[Epidural spinal cord stimulation in therapy-resistant angina pectoris].

Spinal cord stimulation (SCS) has routinely been used since the beginning of the 1970s. The initial indications for stimulation were the so-called deafferentation or neurogenic pain. Further work has confirmed that neurostimulation is useful in severe peripheral vascular disease in relieving pain and increasing capillary blood flow and oxygen tension. The effects are similar to those of sympathectomy. In 1964 Apthorp et al. discovered that sympathectomy relieved angina in about 75% of patients. The use of SCS to treat angina follows logically from its use in peripheral vascular disease. METHODS. The pain-relieving effect of SCS was investigated in two patients, 54 and 69 years old, who were hospitalised for 8 and 28 days. Both patients had severe angina pectoris (duration 2 and 15 years, New York Heart Association class III and II), related to three-vessel disease, and one of them had previously undergone his third bypass operation. The other patient was not considered suitable for surgery. The antianginal treatment (long-acting nitrates, beta-blockers, calcium antagonists) was regarded as optimal and was not changed during the observation period (Table 1). SURGICAL TECHNIQUE AND STIMULATION EQUIPMENT. We used the commercially available Medtronic SCS system. The operation was performed under local anaesthesia to allow the patient to answer questions during the intraoperative stimulation. The epidural space was punctured at the level of T7-T8 in one case and T11-T12 in the other. The electrode tip was positioned in the midline or a few millimetres to the left at the T1-T2 level (Figs. 1, 2), so that the patient felt a prickling sensation in the precordial area and into the arms. The distal end of the electrode was sutured to the fascia and connected via a tunnelled extension lead to the external pulse generator. The pulse width was 200 microseconds, frequency 80 Hz. An appropriate amplitude (usually 8-10 V) was used for comfortable paraesthesia. The study consisted of two parts: a run-in period (1 week) to standardise the stimulation when mobilisation was performed. A treatment period (18 months) to determine the patient's working capacity after continuous stimulation (Table 2). After a successful run-in period a Medtronic receiver was implanted, connected to the electrode and stimulated by external pulse generator. Different variables were used to assess the effect: pulse rate, blood pressure, the product of pulse rate and systolic blood pressure, estimated anginal pain, and ST changes in the electrocardiogram (ECG) before, during and after mobilisation. RESULTS. The stimulation was carried out for 30 min 10-12 times a day during the run-in period and five to six times a day during the treatment period. Altogether there was slight lowering of heart rate and systolic blood pressure. Consequently the product of heart rate and systolic blood pressure was diminished. In one case (NYHA II) the distinct disorder of repolarisation reverted to the normal condition as shown on ECG. In the other case (NYHA III) the ECG remained unchanged because of a severe aneurysm of the cardiac wall. Both patients experienced nearly complete pain relief after a few days for 6 and 12 months respectively. However, an increasing effort tolerance could be demonstrated in both patients by reducing the extent of the heart failure (NYHA II/III to NYHA I/II) (Table 2). DISCUSSION. Our two hospitalised patients had clinically intractable angina pectoris and severe manifestations of heart disease corresponding to at least NYHA functional class II-III. Both were unsuitable for operation and showed no improvement on individually titrated maximal oral antianginal drug treatment. During SCS treatment significant improvement was obvious: chest pain, ST-segment depression, and the extent of heart failure could be reduced. Both patients reached a better NYHA functional class, exhibited increased working capacity and reported reductions in anginal attacks and pain. Th