Causes of death in aneurysms of the heart

American Federation for Clinical Research

668 Wayne cine,

University and

the

City

College of Detroit

of

Medi-

Receiving

Hospital.) The present methods of estimating the megakaryocyte content of aspirated sternal bone marrow are not satisfactory. Methods based on examination of marrow smears are unsatisfactory because the aspirated marrow is unavoidably diluted with sinusoidal blood; the distribution of megakaryocytes on smears is irregular; the total nucleated cell content of bone marrow is variable from patient to patient and the incidence of megakaryocytes may vary independently of the incidence of other nucleated cells. Hemocytometer counts of megakaryocytes are subject to error introduced by variable dilution with sinusoidal blood and also by the variable base of total nucleated cells. The present study showed that neither the smear nor chamber count method yields results which correlate with those obtained by study of actual marrow tissue sections. Instances of low counts obtained by the smear or chamber methods in patients with high megakaryocyte content, as revealed in marrow sections, were encountered. Even the section count produces arbitrary values which cannot be converted into terms expressive of the actual number of megakaryocytes per unit volume of marrow. Hence all section counts obtained from patients must be compared with counts made by identical means from suitable controls. Since the error of underestimating the megakaryocyte content of aspirated marrow samples may be of clinical importance, especially when the question of splenectomy for thrombocytopenic purpura is presented, examination of marrow sections for megakaryocytes should not be omitted whenever the chamber or smear methods yield values suggestive of decreased megakaryocytogenesis.

CLINICAL EVALUATION OF TETRAETHYLAMM~NIUM CHLORIDE IN CORONARY HEART DISEASE. Harold W. Christy, M.D., (introduced by Howard A. Lindberg, M.D.), Chicago, Illinois. Ten patients presenting symptoms that were considered classical of chronic coronary insufficiency with the angina1 syndrome, most of whom had abnormal electrocardiograms, were treated with bi-weekly intramuscular injections

of tetraethylammonium chloride. The dosage ranged from 200 to 800 mg. per injection. No reactions of moment were encountered in this group. Some of the patients received injections over a period of at least a year. Two patients had complete disappearance of their angina1 syndrome with improvement in the electrocardiogram during the course of treatment. Five patients reported considerable improvement in their symptoms. None developed what might be considered angina1 equivalents. Two had improvement in their electrocardiograms. Two patients reported no improvement whatsoever and one of them was the only one that did not have electrocardiographic or physical findings to support a diagnosis of coronary insufficiency. The tenth patient did not report for continuation of therapy and the results of treatment in this case are not known.

CAUSES OF DEATH IN ANEURYSMS OF THE HEART. Wendell A. Shullenberger, M.D., Indianapolis, Indiana. (From the Division of Internal

Medicine,

Methodist

Hospital.)

It is frequently stated that cardiac aneurysm is not incompatible with a considerable degree of physical activity and it is a fact that despite their spectacular pathologic features these when fully healed and fibrosed aneurysms undergo rupture infrequently. The usual causes of death following establishment of this condition in the heart are congestive failure, rupture and “sudden death.” The last group deserves more attention than it has received. The case reported here is believed to be unusual in the nature of the terminal event. A diagnosis of acute coronary thrombosis was made in a fifty year old male after he had suffered three attacks of epigastric pain in a period of eleven days. Aneurysm of the left ventricle was diagnosed by roentgenogram after three weeks in the hospital. He became ambulatory and carried on fairly normal business activities for thirteen months but died suddenly after several attacks of epigastric pain. Autopsy showed a large aneurysm of the left ventricle and a fresh thrombosis of the circumflex branch of the right coronary artery. Statistics obtained from analysis of forty-six well studied cases selected from the literature show that somewhat less than 50 per cent of patients may be expected to survive from a few months to several years. It is further shown that AMERICAN

JOURNAL

OF

MEDICINE

American

Federation

when aneurysm of the heart has been established, 46 per cent died of congestive failure, 11.5 per cent of rupture of the aneurysm, 11.5 per cent of acute coronary thrombosis, 8 per cent of left ventricular failure and 8 per cent of other causes. The remaining 15 per cent are classified as “sudden deaths.”

