Markers of coagulation and platelet activation during percutaneous mitral valvuloplasty

被引:4
作者
Fernández, MA
Villa, P
España, F
Aznar, J
de Arellano, AR
Cebolla, R
机构
[1] La Fe Univ Hosp, Dept Clin Pathol, Valencia, Spain
[2] La Fe Univ Hosp, Res Ctr, Valencia, Spain
[3] La Fe Univ Hosp, Hemodynam Unit, Valencia, Spain
关键词
percutaneous mitral valvuloplasty; markers of coagulation; platelet activation; F1+2; TAT;
D O I
10.1097/00001721-199810000-00003
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
The effect of percutaneous mitral valvuloplasty (PMV) on markers of coagulation and platelet activation was investigated to assess whether coagulation or platelet activation take place during and after PMV even under conditions of full heparinization. Before PMV, all the hemostatic parameters studied were in the normal range compared with those of a control group. Two hours after PMV the levels of prothrombin fragment F1 and 2 (F1 + 2) (1.6 +/- 0.6 nmol/l versus 0.8 +/- 0.3 nmol/l, P < 0.005), plasma thrombin-antithrombin III (TAT) complexes (5.4 +/- 3.2 ng/ml versus 2.2 +/- 0.9 ng/ml) and beta-thromboglobulin (119 +/- 70 ng/ml versus 42.2 +/- 41 ng/ml) had increased significantly compared with those measured at basal conditions. Activated partial thromboplastin time was significantly prolonged (152 +/- 40 s versus 21 +/- 5 s), reflecting full heparinization. Levels of fibrinogen, F1 + 2, TAT and beta-thromboglobulin remained increased 72 h after PMV. We conclude that patients with severe, symptomatic mitral stenosis undergoing PMV need a more specific antithrombotic therapy or a more prolonged and perhaps less intensive heparinization. (C) 1998 Lippincott Williams & Wilkins.
引用
收藏
页码:581 / 585
页数:5
相关论文
共 27 条
[1]
ALTMAN R, 1976, J THORAC CARDIOV SUR, V72, P127
[2]
BOISCLAIR MD, 1993, THROMB HAEMOSTASIS, V70, P253
[3]
BRISTER SJ, 1993, THROMB HAEMOSTASIS, V70, P263
[4]
DANA CA, 1992, BR J HEART, V67, P170
[5]
SYSTEMIC EMBOLISM AS A COMPLICATION OF PERCUTANEOUS MITRAL VALVULOPLASTY [J].
DROBINSKI, G ;
MONTALESCOT, G ;
EVANS, J ;
NIVET, M ;
THOMAS, D ;
GROSGOGEAT, Y .
CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS, 1992, 25 (04) :327-330
[6]
ACTIVATED PROTEIN-C-ALPHA-1-ANTITRYPSIN (APC-ALPHA-1AT) COMPLEX AS A MARKER FOR INVITRO DIAGNOSIS OF PRETHROMBOTIC STATES [J].
ESPANA, F ;
GILABERT, J ;
VICENTE, V ;
ESTELLES, A ;
VAZQUEZ, L ;
HENDL, S ;
AZNAR, J .
THROMBOSIS RESEARCH, 1992, 66 (05) :499-508
[7]
COMPLEX-FORMATION BETWEEN PROTEIN-C INHIBITOR AND TISSUE-PLASMINOGEN ACTIVATOR DURING THROMBOLYTIC THERAPY - EVIDENCE OF ACTIVATION OF PROTEIN-C PATHWAY [J].
ESPANA, F ;
VICENTE, V ;
ESTELLES, A ;
VAZQUEZ, L ;
HENDL, S ;
SANCHEZCUENCA, J ;
AZNAR, J .
FIBRINOLYSIS, 1993, 7 (05) :308-315
[8]
DETERMINATION OF PLASMA PROTEIN-C INHIBITOR AND OF 2 ACTIVATED PROTEIN-C-INHIBITOR COMPLEXES IN NORMALS AND IN PATIENTS WITH INTRAVASCULAR COAGULATION AND THROMBOTIC DISEASE [J].
ESPANA, F ;
VICENTE, V ;
TABERNERO, D ;
SCHARRER, I ;
GRIFFIN, JH .
THROMBOSIS RESEARCH, 1990, 59 (03) :593-608
[9]
FAILURE OF FIXED-DOSE INTRAVENOUS HEPARIN TO SUPPRESS INCREASES IN THROMBIN ACTIVITY AFTER CORONARY THROMBOLYSIS WITH STREPTOKINASE [J].
GALVANI, M ;
ABENDSCHEIN, DR ;
FERRINI, D ;
OTTANI, F ;
RUSTICALI, F ;
EISENBERG, PR .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1994, 24 (06) :1445-1452
[10]
HYNES TM, 1986, CHEST, V89, pS26