Serum chromium in patients old myocardial infarction
with
recent
and
Abraham S. Abraham, M.D., F.R.C.P. Moshe Sonnenblick, M.D. Maya Eni Ovadiah Shemesh, M.D. Ahron P. Batt Jerusalem, Israel
Persons dying of coronary heart disease were found to have virtually no chromium in their aortas, whereas those dying of accidents or other diseases had aortic chromium.’ Chromium levels in tissues of Americans tended to be low and declined with age,‘. 2 whereas tissues of Africans and Orientals contained much higher concentrations. Tissues of Thailanders had more chromium than any other group and they also had a very low incidence of aortic atherosclerosis.” Chromium deficiency has also been linked with an impairment of glucose tolerance, elevated serum cholesterol levels, and the causation of aortic plaques in animals4. 5 These findings have led to the conclusion that decreased or absent aortic chromium in atherosclerosis reflects the decreased or absent chromium in the coronary arteries and that this condition leads to abnormal metabolism and plaque formation.” The measurement of plasma chromium has until recently presented technical difficulties, and no information is available regarding the blood levels of chromium in patients suffering from acute myocardial infarction or known to have coronary artery disease. From the Department of Medicine, Shaare Zedek Inter-Department Equipment Unit, Hadaasah Hebrew University, Jerusalem, Israel. Received
for publication
Feb. 28, 1979.
Accepted
for publication
July
Hospital, Medical
and the School,
2, 1979.
Reprint Hospital,
requests: Dr. A. S. Abraham, Jerusalem. Israel.
604
May,
Dept.
1980, Vol. 99, No. 5
of Medicine,
Shaare
Zadek
Patients
and
methods
Forty-five patients without serious disease who were seen in the outpatient clinics and healthy volunteers were taken as controls. Diabetic subjects (fasting blood glucose of over 110 mg./lOO ml.) were excluded and no patient had a history or electrocardiographic evidence of ischemic or rheumatic heart disease, arteriosclerosis, hypertension, or congestive cardiac failure. No patient was receiving medication. Thirty-four patients attending the outpatient clinic who had been hospitalized 6 to 12 months previously with proven myocardial infarction were taken as the test group. Any patient with a fasting blood glucose level of over 110 mg./lOO ml. was also excluded from the study. Thirty-seven patients consecutively admitted with a definite diagnosis of myocardial infarction (that is, typical history and electrocardiographic changes, together with elevation of serum GOT and LDH) were also studied and the serum chromium was determined the morning after admission, 1 to 4 days later, and again 5 to 10 days following admission. Finally, the serum chromium was measured in 14 patients who were either diabetic or who were receiving intravenous glucose. The latter were patients with chest pain who did not have any electrocardiographic or enzyme changes. Serum chromium was measured by atomic absorption spectrophotometry as described by Pekarek and associates.’ In each case paired samples were taken in polyethylene test tubes
0OiZ12-8703/80/050604
+ 03$00.30/00
1980
The
C. V. Mosby
Co.
Serum chromium and myocardial infarction
after an overnight until analysis.
fast and were kept at -20”
C.
Results
There were 32 males and 13 females in the control group and their ages ranged from 22 to 90 years (mean, 49.9 years). The mean serum chromium was 1.71 parts per billion (ppb) (SE. z!c0.14). Thirty-four patients (25 males and nine females) aged 42 to 85 years (mean, 59.1 years) with ischemic heart disease (IHD), all of whom had had a proven myocardial infarct 6 to 12 months previously, had a mean serum chromium level of 1.84 ppb (SE. f 0.18). Analysis of both groups showed no significant differences due to sex or age nor was there any significant difference between the mean serum chromium levels of the two groups. Serum chromium levels in 37 patients during the first 24 hours following a myocardial infarction were not significantly different from our control population. However, there was a significant rise during the next four days to a maximum mean level of 6.36 ppb (SE. + 0.51; p < 0.001) and a subsequent fall to normal levels during the next 5 days. The serum chromium in five of these patients were between 2.9 and 3.3 ppb, that is just below the mean plus 2 standard deviations (3.5 ppb) of the control group. The serum chromium levels in 22 patients who were not in cardiac failure was positively correlated with “infarct size” as assessedby the maximum rise in SGOT (r = 0.5036; p < 0.05). There was no evidence of any relationship between serum chromium levels and the presence or absence of cardiac failure. There was no increase in serum chromium levels in the 14 patients with raised blood glucose levels (diabetic subjects or patients receiving glucose infusions), nor was there any correlation between blood glucose levels and serum chromium in the patients with acute myocardial infarction. Discussion
The level of serum chromium found in our normal control group compares with recently published data in which a mean of 1.58 ppb (S.E. -C 0.08) was found in healthy volunteers.’
