When patients with myocardiai infarction were kept in bed for several weeks, thromboemboiic complications were thought to be the casue of death in some 4 per cent of patients.’ Although most cardiologists think that such complications are less common now that patients with myocardial infarction are mobilized more quickly, a third of such patients still develop evidence of ieg vein thrombosis, as detected by the I’?” fibrinogen uptake test,‘ and a proportion of these undoubtedly develop fatal pulmonary embolism. Another serious throm- boembolic complication is cerebral embolism from thrombi on the ventricular wall.

It is recognized that heparin therapy in full dosage effec- tively prevents thromboembolic complications after myocar- dial infarction,” but this benefit has to be weighed against the possible hemorrhagic complications of the treatment. Studies, which were undertaken to denne those patients in whom the risk of thromboembolism would be greater than the risk of the hemorrhagic complications of the anticoagulant therapy, indicated, not unexpectedly, that thromboembolic complica- tions were more likely in the elderly, in those in heart failure, and in those with a significant dysrhythmia.’ Unexpectedly it was also found that leg vein thrombosis after myocardial infarction was significantly more common in non-smokers than in smokers.“- 6

Deciding which patients should be given full dose heparin prophylaxis was a nice exercise in clinical judgment to which the technique of decision theory has been applied,’ but these niceties of clinical decision making have been made less necessary by the advent of low-dose heparin prophylaxis. This has been shown to be effective in preventing thromboembolic complications after surgery8 and several studies have now shown that low-dose heparin prophylaxis is also effective in preventing leg vein thrombosis, and so presumably pulmonary embolism, after myocardial infarctionY-”

The lower incidence of leg vein thrombosis after myocardial infarction in smokers compared to non-smokers is the first reported health benefit of smoking. It is a dubious one, however, because the smoker is more likely to be suffering from a myocardial infarction in the first place.

Why being a cigarette smoker should confirm any protec- tion against leg vein thrombosis after myocardial infarction is not known. It is interesting that a decreased incidence of leg vein thrombosis has also been reported in smokers after gynecologiczl operations.”

One possible explanation is that smokers are likely to be more fidgety people, especially when they have had to stop smoking after admission to a coronary care unit, and start >their own involuntary postoperative or postmyocardial infarc- :ion mobilization earlier.

000%8703/78!0196-0129$00.20/O a 1978 The 6. Y. Mosby Co.

The practicdl conclusion to be diav.n Go::1 tnese observa tions is that low-dose heparin prophylaxis should probably be given to all patients with myocardial infarct ion and cerr.ain!) to those with an increased risk of thromboembolic complica- tions, that is the elderly, those with varicose veins or a previous history of tbromboembo~ism, those in cardiac failure or a dysrrhythmia, and those who are non-smokers. Five thousand units of heparin are given intraireiiorraly and 7,500 subcutaneously as soon as possible after diagnosis and then 7,500 units subcutaneously every 12 hours ui-.tii ;he patiect is mobilized.

The oniy disadvantages of giving low-dose hepatin prophy- laxis are the cost and trouble and the occasional prob!em of bruising at the subcutaneous injection sites. Such bruising can be minimized by careful attention to the &jectlcn technique. Seven thousand five-hundred units of beparin. in 0.2 ml. is drawn up into a tuberculin syringe and injected subcuta- neously mto the anterior abdominal wall near the iliac crest, using a new fine gauge needle, i.e., not the ore which was used for drawing up the heparin. The nurses should be told to inserr.

the needle vertically and to resist. their overwbeiming instinct to rub the site of the injection. There is evidence from a small controlled trial that calcium heparin is less likely to cause bruising than sodium heparin,” but ihe difference is probably marginal.

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IIilden, T., Inversen, K., BaascL::. P.: a.16 dchwa:rz, &I.. Anticoagulants in acute myocardia: iiihrction, LanX:ei 2327, 1961. Murray, T. S., Lcrimer, A, R.; LOX, F. C., and Law&, T. D. V.: Leg vein thrombosis following m,irocardiat infai-c- tion, Lancet 2~792, 1970. Handley, A. J., Emerson, I?. A., and Fleming, P. I?.: Beparii in the prevention of deep vein thrombosis after myocardial infarction, Br. Med. 2;. 2~436, 1972. Simmonds, A. Y., Sheppard, M. A., and Cox, A. F.: Deep vein thrombosis after myocardiai ir: far&on: predis- x&sin8 factors. Br. Heart J, 35:&B. 1373. hand&y, A. ‘I., and Teather, 5.: The influence of smoking on deep vein thrombosis after myocardiai infarction, Br. AMed. J. 3:302, 1974. Marks, P., and Emerson, P. A.: Increased incidence of deep vein thrombosis aft.er myocardid infarction in non- smokers, %r. Med. J. 3532, 1974. Emerson, P. A., Teather, D.. and Handiey, A. 2.: The application of decision theory to the prevention of deep

Annotations

vein thrombosis following myocardial infarction, Q. J. Med. 43:389, 1974.

