Gamma-Glutamyl Transpeptidase and Other Liver Function Tests in Myocardial Infarction and Heart Failure

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1 Gamma-Glutamyl Transpeptidase and Other Liver Function Tests in Myocardial Infarction and Heart Failure M. G. BETRO, M.B., CH.B., F.R.C.P.A., R. C. S. OON, B.SC, AND J. B. EDWARDS, PH.D. Division of Clinical Chemistry, Institute of Medical and Veterinary Science, Adelaide, South Australia 5000 ABSTRACT Betro, M. G., Oon, R. C. S., and Edwards, J. B: Gamma-glutamyl transpeptidase and other liver function tests in myocardial infarction and heart failure. Am. J. Clin. Pathol. 60: , Serum gamma-glutamyl transpeptidase (GGTP) was measured and other liver function tests were performed in patients with myocardial infarction with and without cardiac failure, and in patients with cardiac failure from other causes. No late increase in GGTP occurred in myocardial infarction, and of the 27 patients who did not develop cardiac failure, only five had increased levels at any time. Elevations were more common when cardiac failure developed, and were also common in patients with cardiac failure from other causes. In our opinion, GGTP has little to offer in the diagnosis of myocardial infarction, and increases, when they occur, are the result of impairment of liver function. Abnormalities in other liver function tests, while common in cardiac failure, also occurred in a significant number of patients with uncomplicated myocardial infarction. This suggests that sufficient reduction of hepatic blood flow to cause abnormalities in liver function can occur in heart disease without the usual clinical signs of cardiac failure. SEVERAL INVESTIGATORS have do in fact come from the heart. They demonstrated increases in serum gamma- postulate that increased tissue levels deglutamyl transpeptidase (GGTP) in myo- velop in association with the repair process cardial infarction. Because the increase and that leakage into the bloodstream is late (the peak activity being between occurs. the seventh and eleventh days) and lasts We have measured serum GGTP (and as long as a month, it has been proposed done other liver function tests) serially as a useful test for the diagnosis of myo- in patients with myocardial infarction, but cardial infarction in the later stages. 79 could not demonstrate a late increase; Although the normal heart contains very in fact, only a third of the patients had little GGTP, most authors 2, suggest increased GGTP at any stage. We feel that the increased amounts in the serum that GGTP has little to offer in the diag- 7T!_,, m,., nosisof myocardial infarction, and further- Received December 12, 1972; received revised ' manuscript March 15,1973; accepted for publication more, we would argue that the increases, March 20, when they occur, are due not to the repair Requests for reprints should be addressed to M., _ ^. r, G. Betro, Chemical Pathology Department, Dunedin P r cess, but to impairment of hepatic Public Hospital, Dunedin, New Zealand. function. 679

2 680 BETRO ET AL. A.J.C.P. Vol. 60 ' We have also measured GGTP and done other liver function tests in patients with heart failure from other causes to assess the frequency of increased levels, and to compare them with those seen in patients with myocardial infarction. Materials and Method We studied 26 patients with myocardial infarction without cardiac failure, seven with myocardial infarction in whom rightsided cardiac failure developed, and 27 with right-sided cardiac failure from causes other than infarction. The diagnoses of infarction were confirmed by ECG findings and by aspartate aminotransferase (AAT) and lactate dehydrogenase (LDH) measurements. We measured serum GGTP, bilirubin, alkaline phosphatase (AP), lactic dehydrogenase (LDH), and aspartate aminotransferase (AAT) in all patients. In a few patients we performed the tests only once, but in most cases we performed them on at least three or four occasions up to the seventeenth day. We used the method of Szasz 17 for GGTP, but performed it at 30 C. instead of at 25 C. The precision of the method and the normal ranges obtained are given by us in another paper. 4 For the purposes of this study we took a value of 50 I.U. per 1. as being definitely abnormal. The other tests were performed with the SMA 12/60; the details of the methods are given in the Technicon Manual T Our upper limits of normal for the various tests are: bilirubin, 1.1 mg. per 100 ml.; AP, 90 I.U. per 1.; LDH, 300 I.U. per 1.; AAT, 45 I.U. per 1. Results Figure 1 shows the serial changes in GGTP in the three groups of patients. Only five of the 27 patients with myocardial infarction without cardiac failure had increased GGTP. Although some patients developed increases on days 4 to 10, the mean values did not increase throughout the 17-day period. In fact, they declined slightly from days 6 to 13. Of the five patients in this group who developed elevated values, one had complete heart block, another had pulmonary crepitations due to mild left ventricular failure throughout the 17 days, and a third had repeated episodes of atrial fibrillation. None of the other patients had such complications. Most of the patients in the other two groups had increased GGTP values. These ranged to as high as 200 I.U. per 1. In those with cardiac failure from causes other than infarction, the levels tended to stay up even after the clinical signs of failure had disappeared. Thus, most patients with uncomplicated myocardial infarction have normal GGTP levels, but these increase when heart failure or other complications develop. Furthermore, elevated levels are common in cardiac failure, whatever the cause. Table 1 shows the percentage of patients in each category who developed increased values for the various tests on at least one occasion. Surprisingly, a significant number of patients with uncomplicated myocardial infarction had high bilirubin and AP levels. However, in cardiac failure secondary to infarction the frequencies of increase for both tests were higher and were similar to that seen in cardiac failure from other causes. In patients with cardiac failure, whatever the cause, abnormalities in these tests were common. It is worth noting that increases in LDH and AAT were also quite common in patients with cardiac failure not due to infarction. However, these increases were usually mild (less than twice the upper limit of normal), and the levels were much less than those usually attained in myocardial infarction. Patients with infarction did not show significant changes from their initial bili-

