Control of centrifugal blood pump based on the motor current

In this study, centrifugal pump performance was examined in a mock circulatory loop to derive an automatic pump rotational speed (rpm) control method. The pivot bearing supported sealless centrifugal pump was placed in the left ventricular apex to aorta bypass mode. The pneumatic pulsatile ventricle was used to simulate the natural ventricle. To simulate the suction effect in the ventricle, a collapsible rubber tube was placed in the inflow port of the centrifugal pump in series with the apex of the simulated ventricle. Experimentally, the centrifugal pump speed (rpm) was gradually increased to simulate the suction effect. The pump flow through the centrifugal pump measured by an electromagnetic flowmeter, the aortic pressure, and the motor current were continuously digitized at 100 Hz and stored in a personal computer. The analysis of the cross-spectral density between the pump flow and motor current waveforms revealed that 2 waveforms were highly correlated at the frequency range between 0 and 4 Hz, with the coherence and phase angles being close to 1.0 and 0 degree, respectively. The fast Fourier transform analysis of the motor current indicated that the second harmonic component of the motor current power density increased with the occurrence of the suction effect in the circuit. The ratio of the fundamental to the second harmonic component decreased less than 1.3 as the suction effect developed in the circuit. It is possible to detect and prevent the suction effect of the centrifugal blood pump in the natural ventricle through analysis of the motor current waveform.     

Effects of aging on left ventricle-arterial coupling in man

Twenty-five normotensive men without any cardiac or arterial pathology, aged 22 to 68 years, 12 less than 45 year old, 13 over 45 years, underwent cardiac catheterisation and angiography. The following parameters were calculated: 1) a global index of arterial function (Ea) and its determining factors (Ea = LVESP/SV where LEVSP = left ventricular end systolic pressure and SV = left ventricular stroke volume); Ea = (HR x SVR) + Ea' where HR = heart rate, SVR = total systemic vascular resistance and Ea' = (LVESP - MAP/SV) (MAP = mean arterial pressure); 2) an index of global left ventricular pump function: ELV (ELV = LVESP/LVESV, where LVEDV = left ventricular end systolic volume; 3) an index of LV-arterial coupling: the Ea/ELV ratio. With aging, both Ea (by increase in SVR) and Ea' and ELV increased significantly. Ea/ELV (inverse of the ejection fraction-1) increased with age but ELV less than Ea. Ea/ELV was significantly higher in patients over 45 years of age but the correlation between ejection fraction and age was not statistically significant (p = 0.10). These results suggest that with aging, the improvement in LV pump function approximately corresponds to the degradation in arterial transport function: the left ventricular-arterial coupling as assessed by the Ea/ELV ratio (and therefore the ejection fraction) is maintained in the majority of cases.     

In vivo and in vitro evaluation of the pulsatile mode of a magnetically suspended centrifugal pump

The authors have been developing a magnetically suspended centrifugal pump (MSCP). They have devised a pulsatile mode for the MSCP, which was generated by altering rotational speed. This article describes in vitro and in vivo studies with the pulsatile mode of the MSCP. Hemolysis tests were performed in two identical circuits to compare the nonpulsatile (NP) mode and the pulsatile (P) mode. In vivo studies were performed in sheep. First, biventricular assisted circulation was instituted in the left heart with the MSCP and in the right heart with the Biopump. The native heart was induced to ventricular fibrillation. Second, a left ventricular assisted circulation was instituted as the native heart was beating. An inflow cannula was inserted into the left atrium in one sheep and into the left ventricle in the other. The normalized indices of hemolysis of the NP and P groups were 0.0025 +/- 0.0018 g/100 L, and 0.0032 +/- 0.0024 g/100 L (N = 4, not significant). During ventricular fibrillation in the P mode, the pulse pressure was 14 mmHg (the rotational speed: 1,500 to 2,600 rpm). In a beating heart, at atrial withdrawal, the pulse pressure increased from 10 to 24 mmHg (2,100 +/- 500 rpm), while at ventricular withdrawal, it decreased from 17 to 40 mmHg (2,000 +/- 500 rpm) on P mode. The MSCP in pulsatile mode did not increase hemolysis. At ventricular withdrawal, it was easier to produce a pulsation than at atrial withdrawal. The pulsatile mode of the MSCP is applicable to a left ventricular assist system.     

