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Updated: Aug 18, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
Published on: April 1, 2015
Hypofibrinolytic and atherogenic risk factors for stroke
C J Glueck1, M H Rorick, M Schmerler
1Cholesterol Center, Jewish Hospital, University of Cincinnati, OH 45229.
Insights
Hypofibrinolysis, a condition impairing blood clot breakdown, is common in stroke survivors and their families. This is linked to higher levels of plasminogen activator inhibitor activity, a key clot stabilizer.
Area of Science:
- Cardiovascular Science
- Hematology
- Stroke Research
Background:
- Stroke survivors often have underlying risk factors that are not fully understood.
- Fibrinolysis, the process of breaking down blood clots, plays a critical role in vascular health.
- Impaired fibrinolysis (hypofibrinolysis) may contribute to thrombotic events like stroke.
Purpose of the Study:
- To determine the prevalence of hypofibrinolysis and related risk factors in stroke patients and their relatives.
- To investigate the role of plasminogen activator inhibitor (PAI) and tissue plasminogen activator (t-PA) in stroke pathogenesis.
- To assess familial clustering of hypofibrinolysis.
Main Methods:
- Studied 87 stroke patients and 26 first-degree relatives.
- Measured lipids, lipoprotein (a), basal and stimulated fibrinolytic activity, PAI activity, and t-PA antigen levels.
- Compared findings with 175 normolipidemic control subjects.
Main Results:
- Hypofibrinolysis was prevalent in 21% of stroke patients and 30% of relatives, significantly higher than controls.
- Elevated basal PAI activity (major fibrinolysis inhibitor) was found in 20% of patients and 21% of relatives.
- Higher mean basal PAI activity/antigen and t-PA antigen levels were observed in stroke patients compared to controls.
Conclusions:
- Hypofibrinolysis is a common finding in stroke patients and their first-degree relatives.
- This impairment is associated with increased PAI activity and potentially higher t-PA antigen levels.
- These findings suggest a genetic or familial predisposition to hypofibrinolysis as a stroke risk factor.
Abstract:
In 87 patients (studied on average 1 year after their strokes) and 26 of their first-degree relatives, our specific aim was to assess the prevalence of the following stroke risk factors: hypofibrinolysis, familial hypofibrinolysis, high lipoprotein (a) level, and dyslipidemia. At least 2 months after their strokes (primarily ischemic), 87 patients had measures of lipids and lipoprotein (a); 69 and 67 patients had measures of basal and stimulated fibrinolytic activity, respectively, four new findings were as follows. (1) Hypofibrinolysis was common, with bottom decile-stimulated tissue plasminogen activator activity (the major stimulator of fibrinolysis) in 21% of stroke probands and in 30% of their first-degree relatives, versus 7% of 29 nomolipidemic control subjects (p = 0.09 and 0.026, respectively). (2) The hypofibrinolysis was mediated by top-decile levels of basal plasminogen activator inhibitor activity (the major inhibitor of fibrinolysis), which were observed in 20% of stroke probands and in 21% of their first-degree relatives, versus 8% of 175 nomolipidemic control subjects (p = 0.007 and 0.04, respectively). Mean (SD) basal plasminogen activator inhibitor activity and antigen level were higher in stroke probands (18 +/- 18 U/ml and 35 +/- 31 ng/ml, respectively) than in the 175 normolipemic control subjects (14 +/- 10 [p = 0.002], 28 +/- 34 [p = 0.016]). (3) Levels of basal tissue plasminogen activator antigen, a probable marker for atherosclerosis, were much higher in stroke probands than in the 175 normolipemic control subjects (15 +/- 7.3 ng/ml vs 7 +/- 3.8, p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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