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IJC 0213D

Transcutaneous electrical in angina

nerve stimulation (TENS) pectoris *

(Key words: angina pectoris: transcutaneous electrical stimulation)

Relief of pain is a fundamental requirement in the treatment of angina pectoris not only because of the pain per se but also because pain may secondarily increase

myocardial ischemia by pacing sympathetic activity. It is therefore necessary to break this self-propagating vicious circle.

A new therapeutic possibility has been created by the introduction of transcuta- neous electrical nerve stimulation (TENS) for pain relief. There is now ample evidence that TENS additional to its pain relieving effect may influence autonomic systems mainly by suppressing sympathetic overactivity.

* From the Department of Medicine, Gstra Hospital and the Department of Neurosurgery. Sahlgrenska

Hospital. Goteborg. Sweden.

I~irrmotlonal Journal of Cardrologr, 7 (1985) 91-95

I’ Elsevier Science Publishers B.V.

92

Theoretical Background to TENS

It is well known that pressure, massage, heat or cold over a painful area can reduce the intensity of pain. These clinical observations have led researchers to

attempt to explain how this inhibition occurs. Zotterman (1939) and later Bishop

(1959) and Noordenbos (1959) concluded, on the basis of their own experimental

studies, that the activity in large, non-pain transmitting fibre systems could inhibit the activity in the pain fibre system. These earlier ideas were synthesized by Melzach

and Wall [l] who presented a theoretical model to explain how pain inhibition might

take place on the segmental spinal level. According to their gate control theory. the inhibition of the flow of pain impulses occurs at the first synaptic station in the

spinal cord by means of a special presynaptic neuron system. It was assumed that this system was fed by collateral nerves from both large afferent nerve fibres which

do not transmit pain and small pain-transmitting afferent fibres. The small pain- transmitting fibres inhibited the system and thus prepared the way for increased

synaptic transmission - the gate was open -, while activity in large fibres excited the

system, resulting in the suppression of transmission to the next neuronal chain - the

gate was closed. Their theory also assumed that descending systems of supraspinal origin contributed to the inhibition of pain. These supraspinal control systems were

assumed to be activated by external stimuli via rapidly mediating afference but also triggered directly by internal psychogenic activity. The gate theory is still under

debate and justified criticism has been put forward. Regardless of whether the theory is correct, only partly correct or erroneous it has been a valuable hypothesis for the clinical design of methods of pain inhibiting stimulation.

The next important breakthrough in pain research was the results obtained by

Reynolds [2] in 1969. By electrical stimulation of certain areas in the brain stem in rat, Reynolds succeeded in producing complete abolition of pain. Pain inhibition

was effective enough to allow abdominal surgery in a rat which, although it was

conscious, showed no signs of pain. Today it is well known that there are discrete areas in the brain stem. from which

influx of pain impulses to the brain is controlled. From these structures descending pathways can inhibit the spinal transmission of messages that cause the experience

of pain. Further research led to a common explanation for the mechanism of action of

pain inhibition by electrical stimulation and by morphine. In 1973 it was discovered

that opiate receptors exist in the brain stem and spinal cord and the existence of an endogenous ligand for these receptors could be predicted [3]. Only 2 years later, in 1975, naturally occurring opiates were found in the brain and pituitary [4]. They were collectively called endorphines or endogenous morphines. In animal experi-

ments it has been shown that endorphines, like exogenously administered morphine, have affinity to opiate receptors.

There are studies which indicate that low-frequency stimulation releases beta-en- dorphine, which can be blocked, at least in part, by naloxone; whereas high frequency stimulation may release met-encephaline, which is not blocked by conven- tional doses of naloxone [5]. Previous studies with TENS in different pain conditions

93

have shown that stimulation is only effective when given over painful areas, or near

these areas. One might therefore conclude that if electrical stimulation results in the release of humoral substances with analgetic properties, this activation seems to take place in a somatotopically organized way.

Clinical Effects of TENS

During the last decade TENS has developed as a noninvasive means of therapy

for the control of pain of various aetiology. The results are relatively uniform. TENS

is found to give temporary alleviation of pain in about half of the cases in unselected

series of severe pain conditions. The pain reducing effects vary considerably between different diagnostic groups but there are at present no reliable criteria for patient

selection. No complications of significance have been reported.

TENS has widened its fields of application to include also its use on functional disturbances in autonomic systems [6]. Thus, TENS used to control delivery pain

has been shown to increase placental blood flow. TENS applied suprapubically has been shown to increase functional bladder capacity in patients with interstitial

cystitis. Kaada [7] has shown that TENS can induce peripheral vasodilatation in patients with ischemic pain.

Against this background it seemed logical to test the effectiveness of TENS in patients with severe angina pectoris.

Clinical Application of TENS on Patients with Angina Pectoris [S]

The first objective of the study was to define a current density limit for TENS

shaped currents below which no arrhythmia could be provoked in the adult human heart. TENS was supplied epicardially on patients during open heart surgery. Below a current density of 50 A/m2 no arrhythmias were observed. The expected current

density in the heart from conventional TENS on the chest is below this value. In the following three clinical studies TENS was given via standard electrodes of

silicone conducting rubber applied over the painful area of the chest wall. The

stimulator delivered constant current pulses with a duration of 0.2 msec. The pulse repetition frequency was kept at 70 Hz. The intensity of the stimulation (15-50 mA) was individually adapted to a level immediately below that producing pain.

