Soluble thrombomodulin antigen in plasma is increased in patients with acute myocardial infarction treated with thrombolytic therapy

1996 ◽  
Vol 82 (4) ◽  
pp. 313-322 ◽  
Author(s):  
Ann-Kristin Öhlin ◽  
John Morser ◽  
Hans Öhlin
1999 ◽  
Vol 82 (07) ◽  
pp. 104-108 ◽  
Author(s):  
Franck Paganelli ◽  
Marie Christine Alessi ◽  
Pierre Morange ◽  
Jean Michel Maixent ◽  
Samuel Lévy ◽  
...  

Summary Background: Type 1 plasminogen activator inhibitor (PAI-1) is considered to be risk factor for acute myocardial infarction (AMI). A rebound of circulating PAI-1 has been reported after rt-PA administration. We investigated the relationships between PAI-1 levels before and after thrombolytic therapy with streptokinase (SK) as compared to rt-PA and the patency of infarct-related arteries. Methods and Results: Fifty five consecutive patients with acute MI were randomized to strep-tokinase or rt-PA. The plasma PAI-1 levels were studied before and serially within 24 h after thrombolytic administration. Vessel patency was assessed by an angiogram at 5 ± 1days. The PAI-1 levels increased significantly with both rt-PA and SK as shown by the levels obtained from a control group of 10 patients treated with coronary angioplasty alone. However, the area under the PAI-1 curve was significantly higher with SK than with rt-PA (p <0.01) and the plasma PAI-1 levels peaked later with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PAI-1 levels on admission, the PAI-1 levels after thrombolysis were related to vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the area under the PAI-1 curve were significantly higher in patients with occluded arteries (p <0.002, p <0.04 and p <0.05 respectively).The same tendency was observed in the t-PA group without reaching significance. Conclusions: This study showed that the PAI-1 level increase is more pronounced after SK treatment than after t-PA treatment. There is a relationship between increased PAI-1 levels after thrombolytic therapy and poor patency. Therapeutic approaches aimed at quenching PAI-1 activity after thrombolysis might be of interest to improve the efficacy of thrombolytic therapy for acute myocardial infarction.


2018 ◽  
Vol 24 (4) ◽  
pp. 414-426 ◽  
Author(s):  
Patrick Proctor ◽  
Massoud A. Leesar ◽  
Arka Chatterjee

Thrombolytic therapy kick-started the era of modern cardiology but in the last few decades it has been largely supplanted by primary percutaneous coronary intervention (PCI) as the go-to treatment for acute myocardial infarction. However, these agents remain important for vast populations without access to primary PCI and acute ischemic stroke. More innovative uses have recently come up for the treatment of a variety of conditions. This article summarizes the history, evidence base and current use of thrombolytics in cardiovascular disease.


Circulation ◽  
1996 ◽  
Vol 94 (3) ◽  
pp. 298-307 ◽  
Author(s):  
Gary L. Schaer ◽  
Leo J. Spaccavento ◽  
Kevin F. Browne ◽  
Karol A. Krueger ◽  
Daniel Krichbaum ◽  
...  

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
M Thoegersen ◽  
M Frydland ◽  
O Helgestad ◽  
LO Jensen ◽  
J Josiassen ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Lundbeck Foundation OnBehalf Critical Cardiac Care Research Group Background Approximately half of all patients with acute myocardial infarction complicated by cardiogenic shock (AMICS) present with out-of-hospital cardiac arrest (OHCA). Cardiogenic shock due to OHCA is caused by abrupt cessation of circulation, whereas AMICS without OHCA is due to cardiac failure with low cardiac output. Thus, there may also be differences between the two conditions in terms of blood borne biomarkers. Purpose To explore the potential differences in the admission plasma concentrations of biomarkers reflecting tissue perfusion (lactate), neuroendocrine response (mid-regional proadrenomedullin [MRproADM], Copeptin, pro-atrial natriuretic peptide [proANP]), endothelial damage (Syndecan-1, soluble thrombomodulin [sTM]), inflammation (soluble suppression of tumorigenicity 2 [sST2]) and kidney injury (neutrophil gelatinase-associated lipocalin [NGAL]), in patients with AMICS presenting with or without OHCA. Method Consecutive patients admitted for acute coronary angiography due to suspected ST-elevation myocardial infarction (STEMI) were enrolled during a 1-year period. A total of 2,713 patients were screened. In the present study 86 patients with confirmed STEMI and CS at admission were included. Results Patients with OHCA (had significantly higher median admission concentrations of Lactate (6,9 mmol/L vs. 3.4 mmol/L p &lt;0.001), NGAL (220 ng/ml  vs 150 ng/ml p = 0.046), sTM (10 ng/ml vs. 8.0  ng/ml p = 0.026) and Syndecan-1 (160 ng/ml vs. 120 ng/ml p= 0.015) and significantly lower concentrations of MR-proADM (0.85 nmol/L  vs. 1.6 nmol/L p &lt;0.001) and sST2 (39 ng/ml vs. 62 ng/ml p &lt; 0.001).  After adjusting for age, sex, and time from symptom onset to coronary angiography, lactate (p = 0.008), NGAL (p = 0.03) and sTM (p = 0.011) were still significantly higher in patients presenting with OHCA while sST2 was still significantly lower (p = 0.029). There was very little difference in 30-day mortality between the OHCA and non-OHCA groups (OHCA 37% vs. non-OHCA 38%). Conclusion Patients with STEMI and CS at admission with or without concomitant OHCA had similar 30-day mortality but differed in terms of Lactate, NGAL, sTM and sST2 levels at the time of admission to catheterization laboratory. These findings propose that non-OHCA and OHCA patients with CS could be considered as two individual clinical entities. Abstract Figure. Level of biomarkers OHCA vs. non-OHCA


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