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Fibrinolytic adaptations to a phase ...
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Nagelkirk, Paul Robert.
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Fibrinolytic adaptations to a phase II cardiac rehabilitation program.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Fibrinolytic adaptations to a phase II cardiac rehabilitation program./
作者:
Nagelkirk, Paul Robert.
面頁冊數:
64 p.
附註:
Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4719.
Contained By:
Dissertation Abstracts International66-09B.
標題:
Health Sciences, Medicine and Surgery. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3189714
ISBN:
9780542323881
Fibrinolytic adaptations to a phase II cardiac rehabilitation program.
Nagelkirk, Paul Robert.
Fibrinolytic adaptations to a phase II cardiac rehabilitation program.
- 64 p.
Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4719.
Thesis (Ph.D.)--Michigan State University, 2005.
Fibrinolysis, the process of dissolving a fibrin blood clot, plays a pivotal role in the development of vascular disease. Occlusive blood clots are responsible for most acute cardiovascular events, and patients with coronary artery disease (CAD) typically exhibit a blunted fibrinolytic capacity. Initiation of fibrinolysis involves the conversion of plasminogen to plasmin, which is primarily catalyzed by tissue plasminogen activator (tPA). Depressed tPA and elevations of its primary inhibitor, plasminogen activator inhibitor-1 (PAI-1) are associated with morbidity, mortality, and are independent risk factors for various cardiovascular outcomes. Exercise training promotes enhanced fibrinolytic potential in healthy individuals, and individuals with CAD who undergo 12 or more weeks of regular exercise as part of a cardiac rehabilitation program demonstrate improvements in tPA and PAI-1. Modern day third-party reimbursement practices often necessitate fewer than 12 weeks of exercise training in cardiac rehabilitation programs. It is unclear if training regimens shorter than 12 weeks will elicit fibrinolytic improvements. The purpose of the present study was to evaluate changes in plasma concentrations of tPA and PAI-1, as well as changes in expression of the tPA and PAI-1 genes in whole blood after three and six weeks of participation in a phase II cardiac rehabilitation program.
ISBN: 9780542323881Subjects--Topical Terms:
1017756
Health Sciences, Medicine and Surgery.
Fibrinolytic adaptations to a phase II cardiac rehabilitation program.
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Fibrinolysis, the process of dissolving a fibrin blood clot, plays a pivotal role in the development of vascular disease. Occlusive blood clots are responsible for most acute cardiovascular events, and patients with coronary artery disease (CAD) typically exhibit a blunted fibrinolytic capacity. Initiation of fibrinolysis involves the conversion of plasminogen to plasmin, which is primarily catalyzed by tissue plasminogen activator (tPA). Depressed tPA and elevations of its primary inhibitor, plasminogen activator inhibitor-1 (PAI-1) are associated with morbidity, mortality, and are independent risk factors for various cardiovascular outcomes. Exercise training promotes enhanced fibrinolytic potential in healthy individuals, and individuals with CAD who undergo 12 or more weeks of regular exercise as part of a cardiac rehabilitation program demonstrate improvements in tPA and PAI-1. Modern day third-party reimbursement practices often necessitate fewer than 12 weeks of exercise training in cardiac rehabilitation programs. It is unclear if training regimens shorter than 12 weeks will elicit fibrinolytic improvements. The purpose of the present study was to evaluate changes in plasma concentrations of tPA and PAI-1, as well as changes in expression of the tPA and PAI-1 genes in whole blood after three and six weeks of participation in a phase II cardiac rehabilitation program.
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Fourteen CAD patients (12 male, 2 female) trained three days/week for six weeks. Exercise sessions adhered to American College of Sports Medicine (ACSM) guidelines for intensity and duration. Blood samples were taken at baseline (BL), after three weeks (3W), and after six weeks of training (6W) in a cardiac rehabilitation program and analyzed for tPA activity and antigen, PAI-1 activity and antigen, and relative quantification of tPA and PAI-1 RNA. Linear regression revealed no confounding influences on any outcome variable. Data were then analyzed using repeated measures analysis of variance. Six weeks of training resulted in significant decreases in submaximal exercise heart rate and systolic blood pressure (SBP), and resting SBP (p < 0.05). No significant changes in plasma concentrations of tPA activity (BL = 0.69 +/- 0.44, 3W = 0.94 +/- 0.62, 6W = 0.77 +/- 0.49 ng/ml, mean +/- SD, p = 0.391) or antigen (BL = 13.1 +/- 3.9, 3W = 12.4 +/- 3.7, 6W = 11.8 +/- 3.8, mean +/- SD, p = 0.59) were observed. No change was observed in plasma PAI-1 activity (BL = 17.0 +/- 16.8, 3W = 14.8 +/- 22.5, 6W = 17.9 +/- 18.8 IU/ml, mean +/- SD, p = 0.29) or antigen (BL = 28.3 +/- 15.5, 3W = 24.2 +/- 20.2, 6W = 22.4 +/- 16.1 ng/ml, mean +/- SD, p = 0.15). No change in tPA (p = 0.45) or PAI-1 (p = 0.44) gene expression was observed during six weeks of exercise training.
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The six-week cardiac rehabilitation program yielded significant hemodynamic improvements, but did not alter fibrinolytic capacity. Based on the results of the present study and evidence in the literature, it is recommended that traditional cardiac rehabilitation programs that subscribe to ACSM guidelines include at least 12 weeks of regular exercise.
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