AN ENDOCRINEFINDING APPARENTLY CHARACTERISTIC OF GOUT. VERY Low URINARY 17-KETOSTEROIDEXCRETION,WITH CLINICALLY NORMAL ANDROGENIC FUNCTION. W. Q. Wolfson, M.D., R. Levine, M.D., H. S. Guterman, M.D., C. Cohn, M.D., H. D. Hunt, M.D. and E. F. Rosenberg, M.D., Chicago, Illinois. (From the Department

of Biochemistry

partment

of

Research,

Medical

Michael Clinic

Reese and

Michael the

Metabolic

the

Reese

Department

Albany

Medical

and

De-

Endocrine

Research

Institute,

Hospital;

the

Division Hospital, of

the

and

of

Chicago;

Internal

College,

Arthritis Medicine, and

Medicine,

Albany,

N. Y.)

The urinary 17-ketosteroids (KS) are the chief identified urinary excretory products of male sex hormone metabolism. Urinary KS values depend upon both testicular and adrenal androgen production in men and upon adrenal androgen production in women. Decreased urinary KS output has been found in all of a group of eleven gout patients (average 3.0 mg./day). Decreased excretion occurred in all phases of the disease including asymptomatic gout. Similar decreases did not occur in patients with idiopathic hyperuricemia and in males with rheumatoid polyarthritis or spondylitis. Review of currently available endocrine explanations for decreased 17-ketosteroid output of the degree noted indicated none to be acceptable. Injected testosterone was recovered as urinary l7-ketosteroid to the usual extent and no defects in hepatic function were noted. Renal function was well enough preserved to make “retention” of 17-ketosteroids improbable. In spite of accumulating evidence that altered adrenocortical glycocorticoid production may be important in acute gouty attacks there was stage” endocrine no evidence of “resistance status at other periods. Biologic evidence of androgen activity was normal in nine of the ten men in this group. A MAY,

1949

for Clinical

Research

669

review of a much larger series of patients gave additional evidence that hypogonadism is not clinically prominent in patients with gout. The findings of very low outputs of urinary 17-ketosteroids in the presence of normal biologic androgen activity appears to be a new endocrine finding which is characteristic for gout. Our working hypothesis is that in gout biologic androgen activity is maintained by an androgenic hormone which does not make an important contribution to urinary 17-ketosteroids when metabolized.

COMPARATIVE SYMPATHETICBLOCKING AND ADRENOLYTIC ACTION OF FOUR DRUGS IN THE HUMAN SUBJECT.J. W. Avera, M.D. (by invitation), S. W. Hoobler, M.D., (b)j invitation) S. G. McClellan, M.D. and (by invitation), W. J. Little, M.D., Ann Arbor, Michigan. (From the Department of Internal

Medicine,

University

Hospital.)

Comparative effects of the intravenous injection of tetraethylammonium chloride (TEA), (6 mg./Kg. body weight); priscol, (0.6 mg./Kg. body weight); dihydroergocornine (DHO), (0.005-0.01 mg./Kg. body weight) and piperidomethyl benzodioxane (9 33F) (10 mg./square meter body surface) on peripheral blood flow were studied by means of venous occlusion plethysmograph. As a result of these studies we have arrived at the following conclusions: Tetraethylammonium increases peripheral blood flow solely by a sympathetic blocking action. It does not produce vasodilatation in the denervated extremity and it has no adrenolytic effects. When injected intra-arterially, it has a slight vasoconstrictor action in concentrations well above those usually attained by intravenous injection. Priscol increases blood flow by a direct vasodilator action. It has weak adrenolytic properties when given intravenously and a more marked effect when given intra-arterially. It probably has relatively little sympatholytic action when administered intravenously since the increase in blood flow in the innervated extremity is considerably less than that following paravertebral block or ganglionic blockade with tetraethylammonium and since the innervated and denervated extremity show approximately equal vasodilation following injection of the drug. The increase in peripheral blood flow after