The significance of serum cholesterol and triglyceride values in the post myocardial infarction period

The significance of serum cholesterol and triglyceride values in the post myocardial infarction period

Clin. Biochern. 8, 222-224 (1975) LABORATORY NOTE THE SIGNIFICANCE OF SERUM CHOLESTEROL A N D TRIGLYCERIDE V A L U E S IN THE POST MYOCARDIAL INFARCT...

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Clin. Biochern. 8, 222-224 (1975)

LABORATORY NOTE THE SIGNIFICANCE OF SERUM CHOLESTEROL A N D TRIGLYCERIDE V A L U E S IN THE POST MYOCARDIAL INFARCTION PERIOD P. J. M A R T I N

Department of Chemical Pathology, Royal Infirmary, Infirmary Road, Sheffield $6 $DA, England (Accepted December 11, I975) IT HAS BEEN K N O W N FOR MANY YEARS T H A T after a myocardial infarction, a temporary fall in serum cholesterol and a rise in serum triglyceride can occur 1, 2. It is now widely accepted that these changes in serum lipids are such as to invalidate lipoprotein phenotyping which should, therefore, only be undertaken 3 months or more after infarction, when they are then representative of the patient's true status 3, 4, 5.

This view has not gone unchallenged. Dodds and Mills I found that although serum cholesterol had returned to normal within 30 days, the VLDL fraction (and therefore, presumably, the serum triglyceride) was still elevated 50 days after infarction. E n g e r and Ritland e reported little change in serum cholesterol between the 2rid day and 3rd month after infarction, but serum triglyceride rose and remained elevated even after 3 months. No change in triglyceride could be detected by Kirkeby 7, who followed his patients for only 4 days after infarction, during which period the cholesterol showed a mean reduction of 62 mg/dl. Fyfe et al s found the values of cholesterol and triglyceride to be similar on the m o r n i n g after and 3 months after infarction. The former finding was confirmed by Mundy and McPherson% but they did not study serum triglyceride levels in their subjects. Part of the confusion arising from these reports might be due to the inclusion of patients manifesting large weight changes over the period of observation. For this reason the present study was undertaken to compare the lipid levels on the m o r n i n g after a myocardial infarction with those 3 months later. Twenty-four men and 6 women, who had suffered a definite myocardial infarction as judged by clinical criteria, enzyme elevations and electrocardiographic evidence, were studied. No dietary advice was given, but those patients changing weight by more than 5 kg were excluded. The fasting serum lipids were measured on the m o r n i n g after admission and 3 months later. The cholesterol was measured by .AutoAnalyzer method 24a and the triglycerides by a modification of the method of Soloni lo. As shown in Fig. 1 and Table 1, no significant differences were observed in the mean values for serum cholesterol and triglyceride measured

CHOLESTEROL AND TRIGLYCERIDE

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Fig. 1. The alteration of serum cholesterol and triglyceride values at 3 months compared with the value a t day 1. TABLE 1 1st day triglyceride . . . . . . . . . cholesterol . . . . . . . .

116 ± 53 265 ~- 44

3 months 112 ± 35 mg/dl 245 ~ 40 mg/dl

The mean serum cholesterol and triglyceride values ( ~ S.D.) in 30 patients who had suIfered a definite myocardial infarction.

on the first day or 3 months after infarction, although large fluctuations in individual subjects were sometimes noted. This study, therefore, confirms the conclusions of Fyfe et alS that comparable values for both parameters are obtained at these 2 time intervals. Analysis on the first day is, however, much to be preferred since it enables phenotyping to be rapidly performed and appropriate t r e a t m e n t initiated. Moreover, in the present series raised initial values for cholesterol in two cases and for triglyceride in one case were within normal limits after 3 months. If examination is only carried out at that time, a proportion of subjects with underlying hyperlipoproteinaemia may be missed. ACKNOWLEDGEMENT

I wish to t h a n k D. M. Goldberg for help in the preparation of this manuscript.

224

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1. 2. 3. 4. 5. 6. 7. 8.

Dodds, C. & Mills, G. L. (1959). Lancet i, 1160-1163. Tibblin, G. & Cramer, K. (1963). A c ~ M6& Scan& 174, 451-455. Gustafson, A., Elmfeldt, D., Wilhelmsen, G. & Tibblin, G. (1972). Circ. 46, 709. Patterson, O. & Slack, J. (1972). Lancet i, 393-399. Dyerberg, J.,.Bang, H. O. & Nielsen, J. A. (1970). Ac~a Med. Scan& 187, 3553-365. Enger, S. C. & Ritland, S. (1970). A c t ~ Med. Scan& 1~7, 365-369. Kirkeby, K. (1972). Acf~ Mcd. Scan& 192, 523-~28. Fyfe, T., Cochran, K. M., Baxter, R. H., and Booth, E. M. (1971). Lancet ii, 9971001. 9. Mundy, G. R., and McPherson, D. G. (1973). Med. J. A u s t . 278-282. 10. Martin, P. J. (1975). Clin. Chim. A c t a in press.