In vitro and in vivo assessment of an intravenous axial flow pump for right heart assist

Right ventricular (RV) function is a limiting factor in maintaining systemic circulation with circulatory assist. There is, however, no easy way to institute RV assist, such as the intraarterial axial flow pump (Hemopump) used for left heart assist. In this study, the feasibility and hemodynamic effect of intravenous use of an axial flow pump was examined. A pump system was developed with an outflow cannula and an impeller that were newly designed for intravenous insertion with a Hemopump driving system. The pump system characteristics using goat blood at a hematocrit of 26% indicated that maximum flow at a pressure differential against 40 mmHg is 3.2 l/min at a pump speed of 28,000 rpm. The pump was tested in adult goats by intravenous insertion through a 14 mm, low porosity graft anastomosed to the infrarenal inferior vena cava. The pump was advanced until the tip of the cannula was positioned at the main pulmonary artery, using balloon catheter guidance under fluoroscopy. RV assistance was evaluated by pressure tracing, and aortic flow (AF) measured by electromagnetic flowmeter under 1) induced pulmonary stenosis (PS), and 2) electrically induced ventricular fibrillation (VF) in combination with left heart assist. Under PS, right atrial pressure decreased from 11 to 2 mmHg and AF increased from 1.0 to 4.1 l/min after initiation of the pump. Under VF, AF and aortic pressure were 2.6 l/min and 78 mmHg, respectively, with left ventricular assist. After initiation of the pump, they increased to 4.0 l/min and 98 mmHg, respectively. In chronic experiments using three adults goats for up to 48 hr, levels of plasma hemoglobin and platelet counts were maintained within an acceptable range. There was no prominent damage to the hearts. These data suggest that an axial flow pump introduced by an intravenous approach without thoracotomy is feasible and provides sufficient right heart assist.     

Experimental principles for preserving annulo-ventricular integrity of the mitral valve

Despite numerous improvement in cardiac surgery the results in mitral valve replacement are still not satisfactory, since impaired left ventricular function continues to be a problem during the postoperative course. In order to investigate the effect of mitral valve replacement on left ventricular function canine experiments were performed: During extracorporeal circulation bileaflet mitral valve prostheses were implanted preserving the ventriculo-annular continuity. Flexible wires were slung around the chordae of the subvalvular mitral apparatus and brought to the outside through the left ventricular wall. Left ventricular diameters were measured by sonomicrometry, left ventricular stroke volume, left ventricular enddiastolic volume and ejection fraction by dye dilution technique as well as left ventricular and aortic pressure by catheter tip manometers. After finishing cardiopulmonary bypass control values were registered and different preload values achieved by volume loading with blood transfusions to left ventricular enddiastolic pressures of 12 mm Hg. Subsequently under normovolumic conditions the chordae tendineae of the anterior and posterior papillary muscles of the mitral valve were cut from the outside, while the heart was beating, by application of electrocautery on the steel wires. Following severance of the ventriculo-annular continuity of the mitral valve again function curves of left ventricular hemodynamics were made during volume transfusions. When the chordae had been divided the left ventricular enddiastolic diameter increased by 10% in the major axis, while in the minor axis no significant changes occurred. The systolic shortening was impaired substantially by reduction of 43% during the ejection phase when the subvalvular mitral apparatus had been severed. Left ventricular enddiastolic volume was increased by 18% at any preload level, while left ventricular ejection fraction was reduced by 16%. Consequently left ventricular stroke volume was decreased by 24% at any left ventricular enddiastolic volume, when the chordae had been divided. It can be concluded that left ventricular geometry is changed when the annulo-ventricular continuity has been interrupted at mitral valve replacement: The major axis of the left ventricle is increased and the enddiastolic volume is augmented. The left ventricle is only able to eject the same stroke volume at higher preload levels when the chordae tendineae have been divided. The same cardiac performance can only be achieved by volume loading and at the expense of higher wall tension, which leads to unfavorable conditions in terms of cardiac muscle mechanics with reduced exercise tolerance. These data speak for preservation of the annulo-ventricular continuity in mitral valve replacement. Provided that these results from acute canine experiments can be transferred to humans, one would suggest that preservation of the mitral subvalvular apparatus is of importance in patients with dilated hearts and with impaired left ventricular function.     

