Annotations REFERENCES

1.

2.

3.

4. 5. 6. 7.

8.

Nicolaides, A. N., Harbourne, T., Bowers, R., Kidner, P. H., and Besterman, E. M.: Blood viscosity, red-cell flexibility, haematocrit, and plasma-fibrinogen in patients with angina, Lancet 2:943, 1977. Burge, P. S., Johnson, W. S., and Prankerd, T. A. J.: Morbidity and mortality in pseudopolycythaemia, Lancet 1:1266, 1975. Thomas, D. J., Marshall, J., Ross Russel, R. W., Wetherley-Mein, G., DuBoulay, G. H., Pearson, T. C., Symon, L., and Zilkha, E.: Effect of haematocrit on cerebral blood-flow in man, Lancet 2:941, 1977. Editorial: Haemorheology, blood-flow and venous thrombosis, Lancet 2:113, 1975. Dintenfass, L.: Hyperviscosity in disease, Lancet 1:327, 1978. Haggendal, E. and Norback, B.: Effect of viscosity on cerebral blood flow, Acta Chir. Stand. 364:13, 1966. Haggendal, E., Nilsson, N. J., and Norback, B.: Effect of blood corpuscle concentration on cerebral blood flow, Acta Chir. Stand. 364:3, 1966. Leblond, P. F.. and Weed, R. I.: The peripheral blood in

Nonbacterial myocardial

thrombotic infarction

9.

10.

11.

12.

13. 14.

endocarditis

and

Nonbacterial thrombotic endocarditis (NBTE), an entity characterized by bland fibrin-platelet thrombus on cardiac valves and the absence of microorganisms or valve destruction, may be the cause of significant morbidity and mortality as a result of major arterial embolization. NBTE is no longer regarded as a pathologic curiosity, occurring in about 1.6 per cent of adult deaths.’ It is associated with a variety of diseases, most commonly malignant tumors. Adenocarcinomas, particularly mucin-secreting types, predominate in most series.‘, ? The pathogenesis of NBTE is not clear; disseminated intravascular coagulation and thrombotic phenomena are not infrequently encountered, suggesting a pathogenetic role of coagulation abnormalities (hypercoagulable state) in some cases.” ’ Coronary embolism with myocardial infarction is one of the dreaded complications and was found in 6.7 per cent and 9 per cent of patients with NBTE in two recent studies.‘. ’ Thromboembolism, usually of the intramyocardial arteries, without myocardial infarction, is found more frequently but is not judged to be of clinical significance. All patients described so far have had underlying malignant neoplasms, characteristically of epithelial origin. This complication of NBTE has been reported in patients of both sexes with ages ranging from the third to the eighth decade. Pathologically, the vegetations of NBTE are small, measuring less than 10 mm. and usually situated on the closure or free margins of the valves. As may be expected, most verrucae are located on the mitral and aortic valves. The pathologic alterations in the hearts of patients with myocardial infarction associated with NBTE are not distinctive. The heart may be normal or moderately enlarged. An underlying cardiac disease such as rheumatic valvulitis may be present. The

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polycythaemia vera and myelofibrosis, Clinics Haematol. 4:353, 1975. Kannel, W. B., Gordon, T., Wolf, P. A., and McNbmara, P.: Hemoglobin and the risk of cerebral infarction: The Framingham Study, Stroke 3:409, 1972. Abu-Zeid, H. A. H., Choi, N. W., Maini, K. K., Ping-Hwa, H.. and Nelson. N.: Relative role of factors associated with cerebral infarction and cerebral hemorrhage, Stroke 8: 106, 1977. Gordon, R. S., Kahn, H. A., and Forman, S.: Altitude and CBVD death rates show apparent relationship, Stroke 8:274, 1977. Olesen, J.: Cerebral blood flow, methods for measurement, regulation, effects of drugs and changes in disease, Acta Neurol. Stand. 5O(Suppl. 57):31, 1974. Burch, G. E., and DePasquale, N. P.: Hematocrit, viscosity and coronary blood flow, Dis. Chest 48:225, 1965. Erslev, A. J.: Erythrocyte disorders, in Williams, W. J., Beutler, E., Erslev, A. J., and Rundles, R. W., editors: Textbook of Hematology, New York, 1977, McGraw-Hill Book Company, Inc., p. 255.

Co.

intramyocardial or coronary arteries or both frequently contain thromboemboli. Histologically, multiple acute infarcts of different ages are usual. A single area of infarction may result when the embolus lodges in a coronary artery or a large intramyocardial artery. This was described in three of six cases published recently.’ The pathologic diagnosis should be accepted only in the presence of extensive occlusion of coronary arteries or their branches and in the absence of significant atherosclerosis or other diseases of coronary arteries. The antemortem diagnosis of NBTE-associated myocardial infarction is difficult but not impossible.” Most patients have concomitant neurologic symptoms probably secondary to cerebral embolism. These symptoms may mask the chest pain that would alert physicians to the diagnosis of myocardial infarction. Severe symptoms and signs resulting from embolization to other organs-kidneys, spleen, the gastrointestinal tract-may further complicate the clinical picture. The diagnosis under these conditions would depend on a high index of suspicion. It is suggested that, in the patient at risk (with carcinomatosis or other disseminated malignant neoplasms), there should be intermittent monitoring with noninvasive techniques such as electrocardiograms, cardiac enzyme studies and screening for evidence of disseminated intravascular coagulation, venous thrombosis or hypercoagulable state by determining platelet counts, partial thromboplastin time, prothrombin time, and levels of blood fibrinogen and fibrin split products. The latter, in combination with nonspecific signs such as changing murmurs and purpuric skin lesions”, ’ may indicate the presence of NBTE, thus increasing the potential for the diagnosis of myocardial infarction. In most patients, the clinical status and the severity of the underlying diseases would preclude coronary angiography, coronary

American

Heart

Journal

405

Annotations

embolectomy, or bypass therefore advised.

graft.

