Comparison of peak serum C-reactive protein and hydroxybutyrate dehydrogenase levels in patients with acute myocardial infarction treated with alteplase and streptokinase

Pietilä, K; Hermens, Wim Th.; Harmoinen, Aimo; Baardman, Taco; Pasternack, Amos; Topol, Eric J.; Simoons, Maarten L.

doi:10.1016/s0002-9149(97)00606-1

Cited by 25 publications

(9 citation statements)

References 13 publications

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“…However, Genser et al (19) were unable to demonstrate a close correlation between plasma concentration of D-dimer and PAI-1 levels. Pietila et al (36) have recently shown that AMI treated with accelerated dosing of rt-PA leads to a smaller acute phase reaction than streptokinase, the lower peak of C-reactive protein being significantly associated with complete reperfusion in the infarct-related coronary artery. This indicates that the circulating PAI-1 increase, induced by thrombolysis, could be a marker of this acute inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

Paganelli¹,

Alessi²,

Morange³

et al. 1999

Thromb Haemost

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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.

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Section: Discussionmentioning

confidence: 99%

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

Paganelli¹,

Alessi²,

Morange³

et al. 1999

Thromb Haemost

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“…Nevertheless, the precise basis for the relationship between inflammatory markers and risk in ACS has not been conclusively established. CRP certainly rises as a consequence of the inflammatory response to myocardial necrosis (113 ). However, studies demonstrating elevation of CRP and IL-6 during ACS in the absence of myocyte necrosis refute the position that the rise in these markers is solely a response to necrosis (107,109,110 ).…”

Section: Biochemical Markers Of Inflammation a Pathophysiologymentioning

confidence: 99%

National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes

et al. 2007

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“…Inflammatory biomarkers such as C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor-a (TNF-a) are elevated in patients with acute coronary syndromes and heart failure (Pietilä et al, 1997;Miettinen et al, 2008;Tamariz and Hare, 2010). Similarly, inflammatory markers such as CRP, TNF-a, and IL-6 were significantly increased by 440, 70, and 90%, respectively (each P , 0.001), in serum of doxorubicintreated animals compared with the control group.…”

Section: Resultsmentioning

confidence: 99%

“…TNF-a and IL-6 are elevated in individuals with cardiac dysfunction and heart failure (Miettinen et al, 2008;Tamariz and Hare, 2010). CRP as an inflammatory marker also rises as a consequence of the inflammatory response to myocardial damage (Pietilä et al, 1997;Miettinen et al, 2008). The cardiotoxic effects of doxorubicin are mediated in part by expression of proinflammatory cytokines (Nozaki et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

Ezzat

Gaafary

Sayed

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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The current study aimed to investigate the protective effect of the cardenolide glycoside acovenoside A (AcoA) against doxorubicininduced cardiotoxicity in mice. AcoA was isolated from the pericarps of Acokanthera oppositifolia to chemical homogeneity and characterized by means of one-and two-dimensional nuclear magnetic resonance spectroscopy. AcoA exhibited relatively low toxicity in mice (LD 50 5 223.3 mg/kg bw). Repeated administration of doxorubicin induced cardiotoxicity manifested by reduced activity of myocardial membrane-bound ion pumps and elevated serum biomarkers of myocardial dysfunction, oxidative stress, and inflammation. Pretreatment of doxorubicin-exposed mice with AcoA (11.16 or 22.33 mg/kg bw, i.p.) for 2 weeks after 2 weeks of combined administration of AcoA and doxorubicin protected the animals dose dependently against doxorubicininduced cardiotoxicity as indicated by normalization of the levels of different myocardial markers of oxidative stress (malondialdehyde, nitric oxide, total antioxidant capacity, and cardiac glutathione), serum myocardial diagnostic marker enzymes (serum cardiac troponin T, creatine kinase isoenzyme MB, aspartate aminotransferase, and lactate dehydrogenase), and inflammatory markers (c-reactive protein, tumor necrosis factor-a, and interleukin-6), as well as myocardial Na 1 /K 1 -ATPase activity. These effects were attributed to the negative impact of AcoA on transcription factors nuclear factor kB and interferon regulatory factor 3/7. Thus acovenoside A might act as a cardioprotective agent to prevent doxorubicin-induced cardiotoxicity.

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Comparison of peak serum C-reactive protein and hydroxybutyrate dehydrogenase levels in patients with acute myocardial infarction treated with alteplase and streptokinase

Cited by 25 publications

References 13 publications

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes

The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

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