Heart Associates     Cardiac Health Questions

Cardiac External Counterpulsation (CECP)

"I believe that EECP* has great potential, and could be particularly applicable to patients who are not candidates for revascularization, but who continue to have repetitive episodes of myocardial ischemia.”

Richard Conti, M.D.
Cardiology Professor of Medicine

Journal of American College of Cardiology, vol33,#7,1999.

*Enhanced External Counterpulsation

Coronary artery disease with angina or angina equivalent symptoms is usually treated with antianginal medications (aspirin, nitrates, beta blockers, calcium channel blocking agents, etc.), coronary angioplasty, stenting, or coronary artery bypass surgery. But there still remains a very large pool of patients where all these options have run out, yet they continue to have disabling angina.

In our pursuit for alternative options to treat these patients, several other modalities of treatment have evolved such as transmyocardial laser revascularization, transcutaneous electrical nerve stimulation, spinal cord stimulation, and CECP.

CECP, the subject in point here, is meant for the following subset of patients:

a. Patients who have had multiple angioplasties and coronary artery bypass surgeries, and that such procedures are no longer feasible.
b. Contraindication for bypass graft surgery due to other medical conditions.
c. Coronary anatomy is unsuitable for additional PTCA, stenting, or CABG (diffuse vasculopathy).
d. Severe microvascular coronary artery disease where PTCA or CABG is not an option.
e. When all arterial and venous conduits have been used, and additional bypass surgery is not possible.
f. Patients who are just fed up with multiple procedures with no longstanding benefit.
g. Patients who do not want PTCA or CABG by choice.

What is CECP?

CECP is a novel non-pharmacological outpatient treatment for angina secondary to coronary artery disease. It is a fairly complex cardiac-assist device that will increase the coronary blood flow by increasing the diastolic pressure in the central aorta over and above the systolic pressure by synchronized squeezing of the lower extremity vessels in the diastolic phase of the cardiac cycle.

In order to understand CECP, you should know the fundamentals of coronary circulation. Coronary arteries are the first pair of arteries originating from the root of the aorta that supply the whole cardiac musculature. All the organs of the body (brain, lungs, kidneys, etc.), except the heart muscle, receive most of its blood supply during the contraction phase (cardiac systole) of the left ventricle. The pulse we feel in the arteries is that systolic impulse. However, in systole, the heart muscle is in a contracted state, and therefore blood flow is minimal in the coronary vascular bed (Fig 7). In diastole the heart muscle relaxes, and the coronary vascular bed will fill up with all the blood it can with a sucking effect from the aortic root (Fig 8). Therefore, if we can selectively increase the diastolic blood pressure at the aortic root, we can increase the coronary filling, thereby the coronary circulation at large.

Since the 1960s, scientists have been working to achieve this goal of increasing the diastolic pressure in the aortic root by an assist device. The result was the perfection of the intra-aortic balloon pump, which is commonly used in situations like cardiogenic shock. However, intra-aortic balloon pump is a highly invasive technique with the introduction of a large tube and balloon system into the central aorta, and its use is limited to the Cardiac Catheterization Labs, Operation Suites, as well as Intensive Care Units. CECP is an ingenious external cardiac-assist device that came to fruition after 40 years of research and trials. The equipment is totally noninvasive, and is used in an outpatient setting in the cardiologist’s office. Patients are very carefully screened and selected for this therapy. During the treatment, the patient lies down on a special bed. Three pairs of rapidly inflatable and deflatable pneumatic cuffs (pressure suits) are applied to the calves, thighs, and girdle. Continuous electrocardiographic monitoring for cardiac rhythm, and direct plethysmographic measurements for blood pressures are now established. During the diastolic phase of the cardiac cycle, the CECP pressure cuffs are rapidly inflated in sequence starting from the calf, the thigh, and finally the buttocks (Fig 1-5). The cuffs are inflated with a pressure of 250-300 mmHg. With this squeezing mechanism, blood is forcefully propelled back to the central aorta creating a retrograde blood flow during diastole. This diastolic augmentation of blood pressure, and the resultant increase in blood flow through the coronary arteries, and finally to the myocardium is the crux of this treatment modality. (Fig 6) Similarly, the venous system is also squeezed in a similar fashion resulting in increased venous return to the right atrium and right ventricle, eventually improving the cardiac output.

During the systolic phase of the cardiac cycle, the pressure cuffs are rapidly deflated. At this stage, the compressed and under-filled vessels of the lower extremity will quickly dilate and re-conform sucking in blood from the central aorta. This reduction in the afterload of the left ventricle augments emptying of the contents of the left ventricle into the aorta much more effectively, thereby improving the cardiac output. This synchronized inflation and deflation sequence is continued for one hour as the treatment is continued. Normally, the treatment is scheduled one hour per day for 35 days spread over seven weeks.

The hemodynamic effects and the clinical benefits

Several studies have shown that CECP clearly improves the cardiac function from many different standpoints as briefly mentioned here. First of all, direct plethysmographic studies show that the diastolic augmentation is quite remarkable and comparable to intra-aortic balloon pump treatment. This increase in diastolic pressure at the aortic root certainly augments the pressure as well as the velocity of flow through the coronary arteries. This enhanced diastolic perfusion pressure and velocity facilitates the opening of new collaterals, and in my opinion transforms recruitable dormant collaterals into functional collaterals. The formation of these new collaterals will activate a very large number of endothelial cells, which will in turn liberate nitric oxide and prostacyclin, two important hormones responsible for vasodilatation at the microvasculature level of the coronary arterial system. Although CECP does not affect the ejection fraction or systolic indices in any significant way, a very modest increase in cardiac output, particularly the forward stroke volume by up to 12% has been noted in some selected studies. We have seen a reduction in pulmonary capillary wedge pressure as the treatment has progressed in patients.

