Journal of Postgraduate Medicine
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ARTICLE
 
 
Year : 1979  |  Volume : 25  |  Issue : 1  |  Page : 52-56  

Serum lactic dehydrogenase isoenzymes and serum hydroxy butyric dehydrogenase in myocardial infarction

DS Kanekar, PN Sawant, Saroj P Taskar 
 Cordiovascular and Thoracic Centre, K.E.M. Hospital and Seth G.S. Medical College, Parel, Bombay 400012, India

Correspondence Address:
D S Kanekar
Cordiovascular and Thoracic Centre, K.E.M. Hospital and Seth G.S. Medical College, Parel, Bombay 400012
India

Abstract

Total serum lactate dehydrogenase activity in cases of myocar­dial infarct is difficult to interpret as abnormal values can occur in diseases of liver, kidney and skeletal muscle. The estimation of its isoenzymes is of better diagnostic help because of its tissue specificity. Serum LDH isoenzymes were studied in patients o f myocardial infarction and results are quantitated by densitometry. As LDH 1 represents serum hydroxybutyric dehydrogenase when 2-oxylbutyrate is used as substrate, serum hydroxybutyric dehydro­genase was also estimated in above patients. Greater specificity in diagnosis is achieved with SHBDH because of its myocardial nature and lower incidence of false positive results.



How to cite this article:
Kanekar D S, Sawant P N, Taskar SP. Serum lactic dehydrogenase isoenzymes and serum hydroxy butyric dehydrogenase in myocardial infarction.J Postgrad Med 1979;25:52-56


How to cite this URL:
Kanekar D S, Sawant P N, Taskar SP. Serum lactic dehydrogenase isoenzymes and serum hydroxy butyric dehydrogenase in myocardial infarction. J Postgrad Med [serial online] 1979 [cited 2022 Dec 8 ];25:52-56
Available from: https://www.jpgmonline.com/text.asp?1979/25/1/52/42106


Full Text

 Introduction



Large number of enzymes have been introduced for the diagnosis of myocar­dial infarction. Selection of a suitable enzyme system becomes crucial when electrocardiographic findings are not contributory in the presence of clinical symptoms. Most commonly and widely used enzyme remains to be serum gluta­mic oxaloacetic transaminase (SGOT) but the diagnostic specificity of this en­zyme in myocardial infarction is limited because of its elevations in liver diseases and in patients with right heart failure and shock. [5] The use of SGOT determina­tion for the detection of myocardial in­farction also suffers from the major dis­advantage that elevation following infarction is rapid and transient. An increase in serum lactate dehydrogenase following infarction is on the other hand slow and more prolonged. This is helpful in estab­lishing a diagnosis in cases first seen several days after the event. However, the raised activity of serum lactate dehy­drogenase is also difficult to interpret as the abnormal values can occur in diseases of the liver, kidney or of skeletal muscle. Since Wroblewski and Gregory [6] and Wieme and Van Maercke [4] demonstrated that LDH isoenzymes I and II originate specifically from the cardiac muscle, LDH fractionation has become a better diag­nostic aid than the determination of total lactic dehydrogenase and SGOT. As serum hydroxybutyric dehydrogenase represents the activity of LDHI fraction of the total LDH, the same specificity in diagnosis can probably be achieved by determining serum hydroxybutyric de­hydrogenase using 2-oxybutyrate as the substrate. As very meagre data on LDH iso-enzymes in myocardial infarction in Indian population is available in litera­ture, attempt has been made in this paper to quantitate LDH isoenzymes and to correlate them with the levels of hydro­xybutyric dehydrogenase.

 Material And Methods



One hundred and five patients belong­ing to both the sexes between the age group of 35 and 60 years who had had an attack of myocardial infarction diagnos­ed by W.H.O. criteria and admitted to the Intensive Cardiac Care Unit of K.E.M. Hospital were selected for the present study. The controls selected were 40 healthy normals between the same age group. Blood was collected in heparin bulbs by venepuncture soon after the acute episode of myocardial infarc­tion. Haemolysis was avoided while separating the plasma which was im­mediately subjected to the enzyme assay. The blood samples were collected serially upto three days and a week from the day of infarction.

Total lactic acid dehydrogenase was estimated by a colorimetric method. [2]

Lactate dehydrogenase isoenzymes were fractionated by agarose gel electro­phoresis as described by Cawley and Eberhard. [1] The stained slides were scanned on Chromoscan at 520 mix and the percentages of the fractions were quantitated.

Serum hydroxybutyrate dehydrogenase activity was estimated by the method of Rosalki. [3]

 Results



Total LDH

The mean values of total serum lactic dehydrogenase with S.E. and range in normals and in patients with myocardial infarction are shown in [Table 1]. Follow­-up study of these patients shows that enzyme activity is elevated within the first 24 hours from the time of the episode and reaches a maximum on the second day and then declines towards the normal level after a week.

