Sequential Changes of Plasma Proteins after Myocardial Infarction

Johansson, Benny; Kindmark, C.‐O.; Trell, Erik; Wollheim, Frank A.

doi:10.3109/00365517209102759

Cited by 136 publications

(33 citation statements)

References 17 publications

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“…Certainly a wide variety of substances have been reported to activate C1 or C3 in the absence of detectable antibody and include single-and double-stranded DNA, various polynucleotides, proteolytic enzymes such as trypsin and plasmin, endotoxin, certain viruses, polycations, and C-reactive protein (17). Regarding C-reactive protein, it is noteworthy that the initial and maximum decreases in C1, C4, and C3 reported in the present studies occurred before the reported increase in C-reactive protein and other acute phase reactants in myocardial infarction patients (20).…”

Section: Methodssupporting

confidence: 48%

Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction.

Pinckard¹,

Olson²,

Giclas³

et al. 1975

J. Clin. Invest.

179

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Section: Methodssupporting

confidence: 48%

Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction.

Pinckard¹,

Olson²,

Giclas³

et al. 1975

J. Clin. Invest.

179

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“…In patients with cardiac arrhythmias, there was a two fold variability in disopyramide free fraction, and plasma binding was greater than previously reported values (Meffin et al, 1979). These observations required explanation, especially as earlier work had indicated that disopyramide was bound primarily to albumin (Chien et al, 1974), a plasma protein which is rarely elevated in disease states, and is known to be markedly decreased after acute myocardial infarction (Johansson et al, 1972;Smith etal., 1977). inflammatory arthritis, (Piafsky et al, 1978) and during the acute phase following myocardial infarction (Johansson et al, 1972;Smith et al, 1977).…”

Section: Introductionmentioning

confidence: 91%

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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“…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: 87%