In the first short-term study the pain relieving effect of TENS was studied in 10 male patients with angina pectoris of functional class III or IV. All patients had

been stabilized on long-term maximal oral treatment for at least 6 months. The effects of TENS treatment were evaluated by means of repeated bicycle ergometer tests, and ECG recordings. During TENS treatment all patients had an increased working capacity (16-U%). decreased ST-segment depression and reduced recovery time. No adverse effects were observed.

In another short-term study TENS was effective on pacing induced angina pectoris in patients with severe coronary artery disease in terms of increased

tolerance to pacing, improved lactate metabolism in the myocardium and less pronounced ST-segment depressions at identical pacing rate. These beneficial results

94

may be due to a decreased afterload indicated by a fall in systolic blood pressure and a diminished sympathetic activity.

The favourable effects of TENS in angina pectoris were confirmed in a controlled

long-term study on 23 patients. The treatment group showed decreased ST-segment

depression, increased working capacity on bicycle ergometer tests, decreased

frequency of angina1 attacks and lower consumption of nitroglycerine.

Discussion

The results of all three clinical studies are uniform: TENS reduces pain. increases working capacity (or improves the pacing tolerance) and decreases ST-segment depressions. The operating mechanisms are not explored. Four possible mechanisms may be considered: an unspecific placebo effect, pain inhibition with secondarily

sympathetic inhibition, pain inhibition and sympathetic inhibition as parallel phe- nomena and sympathetic inhibition with secondary pain inhibition.

It is virtually impossible to design a blind study of treatment with TENS since

there is no placebo equivalent for the sensation of stimulation. Therefore an unspecific placebo effect in studies with TENS must be anticipated. Recent data

suggest that placebo analgesia can be reversed by naloxone indicating that the effect

might be exerted via neuronal systems using endorphines. This implies that TENS and placebo may employ a common mechanism and that unspecific placebo effects in an unpredictable way can influence the “real” effect of stimulation. However. the

effect of TENS on ST-segment depressions, and myocardial lactate metabolisms indicate that other mechanisms are of major importance than unspecific placebo

effect. In accordance with the second alternative it is quite possible that the pain

reducing effect of TENS also may inhibit the segmental sympathetic outflow since in the dorsal horn of the spinal cord there are connections between pain fibrea and

sympathetic neurones. With respect to the third alternative it is well known that visceral pain as in

angina pectoris is localized to the body surface. The elicitation of visceral effects by stimulation of the skin is well documented in animal and human experiments. A

recent study showed that low-frequency stimulation of the sciatic nerve gave a

significant decrease of the blood pressure in hypertensive rats [9]. This effect could be reversed by naloxone. Studies in man already mentioned also speak in favour of the assumption that electrical stimulation can influence various organs probably hy

changes in the reflex mechanisms and that this effect can be elicited without influencing the pain transmitting system.

Finally. with respect to the fourth alternative it is quite possible that electrical

stimulation blocks sympathetic activity peripherally or centrally and that thih sympathetic blockade may be responsible for the produced analgesia. Upper thnrncic sympathectomy has been used to treat patients with severe angina1 pain. Although the operation was devised to cut the afferent pain fibre it seems possible that the pain reducing effect was due to the removal of the efferent sympathetic innervation of the heart. Beta-adrenergic blockade has an effect Gmilar to that t>f surgical svmpathectomy. This is in accordance with the concept that the pain reduction and the increased effort tolerance following <ympathcctom\- is primarily a result of

95

interruption of the efferent innervation of the heart rather than section of sensory

pathways.

Conclusion

The results of these studies indicate that the pain relieving effect of TENS in

patients with angina pectoris is associated with a decreased degree of myocardial

ischemia as evidenced by the reduction of ST-segment depression and improved myocardial lactate metabolism. There is now evidence to support the value of TENS

in the treatment of angina1 pain.

Department of Medicine

&tra Hospital

416 85 Giteborp

Sweden

C. Mannheimer C-A. Carlsson

A. Vedin C. Wilhelmsson

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19X2:45:185.

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Mannheimer C. Transcutaneous electrical nerve stimulation (TENS) in angina pectoris. Thesis. (Ztehorg

1984.

‘r.ao T. Andersson S, Thoren P. Long-lastmg cardiovascular depressor response following sciatic

\timulation m spontaneously hypertensive rats. Evidence for the involvement of central endorphin and

\erotonin systems. Brain Res 19X2:244:295.

University of Utah

Appointments and Elections

Dr. William A. Gay, Jr. has been appointed professor of surgery and chairman of the

department at the University of Utah School of Medicine. Salt Lake City, effective 1 October. 1984. Most recently Dr. Gay was professor of surgery and chief of cardiac surgery at the New York Hospital-Cornell Medical Center. New York.

Dr. Gay, who is 48 years old, received his B.A. degree from the Virginia Military Institute. Lexington, VA and his M.D. degree from Duke University School of Medicine. Durham. NC. He trained in general and cardiac surgery at the Duke University Hospital and at the National Heart Institute. Bethesda. MD. Dr. Gay joined the faculty at Cornell in 1971. His principal research interests are in myocardial protection and platelet endothelial interactions.