American Heart Journal
We found no statistical difference in the mean serum chromium levels between patients knotin to have IHD and those without any clinical evidence of the disease. This by no means excludes the possibility that the patients in the control group had pathological coronary (or for that matter any other) arteries; however, they were symptom-free and had no obvious evidence of atherosclerotic disease. All our patients came from Jerusalem and drank the same water, and so presumably had the same intake of chromium. However, solitary plasma chromium levels are said not to provide a valid index of chromium nutritional status.* Nevertheless, we have been unable to find evidence of an association between the serum chromium level and the presence or absence of clinically evident ischemic heart disease. Soon after an acute myocardial infarction, there is a significant though temporary increase in serum chromium levels. This may be due to release from the damaged myocardial tissue, as is suggested by the significant correlation with the maximum rise in SGOT. However, whether the lower concentrations of chromium found in the tissues of patients who have died from their infarct is an acute phenomenon or an accompaniment of their atherosclerotic heart disease is not yet clear. Since all our patients were receiving glucose infusions during the acute stage of their myocardial infarction, and since the infarction itself may lead to a temporary impairment of glucose tolerance, the serum chromium levels may have been influenced by changes in the blood glucose.s Others9 have indeed reported that an oral glucose challenge results in a temporary increase in plasma chromium levels. However, we found no correlation between serum chromium and blood glucose levels in the 14 patients we examined (with raised blood glucose levels), nor was there any correlation between serum chromium and blood glucose levels in the patients with acute myocardial infarction. Summary
The serum chromium in 45 subjects with no clinical evidence of ischemic heart disease was found to be 1.71 parts per billion (ppb) (S.E. + 0.14). In 34 patients with a previously documented myocardial infarction, it was 1.84
605
Abraham
et al.
ppb (S.E. I 0.18). The difference was not significant nor was there any difference with age or sex. In 37 patients with acvte myocardial infarction the serum chromium level rose to a mean of 6.36 ppb (S.E. * 0.51; p < 0.001) during the first five days following the infarct, returning to normal over the next five days. There was no correlation between the serum chromium and blood glucose levels in these patients or in a further 14 patients who were receivihg glucose infusions (chest pain without electrocardiographic or enzyme changes) or who were diabetics. We are grateful to The Joint Research Fund of the Hebrew University and Hadassah and to the Chief Scientist’s Office of the Ministry of Health for their support of this project.
Schroeder, H. A., Nason, A. P., and Tipton, I. H.: Chromium deficiency as a factor in atherosclerosis, J. Chronic Dis. 23:123, 1970.
Information
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4.
5.
6. 7.
a. 9.
REFERENCES 1.
2.
Schroeder, H. A.: The role of chromium in mammalian nutrition, Am. J. Clin. Nutr. 21:230, 1968. Schroeder, H. A.: Degenerative cardiovascular disease in the Orient. I. Atherosclerosis, .J. Chronic Dis. 8:287. 1958. Schroeder, H. A., and Balassa, J.J.: Influence of chromium, cadmium and lead on rat aortic lipids and circulating cholesterol, Am. J. Physiol. 209:433, 1965. Schroeder, H. A.: Chromium deficiency in rats. A syndrome simulating diabetes mellitus with retarded growth, J. Nutr. 88:439, 1966. Schroeder, H. A.: The role of trace elements in cardiovascular diseases, Med. Clin. North Am. 58:381, 1974. Pekarek, R. S., Hauer, E. C., Wannemacher, R. W., Jr., and Beisel, W. R.: The direct determination of serum chromium by an atomic absortpion spectrophotometer with a heated graphite atomizer, Anal. Riochem. 59:283, 1974. Hambidge, K. M.: Chromium nutrition in man, Am. J. Clin. Nutr. 27:505, 1974. Glinsman, W. H., Feldman, F. J., and Mertz, W.: Plasma after glucose administration, Science chromium 152:1243, 1966.
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