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A comparative study of serum histaminase and serum glutamic oxaloacetic transaminase in acute myocardial infarction SK Gupta, TN Mehrotra, VS Singh, GP Elhence, HS Mittal, A MitraDepartments of Medicine and Biochemistry, L.L.R.M. Medical College, Meerut, India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 119046
Serum histaminase and SGOT were estimated in 35 cases of acute myocardial infarction and 34 cases of ischaemic heart disease (Other than acute myocardial infarction) and 30, age and sex matched, healthy subjects which served as controls, to evaluate the comparison of time relation activity, diagnostic and prognostic value of histaminase and SGOT. The enzymes were estimated within 6 hours, then repeated -within 24 hours, 2nd day, 3rd day, 5th day, 10th day and 15th day, ascertained from the time o f pain in the chest.
The diagnostic and prognostic value of clinical judgement and electrocardiography cannot be under-rated; however, in the search of a still better and earlier diagnostic tool, large number of enzymes have been evolved. SGOT is a well recognised enzyme estimated in cases of myocardial infarction. Serum histaminase has recently been added to the list. The present study evaluates the comparison of time relation activity, diagnostic and prognostic value of histaminase and SGOT.
This study has been carried out at the L.L.R.M. Medical College Hospital, Meerut on 30 healthy subjects and 34 cases of ischaemic heart diseases (other than acute myocardial infarction) which served as controls and 35 cases of acute myocardial infarction. The diagnosis of acute myocardial infarction and ischaemic heart disease was made as per WHO criteria. [14],[15] Electrocardiograms were taken on the 1st day, 2nd day, 4th day and 7th day of episode of infarction ascertained from the time of pain in the chest and then weekly for the next 6 weeks. Repeat electrocardiograms were taken in special circumstances as in fresh reinfarction or arrhythmias, LVF and shock. In every case, total and differential white cell count, ESR, blood sugar, blood urea and serum cholesterol were estimated. Estimation of serum, histaminase and glutamic oxaloacetic transaminase (SGOT) was done by volumetric method of Kapeller-Adler [3] and Colorimetric method of Reitman and Frankel [9] respectively within 6 hours of infarction, repeated within 24 hours and then on the 2nd day, 3rd day, 5th day, 1.0th day and 15th day ascertained from the time of pain in the chest. Whenever any complication occurred, repeat estimation was done.
The normal range of serum histaminase in the control group was 0.12-0.76 P.U/ml with a mean of 0.413 ± 0.176 P.U./ml. The minimum diagnostic level was taken 0.8 P.U./ml. The normal range of SGOT in the control group was 1.0-22 I.U./L with a mean of 11.7 ± 5.9 I.U./L. The minimum diagnostic level was taken 30 I.U./L. Serum histaminase levels in ischaemic heart disease (other than acute myocardial infarction) were well within normal limits, the mean being 0.417 ± 0.23 P.U./ml. Similarly SGOT was also found within normal limit with a mean of 11.8 ± 4.72 I.U./L. Of the 35 cases of acute :myocardial infarction, 30 were ECG positive, the remaining 5 cases were ECG negative but had convincing clinical evidence of acute myocardial infarction. 6 cases (5 from the ECG positive group and 1 from ECG negative group) presented within 6 hours of infarction and the remaining 29 presented after 6 hours but earlier than 28 days. Serum hustaminase was found elevated in 34 (97.14%) out of 35 cases of acute myocardial infarction with a range of 1.0-4.60 P.U./ml. There was only one false negative case. While SGOT was found elevated in 32 (91.4%) out of 35 cases with a range of 31-192 I.U./L, there were 3 false negative cases. No false positive case was seen in either group. Out of the 5 ECG negative cases, 2 had LBBB, 1 had old myocardial infarction, 1 had complete heart block and 1 had ventricular tachycardia. Serum histaminase and SGOT were diagnostically raised in all the 5 cases, the range of the parameters being 1.4-4.3 P.U./ml and 32-167 I.U./ L respectively. Serum histaminase started rising within 6 hours of the episode of myocardial infarction and all the 6 cases who presented within 6 hours had diagnostic elevation of serum histaminase. On the other hand in none of these cases SGOT was found to be elevated above the diagnostic levels (i.e. more than 30 I.U./L). This clearly indicates that serum histaminase is an early diagnostic index of myocardial infarction in comparison to more often used enzyme SGOT. Both of these enzymes had maximum activity on the 2nd day (the peak values ranged from 1.7-3.8 P.U./ml with a mean of 2.44 P.U./ml and 23-192 I.U./L with a mean of 65.3 I.U./L. respectively). They started declining from the 3rd day and were elevated in only 47.8% and 39.1% cases respectively on the 5th day. Serum histaminase and SGOT were found elevated in none of the cases on the 10th day. Their levels on different days are shown in [Table 1]. Relation to complications Of the 35 cases of acute myocardial infarction, 18 (51.42%) had one or the other complication during the course of study. Of these 18 cases, 3 (16.66%) had cardiac failure, 5 (27.78%) had cardiac arrhythmias, 3 (16.66%) had cardiogenic shock and 7 (38,88%) had combination of complications. The