EECP creates new channels to the heart
Researchers presented several studies on enhanced external counterpulsation (EECP) at the Biomedicine 97 conference held in April in Washington, DC. All underscored the clinical benefits of the therapy.
• A five-year follow-up of 33 angina patients from the State University of New York at Stony Brook showed 88% survival five years after EECP treatment. Sixty percent had not had heart attacks or required other revascularization therapy and had not been hospitalized for coronary-related problems.
• Another study used Doppler echo to show that optimal results of counterpulsation are related to the magnitude of diastolic augmentation. A range of 1.5 to 2.0 is optimal.
• While patients with one or two blocked arteries fare better that those with three, researchers presented findings that offered insights on treating patients with triple vessel disease. Patients were able to exercise longer before reaching ST segment depression or developing angina. The belief is that EECP may stimulate the development of collaterals into vessels large enough to compensate for blocked arteries.
Around since the 50s
Not until 1989, when the Chinese changed the counterpulsation system from hydraulic to pneumatic, did EECP become feasible in this country. Counterpulsation has been around since the 1950s, but in those early years, the machine was based on hydraulics and was large and cumbersome. By the 70s, attention became focused on coronary artery bypass grafts and other invasive methods.
EECP can be thought of as external intra-aortic balloon pumping. An advantage of EECP over intra-aortic pumping, aside from its being noninvasive, is diastolic augmentation venous return is enhanced.
During therapy, several cuffs placed around a patient’s legs and buttocks inflate and deflate rhythmically, triggered by the patient’s EKG. Starting at the ankles, the cuffs are inflated sequentially upward. This action squeezes blood back to the heart during diastole. The cuffs deflate during systole.
During counterpulsation, cardiac workload decreases and the heart receives more oxygen. Researchers suspect that small channels in the heart open in response and develop into permanent conduits around blocked coronary arteries vessels that previously deprived the heart of oxygen and caused angina.