Annotations reported no prolongation of bleeding time in patients receiving sulfinpyrazone, it is unlikely that the observations of this in vivo test of platelet function were made by the same observer in any one patient, a condition which we found to be necessary to demonstrate an effect. It is not clear whether the reduction of fibrin on dialysers that we have demonstrated recently>, n is mediated by sulfinpyrazone’s action on platelets or by other mechanisms. Since the patients in these studies were to all intents and purposes anephric, the uricosuric action of the drug seems to be unimportant, and any effect it may have on the endothelium irrelevant. Perhaps the fibrin in white thrombi is derived from the platelets themselves, or its deposition may be mediated by platelet factors the release of which sulfinpyrazone inhibits, but which heparin and warfarin fail to influence. In another study of the effects of sulfinpyrazone during use of charcoal hemoperfusion,” we concluded that sulfinpyrazone reduced the stability of platelet aggregates, and it is interesting now to note Relman? invoking a similar mechanism to explain the reduction of sudden deaths with use of sulfinpyrazone after myocardial infarction. Ali and McDonaldl” have proposed inhibition of platelet prostaglandin synthesis as the mechanism by which sulfinpyrazone acts. This observation invites an inevitable but interesting comparison with aspirin, which inhibits platelet thromboxane synthesis and also vessel wall synthesis of the potent anti-aggregant, prostacyclin. A single 300 mg. dose of aspirin inhibits platelet function for up to 10 days, but many trials of aspirin’s antithrombotic potential have been carried out at much higher dosages which may have masked any benefit by blocking vessel wall prostacyclin synthesis.” Is the same true of sulfinpyrazone? And if so. is the 800 mg./day dose correct? Unlike aspirin, sulfinpyrazone does not increase occult gastrointestinal blood loss in healthy volunteers,‘Z an effect which aspirin may mediate by inhibition of gastric prostaglandin synthesis, and we await reports of sulfinpyrazone’s effects on vessel wall prostaglandin synthesis with interest. One wonders whether the organizers of large clinical trials of antithrombotic agents would repeat their investigations in the light of more optimum dosage schedules suggested by their pharmacological colleagues as, for example, with aspirin and dipyridamole?’ : Should other drugs that have been shown to have an inhibiting effect on platelets be subjected to clinical trials? The choice of appropriate drug and dosage schedule have no doubt deterred many trial organizers, but the Anturane Reinfarction Trial Research Group deserve congratulations both for their endeavours and also for their prompt and honest reporting of what may have been a surprise finding. One hopes that the trial will proceed to its conclusion, and no

Of “bends”

October,

for many

trials

King’s

of antithrombotM. J. Weston College Hospital Denmurk Hill London, S.E.5. England

REFhNCES

2. 3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

The Anthurane Reinfarction Trial Research Group: Sulfinpyrazone in theprevention of cardiac death after myocardial infarction, N. Engl. J. Med. 298:289, 1978. Relman, A. S.: New job for an old drug? N. Engl. J. Med. 298295, 1978. Smythe, H. A., Ogryzlo, M. A., Murphy, E. A., et al.: The effect of sulfinpyrazone (anturan) on platelet economy and blood coagulation in man, Can. Med. Assoc. J. 92:818, 1965. Mustard, J. F., Rowsell, H. C., Smythe, H. A.,,et al.: The effect of sulfinpyrazone on platelet economy and thrombus formation in rabbits, Blood 29:859, 1967. Dawson, A., Lavinski, C., Weston, M. J., et al.: Sulfinpyrazone as a method of keeping dialysis membranes clean, in Technical Aspects of Renal Dialysis, edited by Frost, T. H., Belmont, Calif., 1978, Pitman Medical Publishing co., p. 133. Mustard, J. F., Rowsell, H. C., and Murphy E. A.: Platelet economy (platelet survival and turnour), Br. J. Haematol. 12:1, 1966. Weston, J. J., Rubin, M. H., Lanalev. P. G.. et al.: Effects of sulfinpyrazone and dipyridamole on capillary bleeding time in man, Thromb. Res. 10:8X. -. - - -, 1977. -Woods, F., Ash, G., and Weston. M. J.: Sulfinovrazone reduces fibrin deposition on dialyser membranes. Clin. Sci. Molec. Med. 55:19, 1978. Weston, M. J., Hanid, A., Langley, P. G., et al.: Biocompatibility of coated and uncoated charcoal during haemoperfusion in healthy dogs, Europ. J. Clin. Invest. 7:5, 1977. Ali, M., and McDonald, J. W. D.: Effects,of sulfinpyrazone on platelet prostaglandin synthesis and platelet release of serotonin, J. Lab. Clin. Med. 89:868, 1977. Baenzinger, N. L., Dillender, M. J., and Majerus, P. W.: Cultured human skin fibroblasts and arterial cells produces a labile platelet inhibiting prostaglandin, Biochem. Biophys. Res. Commun. 78:294, 1977. Dawson, A., Lavinski, C., Parsons. V.. et al.: Effects of sulfinpyrazone and aspirin on gastrointestinal blood loss in man, Thromb. Res. 12:947~ , 1978 --.-. Moncada, S., and Korbut, R.: Dipyridamole and other phosphodiesterase inhibitors act as antithrombotic agents by potentiating endogenous prostacyclin, Lancet i:l286, 1978. -

