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Blood coagulability and fibrinolytic activity before and after physical training during the recovery phase of acute myocardial infarction
Author(s) -
Suzuki Toshikazu,
Yamauchi Kazunobu,
Yamada Yoshiji,
Furumichi Takeo,
Furui Hirohiko,
Tsuzuki Jitsuki,
Hayashi Hiroshi,
Sotobata Iwao,
Saito Hidehiko
Publication year - 1992
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960150510
Subject(s) - medicine , fibrinogen , partial thromboplastin time , plasmin , tissue plasminogen activator , fibrinolysis , antithrombin , myocardial infarction , plasminogen activator , prothrombin time , physical exercise , hematocrit , coagulation , endocrinology , heparin , biochemistry , enzyme , chemistry
The effects of physical training on hemostatic parameters were evaluated in 56 postmyocardial infarction (MI) patients before and after one month of systematic physical training and in 30 control post‐MI patients, who did not undergo such training. There were no significant changes in prothrombin time (PT) and alpha 1 ‐ antitrypsin (α 1 AT) at the beginning and end of the study in either group. Levels of fibrinogen, Factor VIII: C (VIILC) and von Wildebrand antigen (vWf:Ag), and activities of ATIII and plasminogen (Plg) were significantly decreased in the group with physical training (p<0.05), while values were unchanged in the control group. Hematocrit, platelet counts, and alpha 2 ‐plasmin inhibitor (α 2 PI) activities also decreased in the physical training group (p< 0.05). In contrast, these variables increased in the control group (p <0.05). Activated partial thromboplastin time (aPTT) tended to be prolonged in the group with physical training, while it was shortened in the control group. In a subset of 20 patients with physical training, resting levels of plasmin‐α 2 PI complex (PIC), thrombin‐antithrombin III complex (TAT), protein‐C (P‐C:Ag), plasminogen activator inhibitor‐1 (PAI‐1), VII:C, and P‐C activities had significantly decreased after one month of physical training (p<0.05), although tissue plasminogen activator activities remained unchanged. Physical training appeared to suppress coagulability as indicated by the decrease in fibrinogen, VIII:C, vWf:Ag, VII:C, and TAT, and prolongation of aPTT. The decrease in plasminogen, t‐PA:Ag, α 2 PI, PAI‐1, and PIC after physical training may result from the decreased coagulability. In conclusion, physical training appears to induce a suppression of the coagulation system in patients in the recovery phase of MI.

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