The effects of left ventricular load and contractility on mitral regurgitant orifice size and flow in the dog

Acute mitral regurgitation (MR) was produced in 12 dogs by closed chest partial valvulectomy and the relative contributions of MR pressure gradient (MRG), the time for regurgitant flow (VSI), and the MR orifice area (MRA) to mitral regurgitant volume (MRV) assessed. Aortic and left atrial pressures, biplane left ventricular (LV) angiography, forward flow and mitral regurgitant flow (MRF) were measured following MR induction and following augmentation of left ventricular end-diastolic volume (EDV), increased aortic resistance (angiotensin), and in the presence of increased ventricular contractility (calcium or epinephrine). Mitral regurgitation orifice area was determined by calculation and the diameters of the mitral anulus and subvalvular areas measured angiographically. Angiotensin and volume infusion induced a substantial increase in MRF which was largely dependent on an increase in MRA but not MRG, while augmentation of contractility decreased MRF accompanied by a decrease in MRA, relatively independent of MRG. Left ventricular size and shape are major determinants of MRA and resultant MRF in acute mitral regurgitation. These findings may help to explain the effects of such factors as ventricular loading and volume on the clinical course of mitral regurgitation in man.     

Survival of a patient with postinfarction ventricular septal defect following venoarterial bypass with centrifugal pump and reoperation for residual shunt

A 61-year-old man was hospitalized because of circulatory collapse due to postinfarction ventricular septal defect. As his hemodynamic condition deteriorated despite intraaortic counterpulsation, he underwent patch closure of VSP and patch reconstruction of the anterior left ventricular wall concomitant with coronary artery bypass grafting to the circumflex lesion immediately after admission. Femorofemoral circulatory assist with centrifugal pump was necessitated to wean from cardiopulmonary bypass because of severe left ventricular dysfunction. Circulatory assist was controlled to maintain mixed venous oxygen saturation of more than 70% under mild hypothermia. On the second postoperative day (POD), increased oxygen saturation from right atrium to pulmonary artery developed (Qp/Qs = 2.1). Further surgery was performed on an emergency basis for additional patch closure of VSP. Then he was successfully weaned from cardiopulmonary bypass successfully. The patient was extubated on the 14th POD and was ambulatory when he discharged on the 56th POD. Immediate surgical intervention should be performed for the patient with postinfarction ventricular septal defect when the hemodynamic state deteriorates under intraaortic counterpulsation.     

Effects of preload, afterload and inotropy on dynamics of ischemic segmental wall motion