mean serum histaminase level in complicated cases was 3.07 ± 0.95 P.U./ml which was significantly higher than that in uncomplicated cases (2.36 ± 0.33 P.U/ml) (p < 0.05). The highest levels of histaminase were in cardiogenic shock (mean value 4.46 ± 0.13 P.U./ml) which were significantly higher in comparison to that of left ventricular failure (2.15 ± 0.63 P.U./ml), congestive cardiac failure (2.4 P.U./ml) and arrhythmias (2.4 ± 0.54 P.U./ml). The mean SGOT level in complicated cases was 70.1 ± 37.4 l:U. /L which was significantly higher than that in uncomplicated cases (44.05 ± 9.7 I.U./L) (p < 0.05). Highest levels were recorded in cardiogenic shock (111.2 ± 66.5 I.U./L) which were significantly higher than those in left ventricular failure (55.0 I.U./L), congestive cardiac failure (44.7 I.U./L) and arrhythmias (55.2 ± 13.7 I.U./L). These are shown in [Table 2]. Relation to mortality Out of 35 cases of acute myocardial infarction 12 (34.28%) expired, due to one or the other complications and in these cases histaminase and SGOT levels were significantly higher than in those whc survived (p < 0.05). Cardiogenic shock was the commonest cause of death (7 out of 12, 79.35%) in comparison to other complications like cardiac failure and arrhythmias [Table 3]. There was a direct correlation between the height of raised enzyme levels and mortality. Nine out of 10 cases who had peak histaminase levels above 3.0 P.U.ml expired whereas only 3 expired out of 24 cases whose peak histaminase levels were below 2.9 P.U./ml. Similarly 7 expired out of 7 who had peak SGOT levels above 90 I.U./L and only 5 expired out of 27 who had SCOT levels below 90 I.U./L [Table 4].
In the healthy subjects, the serum histaminase levels were 0.12-0.76 P.U./ml with a mean of 0.413 ± 0.176 P.U./ml SGOT levels in healthy subjects rangec from 1.0-22 I.U./L with a mean of 11.7 ± 5.9 I.U./L. In cases of ischaemic heart disease (other than acute myocardial infarction) the levels of serum histaminase and SGOT were well within normal limits, mean being 0.417:± - - 0.23 P.U./ml and 11.8 :L 4.72 I.U./L respectively. The mean and the range of serum histaminase in healthy subjects and in cases of ischaemic heart disease (Other than acute myocardial infarction) in the present study are in conformity with those obtained by Lahiri et al. [4] but contrary to Sainani et al . [12] who reported raised histaminase levels in 3 out of 5 cases of coronary insufficiency and all the 4 cases of old myocardial infarction. The mean and the range of SGOT values in healthy subjects and cases of ischaemic heart disease (other than acute myocardial infarction) are in conformity with Rosalki and Wilkinson [10] and Pagliaro and Notarbartolo. [7],[8] Among the 35 cases of acute myocardial infarction serum histaminase levels were diagnostically raised in 34 cases (97.15%), thus only 1 false negative case was seen. The rise was 6.2 times above the mean normal values. These observations are in agreement with Lahiri et al [4] and Sainani et al. [12] who found diagnostic elevation of histaminase in 97% and 98% cases respectively whereas Chandwani [1] found diagnostic elevation in all the 25 cases (100 %). SGOT levels were diagnostically raised (5.2 times of mean normal values) in only 32 (91.4%) cases, and there were 3 false negative cases. These observations are in conformity with Rudolph et al [11] and Mathur et al . [6] In majority of cases serum histaminase started rising on the first day (within 6 hours) with a peak on the 2nd day. It started declining from the 3rd day and was elevated in only 47.8% cases on the 5th day and in none on the 10th day. These observations are in agreement with those of Lahiri et al. [4] but contrary to those of Chandwani [1] and Sainani et al. [12] who reported raised histaminase levels for whole of the 1st and 2nd week after infarction. In contrast, SGOT started rising on the first day but only after 6 hours. The peak was recorded on the 2nd day. It started declining from the 3rd day and was found elevated only in 39% cases on the 5th day and in none on the 10th clay. These findings are in conformity with Mathur et al. [6] and West et al. [13] Comparing the two enzymes, it has been found that histaminase is an early diagnostic index, is more sensitive and has high peak rise of levels than SGOT. 18 out of 35 cases (51.42%) of acute myocardial infarction developed one or the other complications and had significantly higher levels of serum histaminase and SGOT as compared to those in uncomplicated cases (p < 0.05). The cases of cardiogenic shock revealed highest degree of enhancement of histaminase and SGOT in comparison to cardiac failure and arrhythmias. Furthermore, a direct correlation has been found between the height of elevation of histaminase and SGOT and prognosis. Nine out of 10 cases expired who had peak histaminase levels above 3.0 P.U./ml whereas only 3 expired out of 24 who had peak histaminase levels below 2.9 P.U./ml. These observations are in conformity with those of Lahiri et al . [4] and Sainani et al. [12] Similarly 7 expired out of 7 who had peak SGOT levels above 90 I.U.//L and only 5 expired out of 27 who had peak SGOT levels below 90 LU./L. This is in conformity with Gour el al. [2] and Marrott et al. [5]
[Table 1], [Table 2], [Table 3], [Table 4]
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