LDH isoenzymes

[Table 2] shows the details of results of lactate dehydrogenase isoenzymes in normal subjects, and in patients with myocardial infarction. In healthy normals largest fraction was found to be that of LDH 2 isoenzyme followed by LDH 1 isoenzyme then LDH 3 and LDH 4 isoenzymes. LDH 5 isoenzyme was found to be the smallest fraction. On serial determination of LDH isoenzymes, in patients with myocardial infarction it was observed that on the first day, LDH 1 enzyme rises sharply. The rise is greater than LDH 2 with simultaneous decrease in LDH 3 and LDH 4 isoenzymes. On the second day of the infarct, LDH 1 isoenzy­me reaches maximum and LDH 2 isoenzy­me is found to be minimal along with a decrease in LDH 3 , and LDH 4 isoenzymes. On the third day of the infarct, LDH 1 isoenzyme decreases with slight increase in LDH 2 , LDH 3 and LDH 4 isoenzymes and after a week, LDH 1 isoenzyme still decreases with an increase in other iso­enzyme fractions tending towards the normal.

[Table 3] demonstrates the mean ratio of LDH 1 /LDH 2 in normal subjects and in patients with myocardial infarction.

[Table 4] shows serum hydroxy butyric dehydrogenase activity in normals and in patients suffering from myocardial infarction

 Discussion



The results obtained in the present study indicate that serum lactic dehydro­genase enzyme activity increases 4-5 folds in the first 24-72 hours after the onset of clinical infarction with a peak on the second day. It then declines gradual­ly towards the normal within two weeks. Thus, determination of total serum LDH is valuable if patients present themselves for clinical check up even after a week from the day of infarct in contrast to SGOT. Although the contribution of myocardium to total serum lactic dehydrogenase is large, its interpretation becomes difficult if the diseases of other organs such as liver, kidney, etc. co-exist.

Electrophoretic separation of serum enzymes characterized by tissue specific isoenzyme patterns are more specific for laboratory diagnosis. Out of the various supporting media such as paper, agar, starch gel, polyacrylamide used for gel electrophoresis, agarose gel was found to have distinct advantage over the others. The staining as well as the separation is better and the scanning on densitometer is easier. (See [Figure 1] and [Figure 2] on page 56A) .

The five isoenzymes present in the :serum of normal subjects are in the fol­lowing typical relative concentrations. LDH 2 > LDH 1 > LDH 3 > LDH 4 > LDH 5 . From [Table 2] and [Table 3], it is seen that LDH 1 , isoenzyme increases during the clinical course of myocardial infarc­tion and LDH 1 :LDH 2 , ratio shifts towards more than unity. Elevated values of LDH 1 and LDH i :LDH 2 ratio above unity persist even after a week unlike those of total serum LDH. Determination of LDH 1 /LDH 2 , is particularly useful when total LDH values are on the higher side of normal or slightly above the normal. This ratio extending beyond unity is a definite indication of myocardial infarc­tion. The greater sensitivity and specifi­city of SHBDH compared to LDH in detecting myocardial injury stems from the facts that only myocardial enzyme is being measured and that there is a low incidence of false positive results.

 Acknowledgements



The authors wish to thank Dr. C. K. Deshpande, Dean, Seth G.S. Medical College and K.E.M. Hospital, Bombay for all facilities and Dr. (Smt.) S. G. Kinare, Professor of Pathology, Seth G.S. Medi­cal College for her keen interest and valuable guidance in the work.

References

1Cawley, L. P. and Eberhard, L.: Simpli­fied gel electrophoresis. Rapid technique applicable to the clinical laboratory, Amer. J. Clin. Path., 38: 539-547, 1562.
2King, J.: J. Med. Lab. Tech., 16: 265­267, 1959. Colorimetric method of estima­tion of total lactic acid dehydrogenase Cited in Practical Clinical Biochemistry by Harold Varley published by A. Heine­mann, 4th Ed., reprinted in 1976.
3Rosalki, S. B.: A simple colorimetric method for the determination of serum alpha hydroxy butyric dehydrogenase activity, J. Clin. Path., 15: 566-568. 1962.
4Wieme, R. J. and Y. Van Maercke: The fifth (electrophoretically slowest) serum lactic dehydrogenase as an index of liver injury, Annals of New York Academy of Science, 94: 898-911, 1961.
5Wroblewski, F. and La Due, J. S.: LDH activity in blood, Proc. of the Society of Experimental Biol. & Med., Paper No. 21585, 90: 210-213, 1955.
6Wroblewski, J. and Gregory, K. F.: Lac­tic Dehydrogenase Isoenzymes and their distribution in normal tissue and plasma in disease states, Annals of New York Academy of Science, 94: 912-932, 1961.

 
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