3 November 1973 GAMMA GLUTAMYL TRANSPEPTIDASE IN HEART DISEASE 681 GGTP IU/ Myocardial Infarction wi thout heart failure Myocardial Infarction with heart failure Heart failure from other causes DAYS FIG. 1. Serial changes in GGTP. For the patients with myocardial infarction, the days refer to the number of days after onset. For the patients with heart failure from other causes, the days refer to days after admission. Asterisks denote patients who had only one estimation. rubin or AP levels on serial measurement. In those with cardiac failure not due to infarction the values for bilirubin, AP, LDH, and AAT were highest on the day of admission and declined slowly thereafter. However, most of those having high initial values still had elevated (but lower) values after clinical signs of failure had disappeared. Discussion We failed to find the late increase in GGTP in patients with myocardial infarction described by others 27 " and, in fact, only 11 of 33 patients developed increased levels at all. These increases were not confined to any one period. Our results are similar to those recently reported by Coodley, 6 who found elevated levels in only eight of 38 patients with infarction, and the increases, when they occurred, were nearly as common on days 1 to 2 as on days 5 to 7. Only one of his patients had high values on days 7 to 14 which, in the other reports, is the period of maximum elevation. We calculated the mean values for the three periods from Coodley's data and found that they decreased slightly rather than increased with time. It is interesting that in the first report of GGTP levels in myocardial infarction 11 it was said that the levels usually remained normal; this is in line with our findings and with those of Coodley. 6 Therefore, we feel that measurement of GGTP has little to offer in the diagnosis of myocardial infarction, in either the early or the late stages. Most of those who have reported high levels in myocardial infarction have suggested that the enzyme is coming from the heart. 28,91214 This theory is based upon the fact that the increase in serum GGTP occurs late and therefore might be related to the repair process, and is supported by the demonstration that the walls of new capillaries contain GGTP. 7 However, Ravens and associates, 12 who found a gradual increase with time in particle-bound GGTP in homogenates from necrotic heart muscle, postulated that the GGTP was present in the lysosomes of invading leukocytes;

