Br Heart3' 1994;71:419-421 419 Does pain relief with spinal cord stimulation for angina conceal myocardial infarction? C Andersen, P Hole, H Oxh0j Abstract because they fear that the stimulation could Objective-To investigate the possibility conceal an acute myocardial infarction. that spinal cord stimulation (SCS) used We sought evidence of acute myocardial for pain relief can conceal acute myo- infarction in patients treated with SCS for cardial infarction (AMI). angina. Design-Prospective evaluation of patients treated with SCS. Setting-University hospital. Patients and methods Patients-50 patients with coronary The study was approved by the local ethics artery disease and severe, otherwise committee and the patients gave their intractable angina treated with SCS for informed consent before enrolment. We 1-57 months. studied 50 patients (40 men and 10 women) Main outcome measures-Necropsy find- treated with SCS for otherwise intractable ings, symptoms, serum enzyme concen- anginal pain (table 1). Eighteen of the patients trations, electrocardiographic changes. had had one myocardial infarction and 15 had Results-Ten patients were considered to had two or more. Forty two of the patients have had AMI. In nine of these SCS did had previously been treated with percuta- not conceal precordial pain and in one neous transluminal coronary angioplasty patient no information about precordial (PTCA) or coronary artery bypass graft pain could be obtained. surgery (CABG) or both. In all the patients Conclusion-There was no evidence that SCS treatment was started because further SCS concealed acute myocardial infarc- medical treatment or revascularisation was tion. regarded as impossible. The patients were reviewed after an average (Br HeartJ_ 1994;71:419-421) of 29 (range 1-57) months of SCS treatment. The minimum observation time for patients who did not die or stop SCS treatment (6 The perception of cardiac pain during patients) was 12 months. During the observa- myocardial ischaemia is mediated via sympa- tion period electrocardiographic changes and Department of thetic afferent nerve fibres.' High thoracic cardiac enzymes, if available, were reviewed Anaesthesiology and for every hospital admission and visit to the Intensive Care epidural anaesthesia can block cardiac C Andersen afferent sympathetic fibres; this technique casualty ward. All admissions to hospital in P Hole therefore reduces cardiac pain during myo- the 3 years before SCS treatment were also Department of cardial ischaemia.2 The same effect is reviewed. Clinical Physiology achieved by spinal cord stimulation (SCS),3 The patients were seen by one of us every 1 and Nuclear Medicine, Odense University which has become a well established treat- to 4 months. At these visits they were ques- Hospital, Odense, ment for chronic pain. SCS was first reported tioned about symptoms and visits to other Denmark as a successful treatment of otherwise medical institutions. If the patient had con- H Oxhoj intractable angina pectoris in 1987.4 sulted a general practitioner, information Correspondence to: Dr Claus Andersen, Precordial pain is the cardinal symptom of about the visit was obtained. Because of Department of acute myocardial infarction (AMI) and it is severe chest pain 44 of the patients were Anaesthesiology and Intensive Care, Odense possible that effective pain relief by SCS treated with opioids before SCS treatment. A University Hospital, DK- may conceal acute myocardial infarction.5 reduction in dose during SCS was used to 5000 Odense C, Denmark. Currently several centres use SCS to treat assess symptomatic relief. Accepted for publication 10 December 1993 angina: other centres are reluctant to use SCS When possible the diagnosis of acute myocardial infarction was established accord- ing to WHO criteria that is, pain, ECG Table 1 Data on Patients changes, increase in myocardial enzymes AMI Non-AMI (creatine kinase B > 20 U/I and lactate dehy- Variable (n = 10) (n = 40) drogenase 1 > 170 U/1).6 7 If this information was unavailable, acute myocardial infarction Age (y) 57 (47-71) 61-5 (43-78) F/M 9/1 9/31 was diagnosed if the patient died suddenly or CABG (%) 8 (80) 31 (78) acute heart failure developed. PTCA (%) 1 (10) 9 (23) AMI (%) 9 (90) 24 (60) A 12 lead ECG was recorded at follow up Hospital admissions before/with SCS* 3-0/1-6 3 0/1-9 and compared with the ECG recorded imme- Opiate consumption before/with SCSt 47 5/0 2 30 4/0-4 Digoxin (No of patients (%)) 4 (40) 10 (25) diately before SCS treatment was started. Any *Mean number of hospital admissions per patient per year. alterations in Q wave, QRS configuration, tMedian opiate consumption equivalent to mg morphine per patient per 24 h. ST/T segment, and T wave were evaluated. 420 Andersen, Hole, Oxh0j Table 2 Data on the 10 patients with acute myocardial infarction one hour later he was found dead in the ward. Case Previous SCS Survival/ Acute myocardial infarction was verified at No Age Sex AMI CABG PTCA (mnth) cause of death CK-B LD-1 necropsy (table 2). One patient refused hospi- 1 49 M 2 1 - 21 Alive 34 219 tal admission; she was treated at home by her 2 3 54 55 M M 1 1 2 1 - 1 13 25 Alive Alive 56 51 294 495 general practitioner an4 died suddenly in 4 59 M 1 2 - 27 Alive 131 901 heart failure. This death was attributed to 5 6 49 53 F M - 3 2 - - - 37 1 Heart failure VF - - - - AMI (case 5, table 2). 