clinical use of biophysical, biochemical, and biostatistical methods; toward more emphasis on genetic factors; toward rationalization of therapy by attempted regulation of physiopathological imbalances; toward increasing at¬ tention to psychological and social factors; and, gener¬ ally speaking, toward greater surgical conservatism. All these trends are developing within the framework of a

cultural pattern that is placing greater emphasis the ideas of process, function, and integration, and the need for individual and group cooperation and altru¬ ism in all departments of human life. Urologists are being influenced by all these trends and are also making large and important contributions to them.

general on

2020 E. 93rd St.

(6).

SERUM AMINOPHERASE (TRANSAMINASE) IN DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION Albert A. Kattus Jr., M.D., Robert Watanabe, A.B., Charles Semenson, A.B., William Drell, Ph.D. and

Clarence Agress, M.D., Los Angeles A rise in the serum aminopherase (transaminase) level following acute myocardial infarction recently ob¬ served by LaDue and co-workers 1 suggests that serum level determinations of this enzyme may aid in ascertain¬ ing the presence or absence of myocardial necrosis. Aminopherase is found in2 many animal tissues, but it was first shown by Cohen to be particularly abundant in cardiac and skeletal muscle. It was this observation that led LaDue and his associates to estimate serum levels of this enzyme following myocardial infarction, with the idea that the necrotic myocardium would be likely to liberate aminopherase into the blood stream. The devel¬ 3 opment by Karmen, Wroblewski, and LaDue of a com¬ paratively simple spectrophotometric method fox the determination of serum aminopherase activity has made it possible to carry out a more detailed study of experi¬ mental and clinical myocardial infarction. One of us (C. A.) and co-workers, in collaboration with LaDue, have shown in experimental myocardial infarction in dogs that the peak serum aminopherase level bears a roughly quantitative relationship to the amount of infarcted muscle.4 Because preliminary observations suggest that the serum aminopherase level may prove to be a valuable test in the differential diagnosis and perhaps prognosis of myocardial infarction, this study was undertaken to extend our knowledge of its clinical applicability. One or more serum aminopherase levels were determined in 11 normal control subjects, 5 patients convalescing from myocardial infarction, 4 patients with congestive heart failure of various causes, 4 patients with acute benign From the Veterans Administration Center and the departments of medicine and physiological chemistry, University of California Medical Center. Autopsy data were furnished by Dr. Leo Kaplan, Chief Pathologist, Wadsworth General Veterans Administration Hospital, Los Angeles. Aspartic acid, \g=a\-ketoglutaric acid, reduced diphosphopyridine nucleotide, and malic dehydrogenase used in this study were supplied by the California Foundation for Biochemical Research. 1. LaDue, J. S.; Wroblewski, F., and Karmen, A.: Serum Glutamic Oxaloacetic Transaminase Activity in Human Acute Transmural Myocardial Infarction, Science 120:497-499, 1954. LaDue, J. S., and Wroblewski, F.: The Significance of the Serum Glutamic Oxalacetic Transaminase Activity Following Acute Myocardial Infarction, Circulation 11:871-877, 1955. 2. Cohen, P. P., and Hekhuis, G. L.: Rate of Transamination in Normal Tissues, J. Biol. Chem. 140:711-724, 1941. 3. Karmen, A.; Wroblewski, F., and LaDue, J. S.: Transaminase Activity in Human Blood, J. Clin. Invest. 34:126-133, 1955. 4. Agress, C. M., and others: Serum Transaminase Levels in Experimental Myocardial Infarction, Circulation 11:711-713, 1955.

\s=b\ Patients with myocardial infarction exhibited a rise of serum aminopherase far above the levels found in normal subjects. The rise began after a lapse of 6 to 12 hours, reached its peak in 24 to 36 hours, and was followed by a decline, reaching normal levels by the fifth or sixth day. Patients with other forms of heart disease had normal values. Patients with liver disease had elevations of the serum aminopherase level, but the time relations differed.

nonspecific pericarditis,

9 patients with miscellaneous cardiac and noncardiac diseases, 4 patients with liver disease, 14 patients with proved cases of myocardial in¬ farction, and 24 patients with anginal pain without defi¬ nite evidence of myocardial infarction. MATERIALS AND METHODS

The normal subjects were healthy laboratory and pro¬ fessional personnel. Patients were selected from the wards of the Wadsworth General Veterans Administra¬ tion Hospital. Blood samples were drawn with the usual precautions for avoiding hemolysis. The proce¬ dure of Karmen and co-workers 3 was followed closely. The malic dehydrogenase diluted 1:25 and the solution of reduced diphosphopyridine nucleotide (1 mg. per milliliter) were poured into small tubes and stored in a frozen state at -20 C. Under these conditions the for¬ mer was stable for at least a month and the latter for a week. Sufficient tubes of each were removed for a day's analysis, thawed, and stored in ice, and any excess solu¬ tion was discarded. The solutions of aspartic and alphaketo-glutaric acids in buffer were adjusted to a final pH

of 7.4.

RESULTS

The serum aminopherase levels obtained are sum¬ marized in tables 1 through 4. Normal Subjects and Patients Not Suspected of Hav¬ ing Acute Myocardial Infarction or Liver Disease.—In the group of 11 normal subjects there were 8 males and 3 females ranging in age from 26 to 64 years. Single serum aminopherase level determinations were obtained on each subject (table 1). Values ranged from 16 to 24 units. The five patients who were studied during con-

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valescence from acute myocardial infarction were all white men ranging in age from 45 to 78 years. Serum aminopherase level determinations were made in the pe¬ riod ranging from the 4th to the 27th day following the onset of the symptoms of myocardial infarction. The range of serum aminopherase levels in this group closely approximates the range of values for the normal sub¬ jects. Four patients were studied during attacks of se¬ vere left and right ventricular congestive heart failure. All patients were white men aged 39 to 62 years. The diagnoses were idiopathic myocarditis, rheumatic aortic stenosis, arteriosclerotic heart disease, and hypertensive heart disease with acute pulmonary edema. Multiple de¬ terminations of serum aminopherase levels were ob¬ tained on all but one of these patients. The range of

ONSET OF

had a serum aminopherase level of 14 units. after x-ray therapy the serum aminopherase was 16 units. A patient who was proved at autopsy to have a dissecting aneurysm with a large hematoma had a serum aminopherase level of 18 units. Two patients with cerebral vascular accidents believed to have been infarctions of the brain had serum aminopherase levels ranging from 17 to 27 units. Thus it is shown that the serum aminopherase level is not necessarily elevated by ischemia of an extremity, myalgia and muscle wasting, irradiation of a leiomyosarcoma, dissecting aneurysm with hematoma, or infarction of the brain. A patient sarcoma

One level

day

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SYMPTOMS

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A patient with myalgia and muscle wasting of un¬ known etiology had serum aminopherase levels of 11 and 16 units. A patient with intra-abdominal leiomyo-

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