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A novel subcutaneous counterpulsation device: acute hemodynamic efficacy during pharmacologically induced hypertension, hypotension, and heart failure.

To the Editor, The debut of a new counterpulsation device (CPD) through experimental testing by Bartoli et al. (1) has struck us as very promising. It is our view that the authors have developed a reliable apparatus for providing acute hemodynamic support in various pathophysiologic states. The potential for chronic or acute circulatory support in heart failure conditions with the advantage of diminished invasiveness during implantation may prove very important to improved future treatment. This is especially true for patients on the margin, not yet indicated for a full sternotomy and ventricular assist device insertion but in need of hemodynamic stability. This study builds on this need through an innovative design and device, but questions still remain. The pathophysiological model for hypertension the authors utilize relies on phenylephrine, which is an alpha-1 receptor agonist and acts to constrict the peripheral vasculature and increase total peripheral resistance. Studies on human hypertension have, however, shown that early blood pressure elevation tends to be due to increased heart rate and cardiac output (2). Considering the ultimate applicability of this device to humans, it would be better to induce the same physiological state in the animal models of hypertension. The animal model nature of this study may also make its applicability to human subjects tenuous. Studies have shown a marked difference in compliance and vascular resistance between bovine and human models (3).The authors note that this is likely to raise the CPD’s efficacy at improving hemodynamic states in a system with lower compliance and greater impedance.This may, however, come at the cost of the CPD’s ability to reduce cardiac afterload as it must fill through a greater pressure barrier. Conversely, the stiffer, less compliant vessels in the human may retain architecture better in the face of the CPD’s negative pressure and allow for increased device filling. Regardless, the CPD’s performance and results are likely to be attenuated in a tenser system (4). Vasculature differences between model and human systems are also likely to result in different pressure dynamics (3). Intra-aortic balloon pump and CPD involvement is usually indicated for diastolic dysfunction that results in insufficient coronary perfusion. This compromise in coronary blood flow is often caused and exacerbated, in part, by the lowered compliance and increased impedance of peripheral arterial vasculature. This phenomenon may be explained by the mismatch in timing of the reflection wave which takes place prematurely thereby reaching the heart while it is still in systole and before the aortic valve has closed, thus diminishing coronary perfusion (5,6). Clinical application of a CPD will often be in patients with stiffened arteries, significantly more than calf models, and pressure dynamics of earlier and more proximately originating reflection waves. In calf models where compliance is high, the reflection waves are likely to be well timed and have a small effect in hemodynamic dysfunction while they will play a larger role in human hemodynamics The larger role waveform dynamics play in clinical cases and lessened exposure of the CPD to whole blood flow may show a different picture when applied to humans. Cerebral autoregulation is another area that deserves close attention. Cerebral blood vessels have the unique ability to provide uniform blood flow to the brain within a specific arterial pressure range (60– 160 mm Hg) (7).This regulatory mechanism prevents edema and ischemia in brain tissue during times of hemodynamic instability.The lack of normal pressure rhythms leads to disrupted autoregulatory functions, which, when in the cerebrum, can cause disastrous effects. Proof of concept that a CPD when anastomosed to the axillary artery can achieve hemodynamic efficiency and stability in volatile conditions as shown by our respectable colleagues is indeed very valuable. However, stronger model mimicry can lead to increased certainty. Also, whereas this interesting device definitely appears to help the heart, it does not significantly improve the cardiac output. If the intent is to help patients with chronic heart failure, it would be critical to take into account measures that would enable such a device to help increase the cardiac output in order to ensure that more flow to end organs is provided. We hope that some of the concerns noted in this commentary will be doi:10.1111/j.1525-1594.2010.01176.x Artificial Organs 35(1):92–98, Wiley Periodicals, Inc. © 2011, Copyright the Authors Artificial Organs © 2011, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.