The

Conservative

management

is

A. Olusegun Fayemi, M.D. Department of Pathology Holy Name Hospital Teaneck, N. J. 07666 Ludwig M. Deppisch, M.D. Department of Laboratories Youngstown Hospital Association Youngstown, Ohio 44501

2.

Deppisch, L. M., and Fayemi, A. 0.: thrombotic endocarditis. Clinicopathologic AM. HEART J. 92:723, 1976. Rosen, P., and Armstrong, D.: Nonbacterial

Absence following

Non-bacterial correlations,

March,

5.

7.

thrombotic

of any change in thyroid function acute myocardial infarction

Since thyroid hormones specificially stimulate one of the adenyl cyclase systems in myocardium,l any change in thyroid function, which occurs after acute myocardial infarction would be of potential clinical significance. Previous observations in this regard have produced conflicting findings.? The object of the present study was to determine the effect of acute myocardial infarction on the function of the hypothalamic-pituitary-thyroid axis. Ten patients admitted to hospital with acute myocardial infarction were studied. The diagnosis was confirmed by ECG and enzyme changes and informed consent was obtained in each case. Total thyroxine (TT,), free thyroxine (FT,), total triiodothyronine (TT,), free triodothyronine (FT.,) and thyroid stimulating hormone (TSH) were measured and a thyrotrophin releasing hormone (TRH) test was performed 24 hours after the acute incident. These tests were repeated 14 days later. Total thyroxine, TT,% and TSH were measured by radioimmunoassay by the methods of Challand and associates’ and Hall and colleagues.’ Free thyroxine and FT., were derived from the TT, and TT,, and the dialysable fractions obtained by equilibrium dialysis.” All data were subjected to Student’s t test for paired data. The results obtained are shown in Table I. All results for individual patients were within the normal ranges and there were no significant differences between any of the baseline parameters nor in the TSH response to TRH at 24 hours and 14 days after acute myocardial infarction. It has been suggested by Vanhaelst and co-workers’ that previous investigators were unable to demonstrate changes in thyroid function in patients with myocardial infarction because of inadequate diagnostic criteria. In the present study the same criteria as theirs were used but nevertheless we have failed to demonstrate any change in thyroid function, thyroid

406

4.

6.

REFERENCES 1.

3.

endocarditis in patients with malignant neoplastic diseases, Am. J. Med. 54:23, 1973. McKay, D. G.: Disseminated intravascular coagulation, New York, 1965, Hoeber Medical Division, Harper & Row Publishers. Fayemi, A. O., and Deppisch, L.: Coronary embolism and myocardial infarction associated with nonbacterial thrombotic endocarditis, Am. J. Clin. Pathol. 68:393, 1977. Guinn, G. A., Ayala, A., and Liddicoat, J.: Clinical and therapeutic considerations in nonbacterial thrombotic endocarditis, Chest 64:26, 1973. Weinstein, L., and Schlesinger, J. J.: Pathoanatomic, pathophysiologic and clinical correlations in endocarditis, N. Engl. J. Med. 291:1122, 1974. Goldstein, R. S., and Zak, F. G.: Skin lesions caused by embolism from heart valves with nonbacterial endocarditis, Arch. Dermatol. 93:585, 1966.

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97, No.

3

Table

I Time after acute myocardial infarction 24 hours (mean r SD)

TT, (nmol./L.) TT, (nmol./L.) FT, (pmol./L.) FT, (pmol./L.) TSH-basal-(mu/L.) TSH-20 minutes TRH-(mu/L.)

after

78 -+ 1.6& 20 + 3.3+ 3.52 11.5-c

14 0.4 6.0 1.6 1.3 4.5

14 days (mean f SD) 81 ?I1 1.6+ 22 r 3.4* 3.1 z!z 9.6a

0.4 7.0 1.0 1.6 2.5

hormone binding, or in the hypothalamic-pituitary-thyroid axis after acute myocardial infarction. It is possible that these discrepancies are due to differences in the severity of the patient’s illness rather than in the diagnostic criteria used. J. E. Thomson, M.B., M.R.C.P.(U.K.) Registrar in Endocrinology University Dept. of Medicine and Radioimmunoassay Unit Royal Infirmary Glasgow, Scotland Present address: Senior Registrar Stobhill General Hospital, Glasgow S. G. Baird, B.Sc. Senior Biochemist J. A. Thomson, M.D., F.R.C.P. Senior Lecturer

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Co.

Nonbacterial thrombotic endocarditis and myocardial infarction.

Annotations REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. Nicolaides, A. N., Harbourne, T., Bowers, R., Kidner, P. H., and Besterman, E. M.: Blood viscosit...
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