Impact of percutaneous coronary intervention on biomarker levels in patients in the subacute phase following myocardial infarction: the Occluded Artery Trial (OAT) biomarker ancillary study

BMC Cardiovascular Disorders

Judith Hochman²  Daner Li⁶  Sandra Forman⁶  Grzegorz Skonieczny⁹  Anna Raczynska⁹  Krystyna Jaworska⁹  Wojciech Jablonski⁸  Elzbieta Zinka⁸  Benita Busz-Papież⁴  Michal Kurowski⁴  Piotr Czunko⁵  Krzysztof Zmudka⁵  Grzegorz Opolski³  Marek Roik³  Jadwiga Janas⁷  Witold Rużyłło⁷  Zygmunt Sadowski⁷  Jacek Kądziela⁷  Venu Menon¹  Mariusz Kruk⁷ 

[1] Cleveland Clinic, Cleveland, Ohio, USA;New York University School of Medicine, New York, New York, USA;Medical University, Warsaw, Poland;County Hospital, Szczecin, Poland;John Paul II Hospital, Krakow, Poland;Clinical Trials and Surveys Corporation, Owings Mills, MD, USA;Institute of Cardiology, Warsaw, Poland;County Hospital, Koszalin, Poland;County Hospital, Toruń, Poland

关键词: Remodeling;    Heart failure;    Biomarkers;    Percutaneous coronary intervention;    Acute coronary syndrome;   

Others  :  856750
DOI  :  10.1186/1471-2261-13-91

 received in 2012-12-18, accepted in 2013-09-18,  发布年份 2013

【 摘 要 】

Background

The purpose of the Occluded Artery Trial (OAT) Biomarker substudy was to evaluate the impact of infarct related artery (IRA) revascularization on serial levels of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and dynamics of other biomarkers related to left ventricular remodeling, fibrosis and angiogenesis.

Methods

Patients were eligible for OAT-Biomarker based on the main OAT criteria. Of 70 patients (age 60.8 ± 8.8, 25% women) enrolled in the substudy, 37 were randomized to percutaneous coronary intervention (PCI) and 33 to optimal medical therapy alone. Baseline serum samples were obtained prior to OAT randomization with follow up samples taken at one year. The primary outcome was percent change of NT-proBNP from baseline to 1 year. The secondary outcomes were respective changes of matrix metalloproteinases (MMP) 2 and 9, tissue inhibitor of matrix metalloproteinase 2 (TIMP-2), Vascular Endothelial Growth Factor (VEGF), and Galectin-3.

Results

Paired (baseline and one-year) serum samples were obtained in 62 subjects. Baseline median NT-proBNP level was 944.8 (455.3, 1533) ng/L and decreased by 69% during follow-up (p < 0.0001). Baseline MMP-2 and TIMP-2 levels increased significantly from baseline to follow-up (p = 0.034, and p = 0.027 respectively), while MMP-9 level decreased from baseline (p = 0.038). Levels of VEGF and Galectin-3 remained stable at one year (p = NS for both). No impact of IRA revascularization on any biomarker dynamics were noted.

Conclusions

There were significant changes in measured biomarkers related to LV remodeling, stress, and fibrosis following MI between 0 and 12 month. Establishing infarct vessel patency utilizing stenting 24 hours-28 days post MI did not however influence the biomarkers’ release.