OBJECTIVES: This study sought to explore the separate and combined effects of changes in preload, afterload and contractility on the dynamics of systolic bulging. BACKGROUND: The extent of ischemic systolic bulging has been shown to be mechanically disadvantageous to left ventricular pump performance. The factors that determine ischemic segmental wall motion have not been systematically studied. METHODS: Fourteen beagles were instrumented with sonomicrometers, micromanometer pressure gauges and a balloon in the inferior vena cava. Regional function was evaluated before and after 90 s of proximal left circumflex coronary artery occlusion. Occlusions were repeated after increasing systolic pressure by 5 to 10 (afterload I) and 15 to 20 mm Hg (afterload II) with graded aortic occlusion during inotropic stimulation with dobutamine (2.5 and 5 micrograms/kg body weight per min intravenously), with simultaneous 5 micrograms/kg per min dobutamine infusion and afterload II and during 2.5% halothane (negative inotrope) concentration. A 20-min recovery period was allowed between each stage of the experiment so that regional function returned to its preocclusion level. Ischemic wall motion was characterized by percent systolic bulging and its peak positive systolic lengthening rate (+dL/dt). RESULTS: Because bulging is markedly influenced by regional preload, systolic bulging was characterized over a wide range of end-diastolic lengths of the ischemic segment during caval balloon occlusion. During each intervention, a decrease in regional preload increased the extent of percent systolic bulging. This preload dependency was more pronounced with dobutamine infusions. An increase in afterload was not associated with increased percent systolic bulging at any given preload. At a predetermined preload, bulging was not appreciably altered when an increase in left ventricular systolic pressure was not associated with a change in peak positive first derivative of left ventricular pressure (+dP/dt) but was significantly worse when peak +dP/dt increased. Dobutamine caused a dose-dependent increase in percent systolic bulging and peak +dL/dt that was positively correlated with peak +dP/dt. CONCLUSIONS: By using different loading and inotropic interventions and analyzing the regional wall motion behavior over a range of regional preloads, we can conclude that preload and rate of pressure (tension) development are the principal determinants of systolic bulging. Increases in left ventricular pressure alone had a minimal effect on systolic bulging.     

Load relaxation and forces with activity in Hoffman external fixators: a clinical study in patients with Colles'' fractures

OBJECTIVE: To determine postoperative left ventricular mechanics following the arterial switch operation (ASO). DESIGN: Prospective, cohort study. SETTING: Pediatric cardiac recovery room. PATIENTS: Nine neonates with transposition of the great arteries undergoing the ASO within the first week of life. INTERVENTIONS: Noninvasive ejection phase indices: shortening fraction (% SF), corrected mean velocity of circumferential shortening (VCFc), and wall stress analysis were used to calculate indices of specific left ventricular systolic mechanics. The % SF and VCFc were respectively adjusted for left ventricular afterload (end-systolic wall stress) to derive an index for left ventricular performance (stress-shortening relation) and contractility (stress-velocity relation). Left ventricular preload was assessed as the variance between the performance and contractility indices. All indexed data are reported as mean Zscore (i.e., number of standard deviations from the mean of a normal age- and body surface area-adjusted population). A mean Zscore of < -2 or > 2 was regarded as a significant variance from normal. Transmitral Doppler flow patterns were recorded at each postoperative interval and analyzed for isovolumic relaxation time (IVRT) as an index of left ventricular compliance. MEASUREMENTS AND MAIN RESULTS: All nine patients did well clinically and completed the study. Noninvasive parameters were measured at mean intervals of 3 (early), 23 (intermediate), and 48 hrs (late postoperative) relative to the time of arrival in the cardiac recovery room. Postoperative left ventricular performance was decreased throughout the early (-4.0 +/- 1.5 SD), intermediate (-4.1 +/- 2.8), and late (-3.5 +/- 1.3) phases of recovery. In contrast, the overall left ventricular contractility remained normal throughout the three postoperative intervals (0.2 +/- 1.8, -1.2 +/- 1.9, and -1.0 +/- 1.6, respectively), although three of the nine patients had a diminished stress-velocity index during the study period. Left ventricular afterload was within normal range in the early (0.1 +/- 1.7) and intermediate (1.5 +/- 1.9) phases of recovery, but increased in the late postoperative period (2.5 +/- 2.9). Left ventricular preload was decreased significantly throughout the early (-4.2 +/- 1.3), intermediate (-2.8 +/- 2.0), and late (-2.5 +/- 1.0) postoperative phases. All nine patients demonstrated decreased preload during the recovery period. IVRT was decreased in the post-ASO patients at each phase of recovery compared with normal data (p < .001). CONCLUSIONS: Left ventricular performance is impaired in infants during the period immediately following the ASO. A persistent preload deficit closely matches the pattern of impaired ventricular performance. Decreased IVRT points to impaired ventricular compliance as the etiology of the altered preload. In contrast, left ventricular contractility remains normal in the majority of post-ASO patients. Decreased contractility may account for impaired ventricular performance in selected cases.     