8. An International Multicentre Trial. Prevention of fatal postoperative pulmonary embolism by low doses of heparin, Lancet 2:45, 1975.

9. Steffensen, K. A.: Coronary occlusion treated with small doses of heparin, Acta Med. Stand. 1 X6:519, 1969.

10. Warlow, C., Beattie, A. G., Terry, G., Ogston, D., Kenmure, A. C. F., and Douglas, A. S.: A double blind trial of low doses of subcutaneous heparin in the preven- tion of deep vein thrombosis after myocardial infarction, Lancet 1:934, 1974.

Of how non-invasive is non-invasive?

When a treadmill exercise test is obtained along with echocar- diogram (ECHO), Holter monitoring, vectorcardiogram (VCG), apexcardiogram, carotid pulse tracing, and jugular phlebogram, as well as with routine urinalysis, ECG, EPA of the chest, SMA 12 and often repeats of the same, etc., the special procedures are considered “non-invasive.” But, how non-invasive are they psychologically and economically? All experienced physicians know how disturbing the mere mention of the existence of a “slight murmur” can be to a patient. Some patients never recover from such a casual remark. Unfortunately, the terms “invasive” and “non-inva- sive” are now used and interpreted to mean only physical

11. Emerson, P. A., and Marks, P.: Prevention of throm- boembolism after myocardial infarction: Effect of low dose heparin or smoking, Br. Med. J. 1: 18, 1977.

12. Clayton, J. K., Anderson, J. A., and McNicol, G. P.: Pre- operative prediction of post-operative deep vein throm- bosis, Br. Med. J. 2:910, 1976.

13. Whitehead, M. L., and McCarthy, T. G.: In Kakkar, V. V., and Thomas, D. P., editors, Heparin chemistry and clinical use, London, 1976, Academic Press, p. 361.

invasion. This is inadequate consideration. People have minds, too. Disturbance of mind and thought can be even more troublesome, crippling, and “invasive” than casual considera- tion might suggest. Remember always, patients are people with minds as well as bodies. And, finally, remember that the unnecessary use of these “non-invasive” studies definitely does invade the pocketbook.

George E. Burch, M.D. Tulane University School of Medicine

and Charity Hospital of Louisiana New Orleans, La.

Another link between the left stellate ganglion

and the long Q-T syndrome

Electrical alternation of the T wave, associated with emotional or physical stress, is characteristic of the long Q-T syndrome’ and often precedes life-threatening arrhythmias. This phenomenon has been experimentally reproduced in animals by stimulating the left stellate ganglion.’ Moreover, blockade of the right stellate ganglion, which permits domi- nance of the left cardiac sympathetics, not only lengthened the Q-T interval in long Q-T syndrome, but also evoked T wave alternans and ventricular arrhythmias.’ Excessive sympathetic stimulation of the heart via the left stellate ganglion resulting from a congenitally low activity of the right cardiac sympathetic nerves has been suggested as the patho- genetic mechanigm.a The important role of the left stellate ganglion in cardiac arrhythmias has been recently demon- strated.4 Furthermore, in a patient with long Q-T syndrome at left stellectomy after failure of medical treatment, manipula- tion of the left stellate ganglion consistently produced ventric- ular tachycardia,5 thus confirming this ganglion’s modulation of dangerous ventricular arrhythmias. This report describes temporary abolition of T wave alternation during blockade of

the left stellate ganglion in a patient with Romano-Ward syndrome.

A 26-year-old white housewife had fainted two to three times yearly for 15 years during pleasant and unpleasant emotion. After negative neurologic and EEG examination at age 20, she took phenytoin for a time. At age 21, she fainted upon hearing, in the next room, the voice of an old friend who had visited unexpectedly. Before each faint, she noted heart pounding and had the urge to run away. Asymptomatic long Q-Tc interval was found in the patient’s mother (0.52 sec.), maternal grandmother (0.47 sec.), and son (0.47 sec.). In the patient’s sister (0.45 sec.), and father (0.44 sec.), Q-Tc was normal. Another maternal uncle and his son had childhood syncope which disappeared in adult life. Three maternal aunts died suddenly, at 2 years, at 30 years with childhood cyanosis, and at 33 years in sleep with presumed brain hemorrhage. At age 23, after uneventful induced labor for toxemia of preg- nancy at another hospital, the patient was abruptly separated from her newborn son because of suspected tuberculosis. She lapsed into hysteria, fainted, and convulsed whenever she

130 July, 1978, Vol. 96, No. 1 0002-8703/78/0196-0130$00.30/0 0 1978 The C. V. Mosby Co.