Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

Ranjadayalan, Kulasegaram; Umachandran, Velaitham; Davies, Simon; Syndercombe‐Court, Denise; Gutteridge, C. N.; Timmis, A

doi:10.1136/hrt.66.1.10

Cited by 22 publications

(4 citation statements)

References 22 publications

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“…On the one hand, the higher rates of free radical release in the neutrophils of patients with complicated MI is probably caused by the extent of the inflammatory response induced by myocardial ischaemia (since some of the patients with complicated MI were diagnosed with congestive heart failure or cardiogenic shock, the increased superoxide release may also be due to the existence of these secondary conditions). A recent study [23] reported that streptokinase therapy in acute myocardial infarction is associated with an abrupt reactive neutrophil response; however, this abrupt response was seen in only a few patients. Our results demonstrating that higher rates of superoxide are produced soon after symptoms appear (Fig.…”

Section: Discussionmentioning

confidence: 98%

“…In support of our results, others have shown [19,22] that thrombolysis elevated neither plasma neutrophil elastase nor lipid peroxidation. A recent study [23] reported that streptokinase therapy in acute myocardial infarction is associated with an abrupt reactive neutrophil response; however, this abrupt response was seen in only a few patients.…”

Section: Discussionmentioning

confidence: 98%

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Neutrophil superoxide release and interleukin 8 in acute myocardial infarction: distinction between complicated and uncomplicated states

Riesenberg¹,

Levy²,

Katz³

et al. 1997

Eur J Clin Investigation

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Superoxide release in neutrophils and sera levels of interleukin 8 (IL-8) were determined in 15 patients with complicated acute myocardial infarction (MI) and 15 patients with uncomplicated MI. All patients showed increased superoxide release in unstimulated and stimulated neutrophils compared with healthy control subjects, indicating priming of these cells. Superoxide release of unstimulated or stimulated neutrophils was found to be significantly higher in patients with complicated MI than in patients with uncomplicated MI. Thrombolytic therapy did not affect the rates of superoxide release. The neutrophil chemoattractant/activator IL-8 was detected in the sera of all patients, with significantly higher levels in those with complicated MI. The highest levels of IL-8 were detected at admission to the Coronary Care Unit and significantly decreased thereafter, suggesting its contribution to neutrophil-mediated tissue injury. The high levels of IL-8 may be one of the major contributors to the priming of neutrophils in these patients.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Neutrophil superoxide release and interleukin 8 in acute myocardial infarction: distinction between complicated and uncomplicated states

Riesenberg¹,

Levy²,

Katz³

et al. 1997

Eur J Clin Investigation

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“…The induction of these factors is probably triggered by soluble inflammatory mediators, such as interleukin-1 and tumour ne crosis factor (25)(26)(27)(28). In patients with acute myocardial infarction, the plasma levels of tumour necrosis factor-α and of neutrophil elastase have been related to the extent of myocardial necrosis (29,30). Patients in whom thrombolytic therapy achieves early coronary recanalisation have a faster and reduced acute-phase response compared to patients with persistent infarct artery occlusion (5,6).…”

Section: Discussionmentioning

confidence: 99%

Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

et al. 1992

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SummaryPlasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and ≥ 50% resolution of maximal ST-deviation on the electrocardiogram.Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.

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“…Hypertriglyceridaemia in diabetics can increase monocyte free radical production [13,14]. CRF patients frequently have hypertriglyceridaemia which may contribute to production of ROS.…”

Section: Advanced Glycation Endproducts (Age) and Hypertrigyceridaemiamentioning

confidence: 99%

The therapeutic implications of oxidative stress in patients receiving haemodialysis

Crowe

Bell²

1999

AJN

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Oxygen-derived free radicals are highly reactive chemical species containing an unpaired electron. They are capable of reacting with lipids, proteins and nucleic acids and are thought to have a major role in the pathogenesis of a variety of diseases including atherosclerosis, diabetes and cancer. Antioxidants protect and limit free radical damage and it is the balance between free radical activity and antioxidant mechanisms that determine the potential for tissue damage [1,2]. Oxidative stress exists when there are either low levels of these antioxidants or increased production of reactive oxygen species (ROS).

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Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

Cited by 22 publications

References 22 publications

Neutrophil superoxide release and interleukin 8 in acute myocardial infarction: distinction between complicated and uncomplicated states

Neutrophil superoxide release and interleukin 8 in acute myocardial infarction: distinction between complicated and uncomplicated states

Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

The therapeutic implications of oxidative stress in patients receiving haemodialysis

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