H. Schima

Neurocognitive function in patients with ventricular assist devices: a comparison of pulsatile and continuous blood flow devices.

The effect of successful ventricular assist device (VAD) implantation on neurocognitive function in terminal heart failure is uncertain. Additionally, the different impact of continuous versus pulsatile blood flow devices is unknown. A total of 29 patients (mean age 53 years), surviving implantation of a ventricular assist device as bridge to transplantation were prospectively followed (continuous flow: Micromed DeBakey, n = 11; pulsatile flow: Thoratec and Novacor, n = 18). Normative data were obtained in 40 age- and sex-matched healthy subjects (mean age 54 years). Neurocognitive function was objectively measured by means of cognitive P300 auditory evoked potentials before operation (baseline), at intensive care unit (ICU) discharge, and at the 8-week and 12-week follow-up. Before implantation of the VAD, cognitive P300 evoked potentials were impaired (prolonged) compared with age- and sex-matched healthy subjects (p < 0.001). After successful VAD implantation, P300 evoked potentials markedly improved compared with before operation (ICU discharge, p = 0.007; 8-week follow-up, p = 0.022; 12-week follow-up, p < 0.0001). Importantly, there was no difference between continuous and pulsatile VADs (before operation, p = 0.676; ICU discharge, p = 0.736; 8-week follow-up, p = 0.911 and 12-week follow-up, p = 0.397; respectively). Nevertheless, P300 peak latencies did not fully normalize at 12-week follow-up compared with healthy subjects (p = 0.012). Successful VAD implantation improves neurocognitive impairment in patients with terminal heart failure. Importantly, this effect is independent of the type of VAD (pulsatile vs. continuous blood flow).

The erythrocyte-perfused “working heart” model: Hemodynamic and metabolic performance in comparison to crystalloid perfused hearts

A brief period of ischemia was used to evaluate an erythrocyte-enriched Krebs-Henseleit (KH) buffer (n=8) compared to KH only (n=8) in an isolated working rabbit heart. Experimental protocol was as follows: preischemic baseline, 5 min of global ischemia followed by 45 min of reperfusion. Preischemic heart rate was identical, coronary flow was significantly lower (2.7 versus 5.6 mL/min/g wet wt, p<0.01), the other hemodynamic and biochemical values were significantly higher in erythrocyte-perfused hearts: aortic flow 23.5 versus 12.0, p<0.01; cardiac output 26.2 versus 17.6, p<0.01; all in mL/min/g wet wt; dp/dt max 1286 versus 997 mmHg/s, p<0.01; myocardial oxygen consumption 3.5 versus 2.3 micromol/min/g wet wt, p<0.05. During early reperfusion, in the erythrocyte-perfused hearts, coronary flow further increased (p<0.003), the other hemodynamic parameters returned to baseline values in both groups. High-energy phosphates showed significantly higher values (ATP 2.0+/-0.1 versus 1.3+/-0.1, p<0.05; CrP 2.0+/-0.2 versus 1.6+/-0.1, p<0.05 all in micromol/g wct wt), water content was significantly lower (81% versus 74%, p<0.05) in erythrocyte-perfused hearts. It can be concluded that the erythrocyte-perfused working heart model provides excellent oxygenation, leading to superior hemodynamic and metabolic performance. Additionally, in the erythrocyte-perfused hearts preservation of coronary flow reserve underlines the physiological competency of this preparation.

Effect of Stationary Guiding Vanes on Improvement of the Washout Behind the Rotor in Centrifugal Blood Pumps

In centrifugal pumps, there always exists an area of stagnation between the rear of the rotor and the rear housing wall that promotes thrombus formation around the axle. Some current devices overcome the problem by using holes in the rotor plane, leading to increased hydrodynamic losses and shear stress. In this study, a simple apparatus was developed to overcome this problem. Guiding vanes were fixed to the rear housing wall. These vanes decrease the tangential velocity of the fluid and thus the centrifugal force, leading to an increased secondary flow toward the axle. The effect of such vanes was studied in videographic and ultrasound studies. An increase of washout and mixing between the flow layers could be demonstrated (stay time < 200 msec versus several seconds without vanes). In the first animal experiment using nonoptimized vanes, there was no thrombus at the back plane or the seal, and only a small thrombus at the transition between axle and rotor. Hemolysis was slightly elevated (3.2 mg/dl versus 2.5 mg/dl in control experiments). In conclusion, it is highly likely that this simple system will improve the flow characteristics in centrifugal pumps.

