Key result
Acute MI is linked to scorbutic-level leukocyte ascorbic acid depletion in ~100% of patients.
Observational (n=31)
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Leucocyte ascorbic acid was measured in 3I patients who had sustained an acute myocardial infarction. Nine of the patients were seen within 6 hours of the infarction and 22 patients within 12 hours. It was found that there was a significant fall in the leucocyte ascorbic acid to scorbutic levels within I2 hours of the infarction in each case, and this occurred when the white blood cell count was at its maximum. The fall also coincided with the peak plasma cortisol level. The level remained less than normal for the next two weeks and the reduction in leucocyte ascorbic acid at two weeks was related to the size of the myocardial infarction as reflected by the serum aspartate aminotransferase level. It is suggested that thefall in leucocyte ascorbic acid is due to the migration of ascorbic acid laden leucocytes to the site of the infarction and the dilution of the white cell pool by cells which have not yet taken up their ascorbic acidfrom the plasma. This is in keeping with
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Hume et al. (1972) conducted an observational in Acute myocardial infarction (n=31). Acute myocardial infarction was evaluated on Fall in leucocyte ascorbic acid to scorbutic levels within 12 hours of infarction. Acute myocardial infarction was associated with a significant fall in leucocyte ascorbic acid to scorbutic levels within 12 hours in 100% (31/31) of patients, remaining subnormal for 2 weeks.
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