Although ECP devices are cleared by the Food and Drug Administration (FDA) for use in treating a variety of cardiac conditions, including stable or unstable angina pectoris, acute myocardial infarction and cardiogenic shock, the use of this device to treat cardiac conditions other than stable angina pectoris is not covered, since only that use has developed sufficient evidence to demonstrate its medical effectiveness. Non-coverage of hydraulic versions of these types of devices remains in force.
Coverage is provided for the use of ECP for patients who have been diagnosed with disabling angina (Class III or Class IV, Canadian Cardiovascular Society Classification or equivalent classification) who, in the opinion of a cardiologist or cardiothoracic surgeon, are not readily amenable to surgical intervention, such as PTCA or cardiac bypass because:
- Their condition is inoperable, or at high risk of operative complications or post-operative failure;
- Their coronary anatomy is not readily amenable to such procedures; or
- They have co-morbid states which create excessive risk.
A full course of therapy usually consists of 35 one-hour treatments, which may be offered once or twice daily, usually 5 days per week. The patient is placed on a treatment table where their lower trunk and lower extremities are wrapped in a series of three compressive air cuffs which inflate and deflate in synchronization with the patient's cardiac cycle.
During diastole the three sets of air cuffs are inflated sequentially (distal to proximal) compressing the vascular beds within the muscles of the calves, lower thighs and upper thighs. This action results in an increase in diastolic pressure, generation of retrograde arterial blood flow and an increase in venous return. The cuffs are deflated simultaneously just prior to systole, which produces a rapid drop in vascular impedance, a decrease in ventricular workload and an increase in cardiac output.
The augmented diastolic pressure and retrograde aortic flow appear to improve myocardial perfusion, while systolic unloading appears to reduce cardiac workload and oxygen requirements. The increased venous return coupled with enhanced systolic flow appears to increase cardiac output. As a result of this treatment, most patients experience increased time until onset of ischemia, increased exercise tolerance, and a reduction in the number and severity of anginal episodes. Evidence was presented that this effect lasted well beyond the immediate post-treatment phase, with patients symptom-free for several months to two years.
This procedure must be done under direct supervision of a physician.