Assessment of coronary stenoses by Doppler wires: a validation study using in vitro modeling and computer simulations

The present study evaluates the use of intracoronary velocity measurements by Doppler guidewires for assessing coronary obstructions. In vitro experiments were performed in a flow model using acrylic phantoms of coronary stenoses with different configurations (stenosis area: 56%, 75% and 89%; stenosis length: 1 and 5 mm; stenosis border: tapering or abrupt). Nonpulsatile laminar flow conditions of a test fluid were established at flow rates ranging from 0.5 to 2.0 mL/s to simulate baseline flow and flow after vasodilation. Peak Doppler velocity was measured proximal to, within and distal to the model stenoses. Computer simulations were employed to calculate radial flow profiles with and without a Doppler wire aligned with the vessel center. In 84 in vitro flow experiments, peak Doppler velocity correlated well with the average flow velocity as calculated from the actual flow rate and the vessels cross-sectional area proximal to (r = 0.98, SEE = 1.4, p < 0.001) and within (r = 0.97, SEE = 16.4, p < 0.001) the stenosis. However, the ratio of calculated average velocity to Doppler-measured peak velocity was significantly different from 0.5, the expected value for a parabolic flow profile (0.76+/-0.08, 0.81+/-0.14; p < 0.001). Acceptable accuracy was found for the Doppler estimation of stenosis severity using the continuity equation (error: 0.9+/-1.2% and -4.6+/-3.5% for stenosis with a length of 5 mm and 1 mm, respectively). Doppler velocity reserve significantly underestimated the true flow reserve for the 56% and 75% stenoses (p < 0.01). Computer simulations demonstrated significant alterations of flow profiles by the wire, which explained the observed underestimation of the true flow reserve by the Doppler velocity reserve. Thus, Doppler guidewire measurements of intracoronary flow velocities are useful to assess the severity of coronary stenoses. However, the in vitro results and computer simulations indicate that guidewires alter the flow profile, so that Doppler velocity reserve may underestimate the true flow reserve.

Prosthetic replacement of the aorta is a risk factor for aortic root aneurysm development

BACKGROUND Noncompliant prostheses are used in aortic replacement. We hypothesized that this leads to increased distension and wall stress in the aortic root because of the loss of ventriculo arterial coupling. METHODS Pressure relations in the aortic root caused by changes of aortic elasticity simulating prosthetic aortic replacement were tested in a computer model. We then developed an in vitro model using porcine aortas and performed in vivo validation. RESULTS Findings in vitro and in vivo confirmed the predicted changes of the computer model. Pressure amplitude increased significantly by 17% after prosthetic replacement (p < 0.01). Pressure-time differential (Dp/dt) and dicrotic notch pressure amplitude both increased significantly. Echocardiography demonstrated systolic aortic root distension with percentage area change increasing in vitro from 28.2%+/-9.7% to 35.9%+/-10% (p < 0.05) and in vivo from 13.3%+/-3.1% to 24.3%+/-3.1% (p < 0.0001). Aortic root wall stress increased markedly. CONCLUSIONS Replacement of the aorta with vascular prostheses causes important negative alterations of hemodynamics and increases in wall stress.

Experimental development of an electrically stimulated biological skeletal muscle ventricle for chronic aortic counterpulsation

OBJECTIVE The chronic shortage of donor organs for cardiac transplantation and the high costs for mechanical assist devices demand the development of alternative cardiac assist devices for the treatment of severe heart failure. Cardiac assistance by stimulated skeletal muscles is currently investigated as such a possible alternative. The goal of the presented study was to construct a newly designed biological skeletal muscle ventricle and to evaluate its possible hemodynamic efficacy in an acute sheep model. METHODS A total of 14 adult sheep were used for acute experiments. The entire thoracic aorta including the aortic root was excised from a donor sheep. An aorto-pericardial pouch conduit (APPC) was created by enlarging the aortic circumference in its middle section with two strips of pericardium. This biological conduit was anastomosed in parallel to the descending aorta of a recipient sheep, using the aortic root as an inflow valve to the conduit. Stimulation electrodes were applicated to the thoracodorsal nerve and the latissimus dorsi muscle was detached from the trunk and wrapped around the pouch. ECG-triggered functional electrical stimulation was applied during cardiac diastole to simulate aortic counterpulsation. Stimulation was performed during various hemodynamic conditions. RESULTS A standardised surgical procedure suitable for long term studies was established during six experiments. An APPC, with 70-80 mm filling volume, was found to be of optimal size. In another eight experiments, hemodynamic measurements were performed. Under stable hemodynamic conditions the stimulation of the biological skeletal muscle ventricle induced a significant increase of mean arterial pressure by 14% and mean diastolic pressure by 26%. During pharmacologically induced periods of cardiac failure, the stimulation of the APPC increased mean arterial pressure by 13% and mean diastolic pressure by 19%. In all eight experiments, the diastolic peak pressure reached supra-systolic values during stimulation. CONCLUSIONS The results demonstrate the hemodynamic efficacy of this newly designed biological skeletal muscle ventricle as an aortic counterpulsation device. Chronic experiments using a preconditioned fatigue-resistant muscle will further help to evaluate its possible clinical significance.

