Juxtaaortic counterpulsation: comparison with intraaortic counterpulsation in an animal model of acute heart failure.
ABSTRACT This study was designed to compare the effects of juxtaaortic balloon counterpulsation (JABC), performed in ascending aorta and the aortic arch, with those yielded by intraaortic balloon counterpulsation (IABC) in descending aorta, in experimental animals during induced cardiac failure. JABC was achieved with a manufactured Dacron prosthesis and a balloon pump placed between the prosthesis and the wrapped aorta. JABC resulted in a significant increase of cardiac output (from 2.33+/-0.82 to 2.61+/-1.12 L/min, p < 0.05), cardiac index (from 0.071+/-0.025 to 0.080+/-0.033 L/min/kg, p < 0.05) and diastolic pressure augmentation evaluated through diastolic and systolic areas beneath the aortic pressure curve (DABAC/SABAC) index (from 0.94+/-0.21 to 1.10+/-0.33, p < 0.01). End diastolic aortic pressure showed a significant decrease with JABC (from 31.90+/-7.09 to 27.83+/-9.72 mm Hg, p < 0.05). A close association between percentage of DABAC/SABAC increases obtained with IABC and JABC was observed (r2 = 0.67; p < 0.001). Counterpulsation obtained by a juxtaaortic catheter placed in the arch and the ascending wrapped aorta results in an effective hemodynamic improvement comparable with that achieved by an intraaortic catheter in open chest sheep.
- SourceAvailable from: Juan Manuel CamusRevista Mexicana de Ingeniería Biomédica. 01/2005; XXVI(2):0-.
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ABSTRACT: The mechanisms that explain intra-aortic balloon pumping (IABP) effects are not completely understood, and attributing them only to pressure-associated changes in cardiac function would be an oversimplification. Since IABP modifies the aortic and systemic blood-flow pattern, flow-related effects could be expected. To characterize effects of acute heart failure (AHF) on the arterial biomechanics; IABP effects on the arterial biomechanics during AHF, and their potential time-dependence; the association between hemodynamics and biomechanical changes during AHF and IABP. Sheep (n = 6) aortic pressure, flow, and diameter were measured: (1) before (Basal) and (2) 1-3 (HF(1-3)) and 28-30 (HF(28-30)) min after starting halothane to induce AHF; and (3) at specific times (1-3, 14-15 and 28-30 min) during IABP assistance. Calculus: aortic characteristic impedance (Z (c)), beta stiffness (β), incremental (E (INC)) and pressure-strain elastic modulus (E (P)); total arterial compliance (C (G)), total systemic vascular resistance and wave propagation parameters. (1) AHF resulted in an acute increase in aortic and systemic stiffness (HF(28-30) % changes with respect to Basal conditions: β +217%, E (P) +143%, E (INC) +101%, Z (c) +52%, C (G) -13%), associated with the reduction in the aortic blood flow; (2) during AHF IABP resulted in acute beneficial changes aortic and systemic biomechanics (% changes in IABP(1-3) with respect HF(28-30): β -62%, E (P) -68%, E (INC) -66%, Z (c) -38%, C (G) 66%), and in wave propagation parameters, (3) IABP-related changes were time-dependent and associated with changes in aortic blood flow. Aortic and systemic biomechanical and impedance properties are detrimentally modified during AHF, being the changes rapidly reverted during IABP. IABP-related beneficial changes in arterial biomechanics were time-dependent and associated with IABP capability to increase blood flow.Heart and Vessels 11/2011; 27(5):517-27. · 2.13 Impact Factor
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ABSTRACT: Acute animal models of cardiac failure are necessary to study new therapeutic options and should be thoroughly characterized from the hemodynamic point of view, including the response of the autonomic nervous system. Thus, the aim of this work was to characterize the pathophysiological adaptation of the autonomic nervous system to acute cardiac failure induced by high doses of halothane (4%). In six sheep, electrocardiogram, aortic pressure and flow were obtained and calculation of systemic vascular resistances was done. Variability analyses in the time and frequency domains were also performed. In the time domain, after heart failure induction using halothane 4%, a significant decrease of both aortic blood flow variability (from 0.13 ± 0.05 to 0.09 ± 0.02 L min−1, p < 0.05) and the broad band spectra (from 1.80 ± 0.66 to 1.25 ± 0.57 L2 min−2, p < 0.005) was observed. Both mean RR (472 ± 44 to 567 ± 68 ms, p < 0.01), and low frequency band of RR intervals (from 6.2 ± 0.9 to 7.7 ± 1.5 ms2, p < 0.05), showed a significant increase, and no change in systemic vascular resistance (from 54.9 ± 29.5 to 50.3 ± 38.4 mmHg min L−1), all of them after heart failure induction. We conclude that in this model of heart failure the autonomic nervous system activity is still functioning, the combination of increased mean and RR low frequency band, with no change in systemic vascular resistance suggest an increase in the sympathetic control (due to maintained SVR), in an attempt to compensate the depression in the cardiac activity and hemodynamic alterations after severe myocardial depression induced by halothane.Cardiovascular Engineering and Technology. 09/2012; 3(3).