Cystatin C levels are decreased in acute myocardial infarction - Effect of cystatin C G73A gene polymorphism on plasma levels

被引:29
作者
Noto, D
Cefalu, AB
Barbagallo, CM
Pace, A
Rizzo, M
Marino, G
Caldarella, R
Castello, A
Pernice, V
Notarbartolo, A
Averna, MR
机构
[1] Univ Palermo, Dept Internal Med & Geriatr, I-90127 Palermo, Italy
[2] Buccheri La Ferla Hosp, Div Cardiol, Palermo, Italy
[3] Villa Maria Eleonora Hosp, Div Cardiol, Palermo, Italy
关键词
cystatin C; coronary artery disease; acute myocardial infarction; unstable angina;
D O I
10.1016/j.ijcard.2004.03.018
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Cystatin C is the most abundant protease inhibitor in the plasma. Low plasma levels have been found in patients with aortic aneurysms and they seem correlated with the extension of the aortic lesions in early aneurysms detected by ultrasonography. Methods: In this study, plasma levels of cystatin C have been investigated in patients with acute myocardial infarction (AMI), unstable angina and controls. The effect on plasma levels of the G73A polymorphism of the CST3 gene has been also evaluated. Results: Patients with acute myocardial infarction showed significantly lower levels of cystatin C compared to unstable angina and controls, but levels were nearly normal in a week after the acute event. The genotype distribution of the G73A polymorphism was not different among the groups. Nevertheless, cystatin C levels decreased proportionally with the number of A alleles. Cystatin C levels were positively correlated with age, triglyceride/HDL cholesterol ratio and creatinine, and negatively with HDL cholesterol and the number of A alleles. All variables, but not HDL cholesterol, were independently correlated in a multivariate analysis. Conclusions: Cystatin C is decreased in acute myocardial infarction. It is still not clear whether lower cystatin C levels are causally linked to the acute event or just represent a negative acute phase response. The CST3 gene G73A polymorphism functionally affects cystatin C plasma levels. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:213 / 217
页数:5
相关论文
共 22 条
[1]   THE HUMAN CYSTATIN-C GENE (CST3), MUTATED IN HEREDITARY CYSTATIN-C AMYLOID ANGIOPATHY, IS LOCATED ON CHROMOSOME-20 [J].
ABRAHAMSON, M ;
ISLAM, MQ ;
SZPIRER, J ;
SZPIRER, C ;
LEVAN, G .
HUMAN GENETICS, 1989, 82 (03) :223-226
[2]   Myocardial infarction redefined -: A consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction [J].
Alpert, JS ;
Antman, E ;
Apple, F ;
Armstrong, PW ;
Bassand, JP ;
de Luna, AB ;
Beller, G ;
Breithardt, G ;
Chaitman, BR ;
Clemmensen, P ;
Falk, E ;
Fishbein, MC ;
Galvani, M ;
Garson, A ;
Grines, C ;
Hamm, C ;
Hoppe, U ;
Jaffe, A ;
Katus, H ;
Kjekshus, J ;
Klein, W ;
Klootwijk, P ;
Lenfant, C ;
Levy, D ;
Levy, RI ;
Luepker, R ;
Marcus, F ;
Näslund, U ;
Ohman, M ;
Pahlm, O ;
Poole-Wilson, P ;
Popp, R ;
Pyörälä, K ;
Ravkilde, J ;
Rehnquist, N ;
Roberts, W ;
Roberts, R ;
Roelandt, J ;
Rydén, L ;
Sans, S ;
Simoons, ML ;
Thygesen, K ;
Tunstall-Pedoe, H ;
Underwood, R ;
Uretsky, BF ;
de Werf, FV ;
Voipio-Pulkki, LM ;
Wagner, G ;
Wallentin, L ;
Wijns, W .
EUROPEAN HEART JOURNAL, 2000, 21 (18) :1502-1513
[3]   Cellular processing of the amyloidogenic cystatin C variant of hereditary cerebral hemorrhage with amyloidosis, Icelandic type [J].
Benedikz, E ;
Merz, GS ;
Schwenk, V ;
Johansen, TE ;
Wisniewski, HM ;
Rushbrook, JI .
AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS, 1999, 6 (03) :172-182
[4]   Intracellular accumulation of the amyloidogenic L68Q variant of human cystatin C in NIH/3T3 cells [J].
Bjarnadottir, M ;
Wulff, BS ;
Sameni, M ;
Sloane, BF ;
Keppler, D ;
Grubb, A ;
Abrahamson, M .
JOURNAL OF CLINICAL PATHOLOGY-MOLECULAR PATHOLOGY, 1998, 51 (06) :317-326
[5]   ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction [J].
Braunwald, E ;
Antman, EM ;
Beasley, JW ;
Califf, RM ;
Cheitlin, MD ;
Hochman, JS ;
Jones, RH ;
Kereiakes, D ;
Kupersmith, J ;
Levin, TN ;
Pepine, CJ ;
Schaeffer, JW ;
Smith, EE ;
Steward, DE ;
Theroux, P ;
Gibbons, RJ ;
Alpert, JS ;
Eagle, KA ;
Faxon, DP ;
Fuster, V ;
Gardner, TJ ;
Gregoratos, G ;
Russell, RO ;
Smith, SC .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2000, 36 (03) :970-1056
[6]   Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation [J].
Carmeliet, P ;
Moons, L ;
Lijnen, HR ;
Baes, M ;
Lemaitre, V ;
Tipping, P ;
Drew, A ;
Eeckhout, Y ;
Shapiro, S ;
Lupu, F ;
Collen, D .
NATURE GENETICS, 1997, 17 (04) :439-444
[7]  
GAMERO P, 1998, J BIOL CHEM, V273, P32347
[8]   Human cathepsin K cleaves native type I and II collagens at the N-terminal end of the triple helix [J].
Kafienah, W ;
Brömme, D ;
Buttle, DJ ;
Croucher, LJ ;
Hollander, AP .
BIOCHEMICAL JOURNAL, 1998, 331 :727-732
[9]   Macrophages and atherosclerotic plaque stability [J].
Libby, P ;
Geng, YJ ;
Aikawa, M ;
Schoenbeck, U ;
Mach, F ;
Clinton, SK ;
Sukhova, GK ;
Lee, RT .
CURRENT OPINION IN LIPIDOLOGY, 1996, 7 (05) :330-335
[10]   MOLECULAR-BASES OF THE ACUTE CORONARY SYNDROMES [J].
LIBBY, P .
CIRCULATION, 1995, 91 (11) :2844-2850