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Enhanced external counterpulsation therapy: significant clinical improvement without electrophysiologic remodeling
Charles A Henrikson1, Nisha Chandra-Strobos
1Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21224, USA.
Insights
Enhanced external counterpulsation (EECP) therapy effectively treats severe coronary artery disease (CAD) but does not cause early electrical remodeling in the heart. This study found no significant changes in ECG parameters after EECP treatment.
Area of Science:
- Cardiology
- Cardiovascular Research
- Medical Technology
Background:
- Enhanced external counterpulsation (EECP) therapy improves hemodynamics in severe coronary artery disease (CAD).
- Other hemodynamic-altering treatments can induce electrophysiologic remodeling, indicated by QT interval changes.
Purpose of the Study:
- To assess if EECP therapy induces electrophysiologic remodeling in patients with severe CAD.
- To investigate changes in electrocardiogram (ECG) parameters following EECP treatment.
Main Methods:
- A study involving 28 patients with severe CAD who completed a 7-week, 35-hour EECP therapy course.
- Electrocardiogram (ECG) parameters, including heart rate, PR, QRS, and QT(c) intervals, were measured before and after EECP.
- Patients were analyzed for clinical response to EECP, ejection fraction, and revascularization history.
Main Results:
- EECP therapy improved anginal patterns in most patients (82%).
- No significant changes were observed in heart rate, PR, QRS, or QT(c) intervals before and after EECP.
- No detectable changes in ECG parameters were found when analyzed by response to EECP, ejection fraction, or revascularization history.
Conclusions:
- EECP is an effective treatment for severe CAD, improving symptoms.
- EECP therapy does not appear to induce early electrical remodeling of the heart.
Background:
Enhanced external counterpulsation therapy (EECP), in addition to improving coronary flow and increasing the time to ischemia, noninvasively alters hemodynamics in patients with severe coronary artery disease (CAD). Other treatments that alter hemodynamics, for example, balloon valvuloplasty, left ventricular assist devices, and pharmacologic antagonism of the rennin-angiotensin system, promote electrophysiologic remodeling, as evidenced by alterations in the QT interval.
Methods:
We studied 28 patients who completed a 7-week, 35-hour session of EECP to assess whether such therapy would also result in electrophysiologic remodeling.
Results:
All patients had class II-III angina, imaging-proven ischemia, and severe, near-inoperable CAD. Of 28 patients, with a mean age 62 +/- 13 years (mean +/- SD), 78% were male, 46% diabetic, 82% hypertensive, 60% had undergone angioplasty, and 67% had undergone bypass surgery. The mean ejection fraction was 44% (range 25-60%). Following EECP, most patients (82%) had at least a one full class improvement in their anginal pattern. In most patients, there was substantial baseline conduction system disease present: a mean QRS of 105 +/- 19 ms. It is to be noted that there was no significant change in heart rate (HR), PR, QRS, or QT(c) intervals before and after EECP in either clinical responders or nonresponders. When analyzed by response to EECP, ejection fraction, or history of revascularization, there were still no detectable changes in ECG parameters (all P = NS).
Conclusions:
While EECP remains an effective treatment for severe CAD, it does not prompt early electrical remodeling of the heart.
