INTRODUCTION
Angina pectoris is severe chest pain that is often accompanied by a heavy oppressive feeling. Angina pectoris occurs because of insufficient blood supply to the heart muscle. In most cases, this is caused by a constriction of the coronary arteries. It often coincides with physical exertion or emotional strain, which causes the heart to beat more rapidly and is associated with higher oxygen consumption.

The pain occurring in case of a sudden occlusion of a coronary artery because of a thrombus or embolus is usually more severe. A complete occlusion eventually leads to a myocardial infarction.

Risk factors of angina pectoris include smoking, obesity, hypertension, diabetes mellitus, and hypercholesterolemia.

Besides coronary obstruction, coronary spasms may also cause symptoms of angina pectoris.

Angina pectoris can be treated with vasodilating drugs or by the reduction of exertion. A reduction of the blood pressure also leads to a lower cardiac workload and to decreased angina symptoms.

Presently, a large number of pharmacological therapies are available.

In addition, revascularization procedures, such as percutaneous coronary angioplasty (PTCA) and coronary bypass surgery (CABG), can help with angina attacks if a single or several discrete areas of obstruction can be identified.

Angina pectoris is termed refractory if the conventional therapies mentioned above have insufficient or no effect.

Patients with refractory angina pectoris generally have a long history of coronary disease and are usually clearly limited in their physical activities.

In addition to extensive anti-anginal pharmacological treatment, these patients have undergone one or more percutaneous coronary angioplasties or even CABG surgery.

Strikingly, most patients with refractory angina pectoris are relatively young, predominantly male, and sometimes have a limited ejection fraction.
Spinal cord stimulation is considered a reasonable treatment option for patients with chronic angina not responsive to more conservative strategies who are not candidates for coronary revascularization surgery.

TREATMENT
All therapies for (refractory) angina pectoris aim to improve the myocardial ischemia by means of either the reduction of oxygen demand (b blockers, calcium channel blockers) or the increase of oxygen supply (nitrates, revascularization procedures, coronary angio- plasty, or CABG). In addition, the patients are often treated with anticholesterol drugs and platelet aggrega- tion inhibitors.

All patients considered for SCS with refractory angina pectoris should have been seen by a cardiologist.

Patients with small vessel disease should be considered for SCS if medical treatment is unsatisfactory.

The differential diagnosis includes

SPINAL CORD STIMULATION
A therapy that has anti-anginal effects, enhances the quality of life of patients with refractory angina pectoris, and is not harmful is a valuable treatment.

The population that should be treated includes patients who experience substantial limitations because of their angina pectoris despite exhaustive conservative and surgical intervention.

It has recently been suggested that the effects of SCS in angina pectoris are in part attributed to the protection of the myocardium and the normalization of the intrinsic nerve system of the heart muscle.


Studies have shown that patients treated with SCS have less angina symptoms, a lower use of short-acting nitrates, and an improved exercise tolerance. Moreover, clear anti- ischemic effects have been demonstrated, such as an increased exercise time without a deterioration of the myocardial symptoms and an increased tolerance for arterial pacing.

The reduced myocardial ischemia and reduced myocardial oxygen consumption (MVO2) result in delayed angina pectoris symptoms.

SCS in patients with refractory angina pectoris results in reduced attacks that may be caused by the increased angina pectoris threshold as a result of the reduced MVO2 and possibly the redistribution of the coronary blood flow.

It has also been suggested that angiogenesis would take place under the influence of SCS. Redistribution of the myocardial blood flow has been demonstrated in studies,and it is proposed that some of the redistribution may be because of the formation of collaterals. Also, there are a number of studies that demonstrate that SCS does not mask acute myocardial infarction.

RECOMMENDATIONS
Based on the present literature, SCS is recommended in patients with chronic refractory angina pectoris that does not respond to conventional therapy who are referred by a cardiologist.