Certainly, the coronary circulation increases in diastole by 20-40%. (Fig 7 & 8) In addition, the carotid, renal, as well as hepatic flow volume have been increased by 20-25%.

Patients who have completed a 35-day treatment have noted increased exercise tolerance with increased exercise duration, as well as increased time to ischemia (1.0 mm of ST depression) for a routine treadmill test. In addition, we also have noted better myocardial oxygen utilization (rate pressure product) at peak exercise, as well as better rate pressure product at 1.0 mm ST depression with exercise. Radionuclide scintigraphic studies have demonstrated reversible myocardial ischemia in several studies. It also has clearly shown increased perfusion of the myocardium following a treatment course. However, no change has been noted on fixed perfusion abnormalities. In all of these cases, it is most important that at least one artery be open to gain the benefits from CECP treatment.

From the clinical standpoint, patients have experienced less anginal episodes, less requirement for Nitroglycerin, increased exercise duration, and better exercise duration to develop 1.0 mm ST depression on exercise treadmill test.

Long-term effects

The mechanism of long-term beneficial effect is unclear. However, there is a reasonable body of evidence that suggests the beneficial effect from one set of treatment continues as long as five years. Formation of new collaterals and recruitment of dormant collaterals into functional circulation are speculated. We have also noted a preservation of this benefit on a long-term basis from thallium scintigraphic studies.

Adverse effects

CECP produces a fair amount of minor adverse effects. No mortality has been reported so far. Some patients do not tolerate the look, noise, as well as the complexity of the machine, and therefore withdraw from the treatment. Skin aberrations, bruises, leg pain, paresthesia, anxiety, dizziness, tinnitus, headache, GI symptoms, palpitations, and angina have been reported. In general, about 5% of the patients enrolled for the treatment discontinue it due to these side effects.

Patients who are not candidates for CECP treatment

Not all patients are ideal candidates for CECP treatment, although the indications are slowly evolving as we gain more experience with this treatment modality. As it stands now, severe congestive cardiac failure, chronic atrial fibrillation, myocardial infarction within the last three months, recurrent DVT, varicose veins, stasis ulcers, severe peripheral vascular disease, aortic insufficiency, uncontrolled hypertension of more than 180/100 mmHg, long-term anticoagulation, or bleeding diathesis are considered to be contraindications. All patients who undergo this treatment must have a coronary angiogram. Non-bypassed left main coronary artery disease with more than 50% stenosis is also considered to be a contraindication.

Fig 1 Fig 1

Schematics of the arterial circulation to the lower limbs. At the end of cardiac systole, the arteries are fully filled and carry blood downstream to the tissues. The long arrow shows direction of blood flow. The small arrow shows deflated pressure cuffs.

 
  Fig 2  

Fig 2

The early diastolic phase of the cardiac cycle. The cuffs against the calf muscles are inflated as shown by the large arrow. The small arrow shows compression of the arteries in the calf, and reversal of blood flow towards the heart.

 

Fig 3
Fig 3

Mid diastolic phase of the cardiac cycle. The large arrow shows the inflated cuffs of the calf and thigh. The small arrow shows compression of the arteries in the calf and thigh with reversal of blood flow towards the heart.

 
  Fig 4  

Fig 4

The late diastolic phase of the cardiac cycle. The cuffs against the calves, thighs, and buttocks are now inflated, as shown by the large arrows. The resultant arterial compression and the reversal of blood flow towards the heart are shown by the long arrows.

 

Fig 5
Fig 5

At the beginning of the next cardiac systole, all the cuffs are suddenly deflated allowing the lower limb arteries to decompress. This decompression helps the arteries to fill in and flow distally, creating an “afterload reduction” and better cardiac output.

 
   

This sequential inflation of the cuffs in the legs and buttocks produces a reversal of blood flow towards the central aorta producing the diastolic augmentation of the central aortic pressure.
 
       
Fig 6

Fig 6

Simultaneous electrocardiogram and finger plethysmogram from a 68-year-old patient recorded during CECP treatment. Systolic pressure 124 mmHg. Peak diastolic augmented blood pressure 160 mmHg. This diastolic augmentation is achieved by the sequential inflation of the lower limb and buttock cuffs during diastolic phase of the cardiac cycle. This diastolic augmentation certainly increases coronary flow velocity, which is the goal of this treatment.

Fig 7

Fig 7

Schematics of coronary circulation during cardiac systole of the left ventricle.

In systole, the heart muscle contracts, the aortic valve opens, and about 60-70% of its contained blood is ejected into the aorta. The small arteries that supply the heart muscle are squeezed in that contractile process, thereby markedly reducing the coronary blood flow in cardiac systole.

AO-aorta. RCA- right coronary artery. LCA-left circumflex artery.

Fig 8

Fig 8

Schematics of coronary circulation in cardiac diastole (the filling phase of the left ventricle). The aortic valve is now closed. The mitral valve (not shown in the schematics) opens into the left ventricle. The cardiac muscle relaxes. The intramyocardial pressure is now relieved. The small coronary vessels dilated creating a relatively negative intramyocardial pressure. The combination of these factors helps the coronary arteries to “suck up” more blood from the aortic root, markedly boosting the coronary blood flow in diastole. In fact, the coronary blood flow in diastole improves by 400-500% when compared to systole.

CECP Video Demonstration

The new treatment for angina


Our video samples are designed to be viewed with the QuickTime plug-in.

Download Quicktime Free

Visit the QuickTime help page if you run into any problems.


Phone: (585) 338-2322

© Copyright 2002, Heart Associates of Rochester. All rights reserved.