyriakou SV, Tziakas DN, Chalikias GK et al. Serum levels of collagen type-I degradation markers are associated with vascular stiffness in chronic heart failure patients. Eur J Heart Fail. 2008;10 (12):1181–1185.
- Spinale F. Matrix metalloproteinases: regulation and dysregulation in the failing heart. Circ Res. 2002;90 (5):520–530.
- Buralli S, Dini FL, Ballo P et al. Circulating matrix metalloproteinase-3 and metalloproteinase-9 and tissue Doppler measures of diastolic dysfunction to risk stratify patients with systolic heart failure. Am J Cardiol. 2010;105 (6):853–836.
- Manhenke C, Orn S, Squire I et al. The prognostic value of circulating markers of collagen turnover after acute myocardial infarction. Int J Cardiol. 2011;150 (3):277–282.
- Ciccone MM, Iacoviello M, Puzzovivo A et al. Clinical correlates of endothelial function in chronic heart failure. Clin Res Cardiol. 2011;100 (6):515–521.
- Naka KK, Tweddel AC, Doshi SN et al. Flow-mediated changes in pulse wave velocity: a new clinical measure of endothelial function. Eur Heart J. 2006;27 (3):302–309.
- Tomiyama H, Yamashina A. Non-invasive vascular function tests: their pathophysiological background and clinical application. Circ J. 2010;74 (1):24–33.
- Shuai XX, Chen YY, Lu YX et al. Diagnosis of heart failure with preserved ejection fraction: which parameters and diagnostic strategies are more valuable? Eur J Heart Fail. 2011;13 (7):737–745.
- Parekh N, Maisel AS. Utility of B-natriuretic peptide in the evaluation of left ventricular diastolic function and diastolic heart failure. Curr Opin Cardiol. 2009;24 (2):155–160.
- Förstermann U. Nitric oxide and oxidative stress in vascular disease. Pflugers Arch. 2010;459 (6):923–939.
- Tasatargil A, Tekcan M, Celik-Ozenci C et al. Aldosterone-induced endothelial dysfunction of rat aorta: role of poly (ADP-ribose) activation. J Renin Angiotensin Aldosterone Syst. 2009;10 (3):127–137.
- An SJ, Boyd R, Zhu M et al. NADPH oxidase mediates angiotensin II-induced endothelin-1 expression in vascular adventitial fibroblasts. Cardiovasc Res. 2007;75 (4):702–709.
- Xie YJ, Wang SQ, Chen JS et al. The effect of Aldosterone on the proliferation and collagen production of cardiac fibroblasts. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2011;27 (4):386–388.
- Maron BA, Zhang YY, Handy DE et al. Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells. J Biol Chem. 2009;284 (12):7665–7672.
- Manso AM, Elsherif L, Kang SM, Ross RS. Integrines, membrane-type matrix metalloproteinases and ADAMs: potential implications for cardiac remodeling. Cardiovasc Res. 2006;69 (3):574–584.
- Deardorff R, Spinale F. G. Cytokines and matrix metalloproteinases as potential biomarkers in chronic heart failure. Biomark Med. 2009;3 (5):513–523.
- Heymans S, Hirsch E, Anker SD et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2009;11 (2):119–129.
- Tyagi SC, Lewis K, Pikes D et al. Stretch-indused membrane-type matrix metalloproteinase and tissue plasminogen activator in cardiac fibroblast cell. J Cell Physiol. 1998;176 (2):374–382.
Koziolova N.A., Cherniavina A.I., Surovtseva M.V. et al. Arterial wall structure and functions in patients with chronic heart failure of ischemic etiology depending on level of left ventricular ejection fraction. Russian Heart Failure Journal. 2011;12(6):350-354.