“ .

.”

cardiomyopathy

People who work under pressures above atmospheric pressure, such as divers, must return to atmospheric pressure slowly and properly. In those who are careless and who attempt to be

535

doubt it will serve as a model ic agents to come.

1979,

Vol.

98, No.

4

decompressed rapidly ment, or equipment throughout the body

0002-8703/79/100538

because failure, including

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of impatience, poor managebubbles of air are released the myocardium.’ The earliest

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C. V. Mosby

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Annotations

BENDS

CARDIOMYOPATHY A.H.,

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Fig. 1. Serial electrocardiograms of a 30-year-old man who developed “bends” cardiomyopathy. was recorded during the bends, whereas the tracing in B was recorded after full recovery. Note QRS complex, ST segment and T waves, particularly in Leads aVF and V,-V,.

and most subtle changes that reflect myocardial injury occur in the configuration of the time course of the ST segment and T wave of the electrocardiogram (Fig. 1). These mild changes rapidly reverse to normal if the damage is detected early and is not too extensive and if the subjects are rapidly recompressed. Extensive damage can occur with extremely rapid decompression or with repeated attacks of “bends.” Cardiac discomfort similar to angina pectoris could possibly occur, but most of the discomfort is in the skeletal muscles and joints and headaches.’ George E. Barth, M.D. Tulane University School of Medicine and Charity Hospital of Louisiana New Orleans, La.

Pathology surgery*

of coronary

artery

by Specialized

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Center

+ 02$00.20/O

of Research

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Grant

1.

2.

bypass

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No.

V6

The tracing in A the changes in the

Balldin, U. I., and Borgstrcm, P.: Intracardial bubbles during decompression to altitude in relation to decompresGon sickness in man, Aviat. Space Environ. Med. 47:113, 1976. Erde, A. and Edmonds, C.: Decompression sickness: A clinical series, J. Occup. Med. 17:324, 1975.

graft

totally occlusive thrombi develop is not clear. Endarterectomy of the native coronary artery is one factor which appears to predispose to thrombosis; trauma to the vein itself at the time of its preparation may be another. Compression of the anastomosis site is seen usually when the native vessel is of small caliber and has insufficient wall to be taken up in a suture line without resulting in lumenal compromise. This mechanism of graft failure occurs both when the native coronary artery is unduly small (< 1 mm.) or when the lumen at the anastomosis site is narrowed unexpectedly by eccentric plaque. Coronary arterial dissection may be a cause of anastomosis failure but it is infrequent, probably because atherosclerotic changes in the coronary artery limit medial hematoma extension. Morphologic changes within the vein graft itself are of little consequence in the early course of coronary bypass surgery,

50-HL-

C. V. Mosby

V5

REFERENCES

Coronary artery bypass surgery is creating a new form of heart disease with considerably altered coronary anatomy. Detailed understanding of the morphology of the heart after coronary bypass surgery is important to sorting out the success or failure of this procedure. A pathologic study of coronary bypass surgery includes evaluation of the anastomosis sites, changes in the implanted bypam graft per se, and an assessment of the effects of this procedure on the myocardium. Most graft occlusions occur at the coronary artery-graft anastomosis site, and the mechanisms responsible are predominately thrombosis, and compression of the lumen by the suture line.’ z Although some thrombotic deposition almost always occurs at the anastomosis site, why in some patients *Supported 17655-04.

30 Wkl

Co.

American

Heart

Journal

539