【 授权许可】

   
2013 Kruk et al.; licensee BioMed Central Ltd.

【 图 表 】

【 参考文献 】

• [1]Sadanandan S, Buller C, Menon V, Dzavik V, Terrin M, Thompson B, Lamas G, Hochman JS: The late open artery hypothesis–a decade later. Am Heart J 2001, 142:411-421.
• [2]Hochman JS, Lamas GA, Buller CE, et al.: Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med 2006, 355:2395-2407.
• [3]Udelson JE, Pearte CA, Kimmelstiel CD, et al.: The Occluded Artery Trial (OAT) Viability Ancillary Study (OAT-NUC): influence of infarct zone viability on left ventricular remodeling after percutaneous coronary intervention versus optimal medical therapy alone. Am Heart J 2011, 161:611-621.
• [4]Levin ER, Gardner DG, Samson WK: Natriuretic peptides. N Engl J Med 1998, 339:321-328.
• [5]Goetze JP, Christoffersen C, Perko M, et al.: Increased cardiac BNP expression associated with myocardial ischemia. FASEB J 2003, 17:1105-1107.
• [6]Goetze JP, Gore A, Møller CH, Steinbrüchel DA, Rehfeld JF, Nielsen LB: Acute myocardial hypoxia increases BNP gene expression. FASEB J 2004, 18:1928-1930.
• [7]Richards AM, Nicholls MG, Yandle TG, et al.: Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardial infarction. Circulation 1998, 97:1921-1929.
• [8]Gackowski A, Isnard R, Golmard JL, et al.: Comparison of echocardiography and plasma B-type natriuretic peptide for monitoring the response to treatment in acute heart failure. Eur Heart J 2004, 25:1788-1796.
• [9]Michtalik HJ, Yeh HC, Campbell CY, et al.: Acute changes in N-terminal pro-B-type natriuretic peptide during hospitalization and risk of readmission and mortality in patients with heart failure. Am J Cardiol 2011, 107:1191-1195.
• [10]Jernberg T, Lindahl B, Siegbahn A, et al.: N-terminal pro-brain natriuretic peptide in relation to inflammation, myocardial necrosis, and the effect of an invasive strategy in unstable coronary artery disease. J Am Coll Cardiol 2003, 42:1909-1916.
• [11]Dzavík V, Buller CE, Lamas GA, et al.: Randomized trial of percutaneous coronary intervention for subacute infarct-related coronary artery occlusion to achieve long-term patency and improve ventricular function: the Total Occlusion Study of Canada (TOSCA)-2 trial. Circulation 2006, 114:2449-2457.
• [12]van Veldhuisen DJ, Genth-Zotz S, Brouwer J, et al.: High- versus low-dose ACE inhibition in chronic heart failure: a double-blind, placebo-controlled study of imidapril. J Am Coll Cardiol 1998, 32:1811-1818.
• [13]Vanhoutte D, Schellings M, Pinto Y, Heymans S: Relevance of matrix metalloproteinases and their inhibitors after myocardial infarction: a temporal and spatial window. Cardiovasc Res 2006, 69:604-613.
• [14]Herzog E, Gu A, Kohmoto T, Burkhoff D, Hochman JS: Early activation of metalloproteinases after experimental myocardial infarction occurs in infarct and non-infarct zones. Cardiovasc Pathol 1998, 7:307-312.
• [15]Peterson JT, Hallak H, Johnson L, et al.: Matrix metalloproteinase inhibition attenuates left ventricular remodeling and dysfunction in a rat model of progressive heart failure. Circulation 2001, 103:2303-2309.
• [16]Spinale FG: Matrix metalloproteinases: regulation and dysregulation in the failing heart. Circ Res 2002, 90:520-530.
• [17]Webb CS, Bonnema DD, Ahmed SH: Specific temporal profile of matrix metalloproteinase release occurs in patients after myocardial infarction: relation to left ventricular remodeling. Circulation 2006, 114:1020-1027.
• [18]Orn S, Manhenke C, Squire IB, Ng L, Anand I, Dickstein K: Plasma MMP-2, MMP-9 and N-BNP in long-term survivors following complicated myocardial infarction: relation to cardiac magnetic resonance imaging measures of left ventricular structure and function. J Cardiac Fail 2007, 13:843-849.
• [19]Kelly D, Cockerill G, Ng LL, Thompson M, Khan S, Samani NJ, Squire IB: Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study. Eur Heart J 2007, 28:711-718.
• [20]Hudson MP, Armstrong PW, Ruzyllo W, et al.: Effects of selective matrix metalloproteinase inhibitor (PG-116800) to prevent ventricular remodeling after myocardial infarction: results of the PREMIER (Prevention of Myocardial Infarction Early Remodeling) trial. J Am Coll Cardiol 2006, 48:15-20.
• [21]Squire IB, Evans J, Ng LL, Loftus IM, Thompson MM: Plasma MMP-9 and MMP-2 following acute myocardial infarction in man: correlation with echocardiographic and neurohumoral parameters of left ventricular dysfunction. J Card Fail 2004, 10:328-333.
• [22]Matsunaga T, Abe N, Kameda K, et al.: Circulating level of gelatinase activity predicts ventricular remodeling in patients with acute myocardial infarction. Int J Cardiol 2005, 105:203-208.
• [23]Goldberg GI, Strongin A, Collier IE, Genrich LT, Marmer BL: Interaction of 92-kDa type IV collagenase with the tissue inhibitor of metalloproteinases prevents dimerization, complex formation with interstitial collagenase, and activation of the proenzyme with stromelysin. J Biol Chem 1992, 267:4583-4591.
• [24]Sato H, Takino T, Kinoshita T, et al.: Cell surface binding and activation of gelatinase A induced by expression of membrane-type-1-matrix metalloproteinase (MT1-MMP). FEBS Lett 1996, 385:238-240.
• [25]Kandalam V, Basu R, Abraham T, et al.: TIMP2 deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activation. Circ Res 2010, 106:796-808.
• [26]Hojo Y, Ikeda U, Zhu Y, et al.: Expression of vascular endothelial growth factor in patients with acute myocardial infarction. J Am Coll Cardiol 2000, 35:968-973.
• [27]Heeschen C, Dimmeler S, Hamm CW, et al.: Prognostic significance of angiogenic growth factor serum levels in patients with acute coronary syndromes. Circulation 2003, 107:524-530.
• [28]de Boer RA, Yu L, van Veldhuisen DJ: Galectin-3 in cardiac remodeling and heart failure. Curr Heart Fail Rep 2010, 7:1-8.
• [29]Sharma UC, Pokharel S, van Brakel TJ: Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Circulation 2004, 110:3121-3128.
• [30]van Kimmenade RR, Januzzi JL Jr, Ellinor PT, et al.: Utility of amino-terminal pro-brain natriuretic peptide, galectin-3, and apelin for the evaluation of patients with acute heart failure. J Am Coll Cardiol 2006, 48:1217-1224.