Plasma tissue plasminogen activator levels in patients with coronary heart disease

Vandekerckhove, Yves; Baele, G; Puydt, H De; Weyne, Antoon E.; Clément, Denis

doi:10.1016/0049-3848(88)90274-5

Cited by 21 publications

(3 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…whether this relationship is causal or coincidental is unclear. Discrepant results have been found in studies of patients without metabolic risk factors (28,29), and the prevalence of increased PA1 activity seems to be higher in young than in unselected post-infarction patients (30). Acute insults such as myocardial infarction result in rapid increases in plasma PAI-1 levels, which may last a number of days before returning to normal.…”

Section: Systemic Increased Pai-1 Concentration and Atherothrombosismentioning

confidence: 97%

Plasminogen Activator Inhibitor 1 and Atherothrombosis

1993

View full text Add to dashboard Cite

Section: Systemic Increased Pai-1 Concentration and Atherothrombosismentioning

confidence: 97%

Plasminogen Activator Inhibitor 1 and Atherothrombosis

1993

View full text Add to dashboard Cite

“…In a prospective, placebo controlled study, we found significant decreases in PAI-1 and t-PA in hyperlipidemic patients treated with pravastatin, while no significant changes were noted with placebo (8). These changes are considered as indicators of improvement in endothelium-related fibrinolysis (21,22). Additionally, we found a concordant reduction in ex-vivo thrombus formation under dynamic flow conditions which correlated only modestly with LDL-C reduction (r 2 = 0.23, p = 0.01) (8); ex-vivo thrombus formation in the specific thrombosis model is considered a surrogate for platelet reactivity (14,15).…”

Section: Discussionmentioning

confidence: 84%

Pravastatin: An Antithrombotic Effect Independent of the Cholesterol-lowering Effect

Dangas¹,

Smith²,

Unger³

et al. 2000

Thromb Haemost

View full text Add to dashboard Cite

SummaryLipid-lowering with statins reduces blood thrombogenicity. However, it is unknown whether this is purely due to LDL-cholesterol reduction, or it is related to a statin or agent specific effect. We investigated the relationship between reduction in blood thrombogenicity and the magnitude of low-density lipoprotein cholesterol (LDL-C) during pravastatin therapy.We prospectively followed for 6 months 57 hyperlipidemic patients who initiated therapy with pravastatin, and 36 patients who were randomized into placebo plus diet. Pravastatin-treated patients were grouped according to the LDL-C reduction at 6 months; (i) “adequate LDL-C reduction”: LDL-C reduction >30% from baseline or LDL-C<125 mg/dl (n = 38; LDL-C reduction 74 ± 4 mg/dl; 6-month LDL-C 119 ± 5 mg/dl); (ii) “inadequate LDL-C reduction”: neither of the above criteria (n = 19; LDL-C reduction 31 ± 5 mg/dl; 6-month LDL-C 158 ± 6 mg/dl). Placebo patients were divided into those “with LDL-C reduction” (n = 17, mean reduction 21 ± 5 mg/dl) and those “without LDL reduction” (n = 19).The following parameters were altered at 6 months in both patients with “adequate” and “inadequate” LDL-C reduction: (1) tissue plasminogen activator decreased by 1.4 ± 0.4 and 1.5 ± 0.5 ng/ml respectively (p = NS); (2) plasminogen activator inhibitor-1 decreased by 8.7 ± 2.0 and 10.1 ± 2.7 ng/ml respectively (p = NS); (3) thrombus formation under dynamic flow conditions decreased by 3.5 ± 0.9 and 2.8 ± 1.2 µm2 × 103 respectively (p = NS). In contrast, no significant changes from baseline were noted in placebo-treated patients, regardless of their LDL-C reduction category, and multivariate analysis eliminated LDL-C reduction as an independent predictor of reduction in thrombogenicity.Therefore, the reduction in thrombogenicity was not proportional to the magnitude of LDL-C reduction suggesting that a class or agent specific property is primarily responsible for the pro-fibrinolytic/antithrombotic effects observed.

show abstract

“…Previous studies have shown a correlation between tPA levels and coronary artery diseases, [ 137 , 138 , 139 , 140 , 141 ] while limited data are available on this molecule’s role in other vascular regions.…”

Section: Coagulation Factors As Markers Of Risk In Peripheral Artery ...mentioning

confidence: 99%

The Role of the Coagulation System in Peripheral Arterial Disease: Interactions with the Arterial Wall and Its Vascular Microenvironment and Implications for Rational Therapies

Miceli

Basso

Rizzo

et al. 2022

IJMS

View full text Add to dashboard Cite

Peripheral artery disease (PAD) is a clinical manifestation of atherosclerotic disease with a large-scale impact on the economy and global health. Despite the role played by platelets in the process of atherogenesis being well recognized, evidence has been increasing on the contribution of the coagulation system to the atherosclerosis formation and PAD development, with important repercussions for the therapeutic approach. Histopathological analysis and some clinical studies conducted on atherosclerotic plaques testify to the existence of different types of plaques. Likely, the role of coagulation in each specific type of plaque can be an important determinant in the histopathological composition of atherosclerosis and in its future stability. In this review, we analyze the molecular contribution of inflammation and the coagulation system on PAD pathogenesis, focusing on molecular similarities and differences between atherogenesis in PAD and coronary artery disease (CAD) and discussing the possible implications for current therapeutic strategies and future perspectives accounting for molecular inflammatory and coagulation targets. Understanding the role of cross-talking between coagulation and inflammation in atherosclerosis genesis and progression could help in choosing the right patients for future dual pathway inhibition strategies, where an antiplatelet agent is combined with an anticoagulant, whose role, despite pathophysiological premises and trials’ results, is still under debate.

show abstract

Plasma tissue plasminogen activator levels in patients with coronary heart disease

Cited by 21 publications

References 10 publications

Plasminogen Activator Inhibitor 1 and Atherothrombosis

Plasminogen Activator Inhibitor 1 and Atherothrombosis

Pravastatin: An Antithrombotic Effect Independent of the Cholesterol-lowering Effect

The Role of the Coagulation System in Peripheral Arterial Disease: Interactions with the Arterial Wall and Its Vascular Microenvironment and Implications for Rational Therapies

Contact Info

Product

Resources

About