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

被引:41
作者
Orn, Stein [1 ]
Manhenke, Cord [1 ]
Squire, Iain B. [2 ]
Ng, Leong [2 ]
Anand, Inder [3 ,4 ]
Dickstein, Kenneth [1 ]
机构
[1] Univ Bergen, Stavanger Univ Hosp, N-4068 Stavanger, Norway
[2] Univ Leicester, Leicester LE1 7RH, Leics, England
[3] Univ Minnesota, Minneapolis, MN USA
[4] VA Med Ctr, Minneapolis, MN USA
关键词
long-term remodeling; scarring; myocardial infarction; natriuretic peptides; gelatinases; cardiac magnetic resonance;
D O I
10.1016/j.cardfail.2007.07.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Altered activity of the matrix metalloproteinases (MMP-2 and -9), has been implicated in the left ventricular (LV) remodeling process occurring after myocardial infarction (MI). In the acute phase, a relation between plasma MMP-9 levels and parameters of LV dysfunction has been demonstrated. The relationship in long-term survivors has not been investigated. We studied the relationships of these biochemical markers, and N-terminal pro-B-type natriuretic peptide (N-BNP), with measures of long-term LV remodeling. Methods and Results: Plasma levels of N-BNP, MMP-2, and MMP-9 were measured at randomization, I month, I year, and > 4 years after complicated AMI. Contrast-enhanced cardiac magnetic resonance (CMR) was performed at 4.4 (+/- 4) years in 52 clinically stable long-term survivors of the index AMI. We assessed the relationships of plasma N-BNP, MMP-2, and MMP-9 with myocardial scarring, and measures of long-term LV remodeling. Compared with a reference population, N-BNP and MMP-9 levels were increased at all time points from the acute phase until > 4 years after MI. Plasma N-BNP and MMP-9 correlated only in the subacute phase (randomization, mean 3.3 days after MI) days after acute MI (r = 0.38, P =.006). At CMR assessment >= 4 years, log MMP-9 level was inversely related to LV ejection fraction (P =.002) and nonscarred myocardial mass (P =.008). This relationship was independent of MMP-2. Log N-BNP was related to end diastolic volume index (P =.0002). There was no correlation between log MMP-9 and LV volumes. Conclusion: There is a time-dependent relationship between plasma N-BNP and MMP-9 levels, these peptides correlating only in the acute phase after MI. In long-term follow-up, plasma MMP-9 and N-BNP levels were related to different parameters of LV remodeling. These findings suggest that in long-term survivors of complicated MI, different mechanisms modulate plasma levels of MMP-9 and N-BNP.
引用
收藏
页码:843 / 849
页数:7
相关论文
共 42 条
[1]   Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonance [J].
Bellenger, NG ;
Davies, LC ;
Francis, JM ;
Coats, AJS ;
Pennell, DJ .
JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE, 2000, 2 (04) :271-278
[2]   REGULATION OF COLLAGEN DEGRADATION IN THE RAT MYOCARDIUM AFTER INFARCTION [J].
CLEUTJENS, JPM ;
KANDALA, JC ;
GUARDA, E ;
GUNTAKA, RV ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (06) :1281-1292
[3]   Defects in matrix metalloproteinase inhibitory stoichiometry and selective MMP induction in patients with nonischemic or ischemic dilated cardiomyopathy [J].
Coker, ML ;
Zellner, JL ;
Crumbley, AJ ;
Spinale, FG .
INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC APPLICATIONS, 1999, 878 :559-562
[4]   Matrix metalloproteinase inhibition after myocardial infarction - A new approach to prevent heart failure? [J].
Creemers, EEJM ;
Cleutjens, JPM ;
Smits, JFM ;
Daemen, MJAP .
CIRCULATION RESEARCH, 2001, 89 (03) :201-210
[5]   Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAL randomised trial [J].
Dickstein, K ;
Kjekshus, J .
LANCET, 2002, 360 (9335) :752-760
[6]   Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction [J].
Gerber, BL ;
Garot, J ;
Bluemke, DA ;
Wu, KC ;
Lima, JAC .
CIRCULATION, 2002, 106 (09) :1083-1089
[7]   Evaluation of impaired left ventricular ejection fraction and increased dimensions by multiple neurohumoral plasma concentrations [J].
Groenning, BA ;
Nilsson, JC ;
Sondergaard, L ;
Kjaer, A ;
Larsson, HBW ;
Hildebrandt, PR .
EUROPEAN JOURNAL OF HEART FAILURE, 2001, 3 (06) :699-708
[8]   Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure [J].
Heymans, S ;
Luttun, A ;
Nuyens, D ;
Theilmeier, G ;
Creemers, E ;
Moons, L ;
Dyspersin, GD ;
Cleutjens, JPM ;
Shipley, M ;
Angellilo, A ;
Levi, M ;
Nübe, O ;
Baker, A ;
Keshet, E ;
Lupu, F ;
Herbert, JM ;
Smits, JFM ;
Shapiro, SD ;
Baes, M ;
Borgers, M ;
Collen, D ;
Daemen, MJAP ;
Carmeliet, P .
NATURE MEDICINE, 1999, 5 (10) :1135-1142
[9]   Plasma levels of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 are increased in the coronary circulation in pa with acute coronary syndrome [J].
Inokubo, Y ;
Hanada, H ;
Ishizaka, H ;
Fukushi, T ;
Kamada, T ;
Okumura, K .
AMERICAN HEART JOURNAL, 2001, 141 (02) :211-217
[10]   Matrix metalloproteinases: A review of their structure and role in acute coronary syndrome [J].
Jones, CB ;
Sane, DC ;
Herrington, DM .
CARDIOVASCULAR RESEARCH, 2003, 59 (04) :812-823