Acute-phase proteins from the liver and enzymes from myocardial infarction; a quantitative relationship

Smith, Steven J.; Bos, G.; Esseveld, M.R.; Eijk, H.G. Van; Gerbrandy, J

doi:10.1016/0009-8981(77)90415-6

Cited by 61 publications

(20 citation statements)

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“…Alternatively, the binding on days 1 and 5 may be influenced by the plethora of endogenous compounds released into plasma in response to tissue injury. Such compounds would include other acute phase reactants and altered lipoprotein fractions (Johansson et al, 1972;Smith et al, 1977). Increased binding in the presence of increased plasma lipoprotein concentrations was recently shown for quinidine and propranolol (Nilsen et al, 1978;Sager et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Prolonged variability in plasma protein binding of disopyramide after acute myocardial infarction.

David¹,

Ilett²,

Whitford³

et al. 1983

Brit J Clinical Pharma

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1 Disopyramide plasma binding was determined in vitro in plasma from 20 patients with acute myocardial infarction (aged 35-79 years) and in 20 age and sex matched healthy subjects. Plasma samples were collected on days 1, 5 and 12 after infarction and when the patient returned to the outpatient clinic. 2 In healthy subjects there was a significant negative correlation between disopyramide free fraction and plasma a,-acid glycoprotein (AAG) concentration. A similar correlation was observed in the patients with myocardial infarction, however this correlation was dependent on time elapsed after infarction. Disopyramide free fraction did not correlate with albumin concentration in either group. 3 Mean plasma AAG concentrations were increased by'63% within 5 days after infarction and had returned to initial levels some months later (73.5 + 7.8 days). On each of the four sampling days, a two to four fold individual variability in plasma AAG concentrations was observed. 4 Maximum increases in disopyramide plasma binding were shown on days 5 and 12 after infarction. These increases were dependent on both drug and AAG concentrations. Increases in fraction bound were greater at the higher drug concentrations. Within the usual therapeutic plasma range for disopyramide (2 to 5 mg/I), the mean increases in fraction bound, compared to day 1 data, varied from 22 to 45% respectively. 5 Sequential alteration in AAG concentration after infarction indicates that disopyramide plasma binding may not reach a'steady state until some months after infarction. Prediction of the time to achieve this steady state would be difficult due to inter-and intra-patient variability in binding.

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Section: Discussionmentioning

confidence: 99%

Prolonged variability in plasma protein binding of disopyramide after acute myocardial infarction.

David¹,

Ilett²,

Whitford³

et al. 1983

Brit J Clinical Pharma

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“…Our results do not support this contention in healthy volunteers; indeed, for a biological phenomenon, there is surprising conformity (Figure 3) Myocardial infarction appears to decrease disopyramide binding in the therapeutic range, but this would not have been inferred when comparing the data of Meffin et al (1979) with previous workers (Figure 3). Decreased binding might be expected in view of the well known decrease in plasma albumin concentrations after infarction (Johansson, Kindmark, Trell & Wollheim, 1972;Smith, Bos, Esseveld, Van Eijk & Gerbrandy, 1977), and the finding by Chien, Lambert & Karim (1974) …”

mentioning

confidence: 88%

Plasma binding of disopyramide.

David¹,

Madsen²,

Ilett³

1980

Brit J Clinical Pharma

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“…In patients with MI, CRP levels increase within 6 h after symptom onset and peak 2–4 days later [36]. CRP increases in response to myocardial injury and the maximum level is correlated to the size of the MI [37]. CRP has been detected in atherosclerotic plaques, but a causal relationship between CRP and coronary events is highly unlikely [38].…”

Section: Biomarkers Of Inflammationmentioning

confidence: 99%

Prognostic Biomarkers in Acute Coronary Syndromes: Risk Stratification Beyond Cardiac Troponins

Eggers

Lindahl

2017

Curr Cardiol Rep

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Purpose of ReviewCardiac troponin (cTn) plays an essential role for assessment of outcome in acute coronary syndrome (ACS). However, the prognostic value of cTn is not absolute. In this mini-review, we summarize the evidence on the utility of established biomarkers of left-ventricular dysfunction, hemodynamic stress, inflammation, and renal dysfunction for risk prediction beyond cTn in ACS.Recent FindingsOnly few biomarkers consistently demonstrate additive prognostic value to cTn levels. The B-type natriuretic peptides (NPs) and growth-differentiation factor-15 (GDF-15) are most promising in this regard. However, there are uncertainties regarding the role of these biomarkers for guidance of treatment decisions, and their prognostic increment to cTn levels measured with high-sensitivity assays is largely unknown.SummaryThe NPs and GDF-15 provide the strongest prognostic increment to cTn levels in ACS. However, the role of these biomarkers for clinical decision-making in contemporary settings has still to be defined.

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Acute-phase proteins from the liver and enzymes from myocardial infarction; a quantitative relationship

Cited by 61 publications

References 20 publications

Prolonged variability in plasma protein binding of disopyramide after acute myocardial infarction.

Prolonged variability in plasma protein binding of disopyramide after acute myocardial infarction.

Plasma binding of disopyramide.

Prognostic Biomarkers in Acute Coronary Syndromes: Risk Stratification Beyond Cardiac Troponins

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