Commentary

Intraaortic Balloon Counterpulsation in Juvenile Pigs

Morton Kern, MD
Morton Kern, MD
Fischi et al.1 sought to model the influence of intraaortic balloon counterpulsation (IABP) on coronary renal and aortic flow in subjects with congestive heart failure. The model involved examining responses in 5 juvenile pigs who had pacemaker implantation and rapid-pacing induced dilated cardiomyopathy. At 4 weeks, with the ejection fraction reduced to 28 ± 8% with a systemic pressure of 64/44 mmHg, the effect of IABP on blood flow across the circumflex coronary artery, the renal arteries and the infrarenal aorta was examined. High-fidelity pressure catheters were used to evaluate dp/dt and cardiac output. After 10 minutes of intraaortic balloon pumping, there appeared to be no significant hemodynamic or myocardial effects. The results of the negative study indicated, in this model and contrary to some coronary artery disease patient studies, that IABP does not significantly alter coronary, renal or infrarenal flow, with contractility and cardiac output likewise unchanged. The authors concluded that IABP did not improve hemodynamics in the pig heart failure model and attributed the failure to the high compliance of juvenile pig aortas. They further indicated that a larger volume intraaortic balloon would merit investigation for this application. See Fischi, et al. on pages 181–183 The hemodynamic effects of IABP are dependent on several systemic and local vascular factors. Vascular compliance is one of the major influences of pressure-flow responses of aortic balloon counterpulsation. The rapid augmentation of a 40 cc volume delivered during diastole produces a pulsed pressure wave with propagation both distally and proximally. The augmented pulse drives blood flow in both directions and if the receiving vascular bed has sufficiently low resistance, flow through the peripheral (carotid and femorals) as well as through the coronary arteries will increase. At the same time, the abrupt deflation of the balloon creates rapid aortic volume reduction, promoting easier left ventricular ejection due to afterload reduction, which may increase cardiac output and myocardial function. These responses require the IABP to increase the pulsatile pressure to at least a minimum for the aortic volume and compliance. Unfortunately, in the model employed, counterpulsation neither augmented diastolic pressure nor reduced systolic pressure in the setting of pacing-induced cardiomyopathy in the juvenile pig. Disappointing as it was to the investigators, this study should not diminish continued investigation of the potential benefits of IABP for patients with heart failure. It remains important that IABP does not significantly decrease renal blood flow, a complication feared by many, especially in patients with renal artery stenosis. Blood flow through the renal arteries predominantly relies on maintaining a mean (driving) pressure and thus a transient decrease in systolic pressure during IABP or modest augmentation of diastolic pressure does not generally significantly impact renal flow. The ineffectual augmentation of the IABP in the pig model is likely (if not exclusively) due to the highly compliant vascular tree accommodating the balloon pulse and not generating a sufficiently large reflected arterial pressure. This type of IABP failure is also observed in some patients, especially the young, with a highly compliant vasculature. IABP hemodynamics can be improved with the administration of vasopressors to increase vascular tone, thus improving augmentation during pulsatile activities, as noted in young adult candidates for cardiac transplantation who require vasoconstrictors to have effective diastolic pressure augmentation. The Fischi et al. study emphasizes the difficulty of determining the impact of IABP in the heart failure model and encourages continued exploration of this problem.
References
1. Fischi MD, Tondato F, Adams R, et al.. Impact of intraaortic balloon counterpulsation on arterial blood flow in juvenile pigs with heart failure. J Invas Cardiol 2004;16:xxx–xxx.