Key result
CTEPH is linked to ~11-fold higher basal t-PA antigen levels despite unchanged enzymatic activity.
Why the study?
The mechanism for poor thrombus dissolution in chronic thromboembolic pulmonary hypertension remains to be explained.
Are there abnormalities in the endogenous fibrinolytic system in patients with chronic thromboembolic pulmonary hypertension compared to age-matched controls?
Case-Control
Are there abnormalities in the endogenous fibrinolytic system in patients with chronic thromboembolic pulmonary hypertension compared to age-matched controls?
Absolute Event Rate: 29.5% vs 2.7%
Neither high resting plasma PAI-1 activity nor a blunted response of t-PA to venous occlusion explains the etiology of poor thrombus dissolution in CTEPH.
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Detected fibrinolytic abnormalities do not implicate PAI-1 activity or blunted t-PA release in CTEPH; leaves open other mechanisms of impaired thrombus resolution.
Olman et al. (1992) conducted a case-control in Chronic thromboembolic pulmonary hypertension (CTEPH). Chronic thromboembolic pulmonary hypertension vs. Age-matched controls was evaluated on Basal platelet-poor plasma t-PA antigen levels (ng/ml). Patients with CTEPH had higher basal t-PA (29.5 vs 2.7 ng/ml) and PAI-1 antigen levels than controls, but no differences in enzymatic activities were detected.
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