Experimental Stent-Graft Treatment of Ascending Aortic Dissection

BACKGROUND This study assessed the feasibility of stent graft treatment of ascending aortic dissections in a porcine in vitro model. METHODS The entire thoracic aortic aorta including the supraaortic branches was harvested from 12 adult pigs and an intimal tear was artificially created. The aortic annulus was then sewn into a silicon ring of a driving chamber. The distal aorta was connected to tubing with adjustable resistance elements. The circulation was driven by a hydraulic motor piston pump to mimic aortic flow and pressure. After creating a dissection by elevating the systolic aortic pressure to 180 mm Hg, a 2- x 2.6-cm covered stent graft was inserted through the brachiocephalic trunk using a specially designed delivery system. Stent graft placement was performed under continuous ultrasound control. RESULTS The longitudinal length of the created ascending aortic dissection was 1.8 +/- 0.39 cm. Ultrasound studies revealed successful deployment of the stent graft and closure of the false lumen in all 12 cases. Diameter and area of the true lumen increased from 0.52 +/- 0.15 cm to 2.54 +/- 0.36 cm (p < 0.05) and from 0.78 +/- 0.27 cm2 to 5.13 +/- 1.35 cm2 (p < 0.05), respectively. The circumference of the true lumen increased from 4.50 +/- 0.52 cm to 7.96 +/- 1.2 cm (p < 0.05). Ultrasound studies also revealed uncompromised function of the aortic valve in all cases. No dislodging of stent grafts was observed. CONCLUSIONS Given ideal anatomy, experimental stent graft placement for ascending aortic dissection is feasible and achieves complete closure of the false lumen.

Can Hypocapnia Reduce Cerebral Embolization During Cardiopulmonary Bypass

BACKGROUND Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures. METHODS Patients were prospectively randomized to either hypocapnia (PaCO2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes. RESULTS Despite significant differences in PaCO2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 +/- 100 (median, 80) in the hypocapnic group and 135 +/- 115 (median, 96) in the normocapnic group, respectively (p = 0.315). CONCLUSIONS Due to the high between-patient variability in embolization, reductions in PaCO2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans.

Mechanical simulation of shear stress on the walls of peripheral arteries

In the last few years many attempts were made to line artificial vascular grafts with in vitro grown endothelial cell layers and thereby to minimize the risk of thromboembolism. However, adherence and resistance against shear stress forces were not tested under physiological pulsatile shear stress forces. In this paper, a mock-circulation apparatus is described, which simulates various forms of pulsatile shear stress, and which at the same time meets the requirements of cell cultivation. It can be sterilized and needs less than 700 ml of culture medium for priming. The generated flow profile can be adapted to a wide range of shear stress and also to different viscosities of used media. To take account of the different viscosities of culture medium and blood, a computerized calculation of the shear stress pattern was performed. Using the results of this computer model, the flow pattern was modified to obtain normal physiological shear stress when using culture medium. Results of pulse generation and simulation for the superficial femoral artery are presented.

NEUROCOGNITIVE FUNCTION IN PATIENTS WITH VENTRICULAR ASSIST DEVICES

The effect of successful ventricular assist device (VAD) implantation on neurocognitive function in terminal heart failure is uncertain. Additionally, the different impact of continuous versus pulsatile blood flow devices is unknown. A total of 29 patients (mean age 53 years), surviving implantation of a ventricular assist device as bridge to transplantation were prospectively followed (continuous flow: Micromed DeBakey, n = 11; pulsatile flow: Thoratec and Novacor, n = 18). Normative data were obtained in 40 age- and sex-matched healthy subjects (mean age 54 years). Neurocognitive function was objectively measured by means of cognitive P300 auditory evoked potentials before operation (baseline), at intensive care unit (ICU) discharge, and at the 8-week and 12-week follow-up. Before implantation of the VAD, cognitive P300 evoked potentials were impaired (prolonged) compared with age- and sex-matched healthy subjects (p < 0.001). After successful VAD implantation, P300 evoked potentials markedly improved compared with before operation (ICU discharge, p = 0.007; 8-week follow-up, p = 0.022; 12-week follow-up, p < 0.0001). Importantly, there was no difference between continuous and pulsatile VADs (before operation, p = 0.676; ICU discharge, p = 0.736; 8-week follow-up, p = 0.911 and 12-week follow-up, p = 0.397; respectively). Nevertheless, P300 peak latencies did not fully normalize at 12-week follow-up compared with healthy subjects (p = 0.012). Successful VAD implantation improves neurocognitive impairment in patients with terminal heart failure. Importantly, this effect is independent of the type of VAD (pulsatile vs. continuous blood flow).