7 57 M 1 - - 6 AMA*t - - During the observation period 37 of the 50 8 9 61 66 M M 1 2 1 1 - - 9 11 Heart failure AMI* - 81 - 160 patients were admitted to hospital. During the 10 71 M 1 2 - 12 VF - - observation period there were 153 admis- *Confirmed at necropsy. tSudden death. sions. The mean number of admissions for CK-B, creatine kinase isoenzyme B; LD-1, lactate dehydrogenase; VF, Ventricular fibrillation. chest pain or angina or observation for acute myocardial infarction during the 3 year period before SCS treatment and during the period STATISTICAL ANALYSIS with SCS treatment were not significantly dif- The groups with and without acute myocar- ferent (P = 0 6) in the 10 patients with acute dial infarction were compared by rank sum myocardial infarction and the patients without test (Mann-Witney) and observations before (table 1). and with SCS were evaluated by the During SCS treatment about 90% of the Wilcoxon/Pratt test. Differences were visits to the casualty ward or the general prac- regarded as significant if P < 0 05. titioner were for prescriptions or socio- economic problems or both. The median number of contacts with a physician was one Results per month. There were, however, large varia- We evaluated 108x6 patient-years of SCS tions between individual patients (0-30 per treatment. During the observation period 10 month). patients were diagnosed as having an acute During the follow up period five patients myocardial infarction while they were being had their antianginal medication adjusted. treated with SCS: six of them died (table 2). One patient .had CABG because coronary Two patients died of other causes: one of angiography showed occlusion of a previously pneumonia and one of progressive heart inserted bypass graft. failure. The symptomatic relief achieved by SCS In the four survivors and one of the patients treatment (assessed from the reduction in opi- who died acute myocardial infarction was ate consumption) was significant; there was, verified by serum enzyme concentrations; the however, no difference between the 10 other patients died before a blood sample was patients with acute myocardial infarction and taken. In an additional patient acute myocar- the others (table 1). Forty three of the 50 dial infarction was verified at necropsy: the patients reported that SCS treatment reduced diagnosis was based on clinical observations angina. All 10 patients who had an acute in the remaining four patients. Two of these myocardial infarction during SCS treatment died in intractable ventricular fibrillation, and claimed to have a considerable reduction in two patients in heart failure died suddenly. angina. Nine of the ten patients with acute myocardial There were no differences in the number of infarction recognised that the precordial pain previous acute myocardial infarctions or in during their acute myocardial infarction was the number of bypass operations between the being clearly different and definitely more ten patients in the acute myocardial infarc- severe than their usual angina and that it was tion-group and the other 40 patients (table 1). not alleviated by SCS. Furthermore, the pain The electrocardiograms recorded before at acute myocardial infarction was accompa- SCS were abnormal in most of the patients, nied by unusual symptoms such as dyspnoea, with a high incidence of Q wave and ST-T general weakness, etc. Patients with previous abnormalities (table 3). In the patients with- myocardial infarction reported that some out acute myocardial infarction a comparison symptoms were the same as at the last of the follow up electrocardiograms with those myocardial infarction. recorded before SCS showed no significant One patient (case 7) died suddenly; it is not changes in Q wave, T wave inversion, or new known whether he experienced any chest bundle branch block (table 3). In the group pain. He was admitted to hospital for a with acute myocardial infarction follow up transurethal resection of the prostate and was electrocardiograms could be recorded only in well when he was given premedication. About the four patients who survived: one patient developed bundle branch block, two had T Table 3 Electrocardiographic abnormalities in the AMI and non-AMI groups before wave changes, and in one no changes were SCS and at follow up seen in the electrocardiogram. The four AMI AMI Non-AMI Non-AMI patients who survived their acute myocardial before afterAMI before follow up infarction have not been admitted to hospital Abnormality (n = 10)(%) (n = 4) (n = 40)(%) (n = 40) since. Qwave 5 (50) - 9 (23) 9 Bundle branch block 1 (10) 1 2 (5) 2 LVhypertrophy 1 (10) - 4 (10) 4 Cohn effect 4 (40) - 10 (25) 10 Discussion Twave 3 2* 21 (53) 21 Recognition of sympathetic afferent fibres as *Changes at acute myocardial infarction (AMI). LV, left ventricular. the pathway for cardiac pain led to efforts to Does pain relief with spinal cord stimulation for angina conceal myocardial infarction? 