angina conceal myocardial infarction by liaoqinmei


									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
                                                                                                     general practitioner an4 died suddenly in
 4     59      M       1            2        -         27        Alive             131        901    heart failure. This death was attributed to
                                                                 Heart failure
                                                                                                     AMI (case 5, table 2).
 7     57      M       1            -        -          6        AMA*t            -           -         During the observation period 37 of the 50
                                                                 Heart failure
                                                                                                     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:
                                 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:
                                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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