4 682 BETRO ET AL. AJ.C.P. Vol. 60 Table 1. Percentages of Patients Showing an Abnormal Result on at Least One Occasion Alkaline Lactic Aspartate GGTP Phosphatase Dehydrogenase Aminotransferase Bilirubin Myocardial infarction without heart failure (n = 26) Myocardial infarction with heart failure (n = 7) Heart failure from other causes (n = 27) but this also postulates the heart as being the source, with local levels increasing because of the repair process. Even if there is GGTP in the walls of new capillaries or in the lysosomes of invading leukocytes, it does not necessarily follow that raised serum levels would result. The repair reaction in the heart is similar to repair processes elsewhere, and these do not result in increased GGTP in serum. No increase is seen, for example, with healing fractures, 10 which also contain abundant leukocytes and new capillaries. In this discussion we present our reasons for thinking that, in myocardial infarction, GGTP comes not from the heart, but from the liver. Abnormalities in other liver function tests, caused by a combination of anoxia and congestion of the liver, are common in congestive cardiac failure We have demonstrated here that serum GGTP, which is usually regarded as originating mainly from the liver, may also increase in cardiac failure. In our patients with cardiac failure secondary to myocardial infarction the values for GGTP were similar to those in patients with cardiac failure from other causes, but only five of the 26 patients with myocardial infarction and no cardiac failure had increases in GGTP. Three of these five patients had complications, such as heart block, atrial fibrillation and mild left ventricular failure, which could well have reduced hepatic arterial blood flow and impaired liver function. It is worth noting that most ofthe previous reports do not state whether the patients with myocardial infarction were in cardiac failure or not, but Dimov 7 states that in his patients the highest GGTP values occurred in those with cardiac failure, and Orlowski 11 states that values were normal in his patients but rose when right ventricular failure set in. Even in patients with uncomplicated myocardial infarction, abnormalities in other liver function tests may occur. We found, for example, that AP was elevated in 35% and bilirubin in 11.5% of such patients. Other authors have also reported abnormalities in liver function tests in myocardial infarction; some of these tests are specific for hepatic disease. 13 ' 7 ' 8 It seems reasonable to assume that in myocardial infarction, even when clinical signs of heart failure are absent, enough impairment of hepatic function might occur to produce rises in GGTP and other liver function tests. This is supported by the fact that hepatic function may by impaired in a variety of other cardiovascular conditions without necrosis, presumably reflecting circulatory effects on the liver. 9,1518 This could explain why increases were uncommon in our patients with uncomplicated myocardial infarction, since most were treated in a well-equipped coronary care unit, and any developing cardiac failure would be immediately spotted and treated. Thus, many would not progress to the stage where hepatic function became impaired. Although abnormalities in hepatic func-

5 November 1973 GAMMA GLUTAMYL TRANSPEPTIDASE IN HEART DISEASE 683 tion are known to be common in cardiac failure from any cause, most accounts state that it is usually bilirubin that is increased, and that AP is usually normal. 13,16 In our patients with cardiac failure, however, AP was increased in 70% and bilirubin in 44%. The two tests did not correlate with each other; many patients had high bilirubin with normal AP levels, whereas others had high AP with normal bilirubin levels. Serum LDH and AAT are not usually mentioned as being elevated in cardiac failure, but were elevated in 78% and 44% of our patients, respectively. This is similar to the experience of Calderon and Alexander. 5 The liver would seem to be the obvious source of these, but in some patients intravascular hemolysis may contribute to the LDH levels. References 1. Aber CP, Brunt PE, Wyn E, et al: Liver function after myocardial infarction. Lancet 1: , Agostini A, Ideo G, Stabilini R: Serum y-glutamyl transpeptidase activity in myocardial infarction. Br Heart J 27: , Albertini A, Cavaliere G, Bonera E, et al: Activities of liver enzymes in serum after myocardial infarction. Enzymologia 38:97-102, 1970 :, 4. Betro MG, Oon RCS, Edwards JB: Gammaglutamyl transpeptidase in diseases of the liver and bone. Am J Clin Pathol 60: , Calderon D, Alexander S: The liver in congestive heart failure. Med Clin North Am 50: , Coodley EL: Evaluation of y-glutamyl transpeptidase activity in myocardial infarction. JAMA 220: , Dimov D: A study of serum y-glutamyl transpeptidase activity in myocardial infarction. Cor Vasa 10: , Ewen LM, Griffiths J: Patterns of enzyme activity following myocardial infarction and ischemia. Am J Clin Pathol 56: , Hedworth-Whitty RB, Whitfield JB, Richardson RW: Serum y-glutamyl transpeptidase activity in myocardial ischaemia. Br Heart J 29: , Lum G, Gambino SR: Serum gamma-glutamyl transpeptidase as an indicator of disease in liver, pancreas, or bone. Clin Chem 18: , Orlowski M: The role of gamma-glutamyl transpeptidase in the internal diseases clinic. Arch Immunol Ther Exp (Warsz) 11:1-61, Ravens KG, Gudbjarneson S, Cowan CM, et al: Gamma-glutamyl transpeptidase in myocardial infarction. Circulation 39: , Richman SM, Delman AJ, Grob D: Alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes. Am J Med 30: , Rosalki SB, Rau D, Lehmann D, et al: Determinations of serum y-glutamyl transpeptidase activity and its clinical applications. Ann Clin Biochem 7: , Runde I, Dale J: Serum enzymes in acute tachycardia. Acta Med Scand 179: , Sherlock S: The liver in heart failure. Br Heart J 13: , Szasz G: A kinetic photometric method for serum y-glutamyl transpeptidase. Clin Chem 15: , Thomas AJ, Rees HA, Saunders RA: Live function in pulmonary heart disease. Br Heart J 27: , 1965

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