421 treat angina with sympathectomy. This treat- group who reported on their symptoms also ment relieved angina in about 75%.8 In 1977 had additional symptoms at the same time as Melzack and Wall published their gate control the pain caused by acute myocardial infarc- theory of pain transmission,9 which led to tion. During follow up none of the 40 patients attempts at relieving pain by electric stimula- without acute myocardial infarction reported tion of the spinal cord. Low-amplitude elec- additional symptoms. tric impulses transmitted through implanted A major problem in investigations is the epidural electrodes attached to a subcuta- uncertainty with which acute myocardial neous neurostimulator stimulate the spinal infarction can be diagnosed or excluded in dorsal columns and alleviate pain. Pain relief patients such as ours. In four of our patients alone, however, does not account for the the diagnosis of acute myocardial infarction improvement in exercise tolerance reported in was based on circumstantial evidence. We patients treated with SCS.'0 Mannheimer et al considered it prudent to include these patients used transcutaneous electrical nerve stimula- in the group with acute myocardial infarction. tion for pain relief in angina and they believe It would not alter our conclusion, however, if that reduction of sympathetic overactivity they were not included. may contribute to its effectiveness." The most critical factor in our investigation Angina may be regarded a warning sign, is the possible occurrence of unrecognised signalling that the patient's myocardium is at acute myocardial infarction in the group with- risk because oxygen supply is insufficient and out acute myocardial infarction. This may that it should be protected by reducing effort. probably never be fully resolved because silent When this warning is abolished it may prevent acute myocardial infarction could remain the patient from recognising acute myocardial completely unrecognised. None the less close infarction. We investigated whether SCS can surveillance in hospital of patients whenever conceal acute myocardial infarction. Ten of chest pain was not alleviated by SCS seems to the 50 patients treated with SCS were indicate that clinically significant acute believed to have had an acute myocardial myocardial infarction did not occur in the infarction during the observation period. The group without acute myocardial infarction. diagnosis was confirmed by enzyme concen- trations or necropsy or both in six of the patients. In the remaining four patients the clinical picture suggested acute myocardial 1 Bonica JJ. The management of pain. Vol II. 2nd ed. infarction and these patients were included in Philadelphia: Lea and Febiger, 1990;1001-30. 2 Blomberg S, Curelaru I, Emanuelsson H, Herlitz J, Ponten the group with acute myocardial infarction. J, Rickten SE. Thoracic epidural anaesthesia in patients Some of the 40 patients without acute with unstable angina pectoris. Eur Heart J 1989;1O: 437-44. myocardial infarction during SCS were 3 Augustinsson LE. Spinal cord electrical stimulation in severe angina pectoris: Surgical technique, interaopera- admitted to hospital with severe precordial tive physiology, complications, and side effects. PACE pain. In all these instances acute myocardial 1989;12:693-4. infarction was ruled out by serum enzyme 4 Murphy DF, Giles KE. Dorsal column stimulation for pain relief from intractable angina pectoris. Pain analysis and electrocardiograpy. We therefore 1987;28:365-8. feel confident that symptomatic acute myo- 5 Dershwitz M, Sherman EP. Acute myocardial infarction symptoms masked by epidural morphine? J Clin Anesth cardial infarction did not occur in this group. 1991;3:146-8. This does not, however, rule out the possibility 6 Gersh BJ, Clements IP, Chesebro JH. Acute myocardial infarction. A: Diagnosis and prognosis. In: Brandenburg that some patients in this group may have had RO, Fuster V, Giuliani ER, McGoon DC, eds. silent AMI, with the pain being overruled by Cardiology-fundamentals and practice. 1987: 1116-52. ScS. 7 Horder M, Thygesen K, Gerhard W, Grande P, Christiansen I, Stender S. Enzymatic diagnosis in acute In the Framingham study 23% of the acute myocardial infarction. Ugeskr LIeger 1 989;151:1447-53. myocardial infarctions documented by elec- 8 Apthorp GH, Chamberlain DA, Hayward GW. The effects of sympathectomy on the electrocardiogram and trocardiography were not accompanied by effort tolerance in angina pectoris. Br Heart J 1964;26: symptoms severe enough to require medical 218-26. 9 Melzack R, Wall PD. Pain mechanisms: a new theory. A attention.'2 However, unrecognised myocar- gate control system modulates sensory input from the dial infarction was rare in patients with prior skin before it evokes pain perception and response. Science 1977;195:471-3. angina. All our patients had prior angina. 10 Mannheimer C, Augustinsson LE, Carlsson CA, Manhem No changes attributable to acute myocar- K, Wilhelmsson C. Epidural spinal electrical stimulation in severe angina pectoris. Br Heart T 1988;59:56-61. dial infarction were seen when the electrocar- 11 Sandrec S, Meglio M, Bellocci F, Montenero AS, Scabbia diogram taken at follow up was compared E, D'Annunzio V. Clinical and electrocardiographic with the one taken immediately before SCS. improvement of ischaemic heart disease after spinal cord stimulation. Acta Neurochirurgica 1 984;(suppl)33:543-6. Absence of electrocardiographic changes does 12 Margolis JR. Clinical features of unrecognized myocardial infarction-silent and symptomatic. Eighteen year follow- not rule out acute myocardial infarction, how- up: The Framingham Study. Am J Cardiol 1973;32: 1. ever, particularly in patients with previous 13 Sullivan W, Vlodaver Z, Tuna N, Long L, Edwards JE. Correlation of electrocardiographic and pathologic find- acute myocardial infarction as in our ings in healed myocardial infarction. Am Y Cardiol patients.67" The nine patients in the AMI 1978;42:724-32.
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