Year : 2019 | Volume
: 22 | Issue : 3 | Page : 283--284
Aortic counterpulsation for myocardial support: Towards a new paradigm
Department of Cardiac Anaesthesia, All India Institute of Medical Sciences, New Delhi, India
Department of Cardiac Anaesthesia, All India Institute of Medical Sciences, New Delhi - 110 029
|How to cite this article:|
Choudhury A. Aortic counterpulsation for myocardial support: Towards a new paradigm.Ann Card Anaesth 2019;22:283-284
|How to cite this URL:|
Choudhury A. Aortic counterpulsation for myocardial support: Towards a new paradigm. Ann Card Anaesth [serial online] 2019 [cited 2020 Oct 19 ];22:283-284
Available from: https://www.annals.in/text.asp?2019/22/3/283/262096
Treatment for the failing heart comprises cardiopulmonary bypass (CPB), extracorporal membrane oxygenation internal/external counterpulsation, and various types of auxiliary pumps (artificial heart) such as ventricular-assist devices. Intra-aortic balloon pump (IABP) is the most commonly available and rapidly instituted form of mechanical support device for the ailing heart. As early as 1953, Arthur and Adrian Kantrowitz (brothers) published “experimental augmentation of coronary flow by retardation of arterial pulse pressure.” There were numerous experimental studies during early 1950s by others with a concept of developing a mechanical device including CPB to support the failing heart. They demonstrated many benefits like increase in mean aortic diastolic pressure, diastolic pressure–time index, endocardial viability ratio, ejection fraction, cardiac output, coronary, cerebral and renal blood flow, myocardial oxygen supply, lactate utilization, and significant decreases in peak systolic aortic pressure, left ventricular end-diastolic pressure, tension time index, left ventricular work, myocardial oxygen consumption, and lactate production. IABP is a form of internal aortic counterpulsation which augments the diastolic pressure during balloon inflation contributing to augmented coronary perfusion pressure, and presystolic rapid deflation helps reduce the left ventricular afterload, potentially reducing myocardial work. The hemodynamic and metabolic benefits of counterpulsation therapy in patients with acute cardiac dysfunction have led to the development of a noninvasive device that could perform diastolic augmentation sans common pitfalls associated with invasive counterpulsation devices (bleeding, thrombosis, limb ischemia etc.).
In 1963, Dennis et al. pioneered systolic unloading and diastolic augmentation by using a gas-filled suit covering the lower extremities till the mid-abdomen, which was inflated and deflated in “sync” with the patients ECG. Since then, many improvements have brought about the modern enhanced external counterpulsation (EECP) device with proven clinical benefits for refractory angina (stable ischemic heart disease) aiming to improve the quality of life in patients with disabling coronary artery disease (CAD). Its utility in modern times has been challenged by the successful pharmacologic therapy for CAD, a time-consuming regimen (35 one-hour sessions, 5 days a week for 7 weeks) and somewhat incomplete understanding of its mechanism of action. In this issue of ACA, Sahebjami Fet al., in their paper entitled “Refractory Angina Frequencies during Seven Weeks Treatment by Enhanced External Counter Pulsation in Coronary Artery Disease Patients with and without Diabetes,” have elucidated the usefulness of EECP in refractory angina in diabetics. From a hydraulic system to a pneumatic one, ECP systems have undergone massive improvements, but while its interest gradually declined in the United States, ECP therapy became popular in China because of its cost-effectiveness and potential for widespread use. Zheng ZS et al. in 1976 transformed single-cuff ECP system into sequential multi-cuff apparatus, which further evolved in 1983 into EECP. Instead of compressing the entire lower limb instantaneously, three separate cuffs inflate and deflate sequentially from distal to proximal fashion synchronized to cardiac cycle. Both central hemodynamics and peripheral sheer stress mechanisms are active when EECP therapy is instituted for chronic stable angina.
The future of EECP therapy is promising as a number of noncardiac applications emerged in recent years. Patients with angina and heart failure with restless leg syndrome, erectile dysfunction, hepato-renal syndrome, non-arthritic ischemic optic neuropathy, and depression have experienced improvement in their symptom after sessions of EECP therapy. Data suggest that EECP is a safe treatment modality for selected patient with obstructive stable CAD. In the light of evidence supporting this low-cost noninvasive therapeutic modality, along with an aging population and decreasing trends in invasive procedures for CAD, EECP might become more widely accepted mode of therapy in the future. Meanwhile, more research investigating the utility and efficacy of EECP is definitely welcome.
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