Effects of load manipulations, heart rate, and contractility on left ventricular apical rotation. An experimental study in anesthetized dogs

BACKGROUND: Left ventricular twist or torsion has been defined as the counterclockwise rotation of the ventricular apex with respect to the base during systole. We have recently shown that since base rotation is minimal, measurement of apex rotation reflects the dynamics of left ventricular (LV) twist. Since the mechanisms by which load and contractility affect twist are controversial, we aimed to determine the relation between apex rotation and volume, contractility, and heart rate under conditions in which dimensions and pressures were accurately measured. METHODS AND RESULTS: Using our optical device coupled to the LV apex, apex rotation was recorded simultaneously with LV pressure, ECG, LV segment length, and minor-axis diameters (sonomicrometry) in 12 open-chest dogs. Using vena caval occlusion and volume loading, a linear end-diastolic (ED) relation between apex rotation and LV area index was obtained (slope, 0.61 +/- 0.06 degrees/percent change; intercept, -60.1 +/- 6.2 degrees; n = 10) that differed from the end-systolic (ES) relation (slope, 1.36 +/- 0.27 degree/percent change; intercept, -132.5 +/- 24.9 degrees; P < .005). With changes in contractility, afterload, or heart rate, for both ED and ES the apex rotation-volume points fell within the range of the relations established by changing preload, suggesting that volume is the major determinant of twist. Vena caval occlusion (preload and afterload decrease) caused an increase in amplitude of apex rotation, with maximal apex rotation occurring earlier in ejection. In contrast, acute volume loading (predominant preload increase) caused a small decrease in the amplitude of apex rotation, and twist relaxation was delayed into the isovolumic relaxation period. Likewise, with single-beat aortic occlusion (increased afterload), there was a slight decrease in the amplitude of apex rotation, and maximal apex rotation was delayed into the isovolumic relaxation period. Paired pacing (increased contractility) increased the total amplitude of apex rotation by 42% and caused a delay in untwisting until the end of the isovolumic relaxation period. An increase in heart rate over 150 beats per minute resulted in a significant decrease in the amplitude of apex rotation with a similar delay of twist relaxation into the isovolumic relaxation period. CONCLUSIONS: The effects of load, contractility, and heart rate manipulations on LV twist as measured throughout the cardiac cycle by the optical apex rotation method are manifested by changes in both the amplitude and dynamics of torsion. LV twist at ED and ES is primarily a function of volume; this relation appears to be unaltered by heart rate, afterload, and contractility. Whereas decreased load caused early untwisting, increases in preload, afterload, heart rate, and contractility caused a consistent pattern of delay in twist relaxation.     

Structural basis for changes in left ventricular function and geometry because of chronic mitral regurgitation and after correction of volume overload

Left ventricular function and myocyte structure were examined in three groups of dogs: (1) 3 months of mitral regurgitation caused by chordal rupture (n = 7); (2) chronic mitral regurgitation followed by mitral valve replacement and a 3-month recovery period (n = 7), and (3) sham controls (n = 8). The left ventricular end-systolic stiffness constant (Kess) was measured as an index of left ventricular contractile function with stress-strain relationships obtained by cinecatheterization. Isolated myocyte structure and composition were examined with computer-assisted morphometry and nuclear area computed with deoxyribonucleic acid fluorescence. Left ventricular contractile function was significantly depressed with chronic mitral regurgitation compared with control values (Kess, 2.1 +/- 0.1 versus 3.6 +/- 0.2; p < 0.05) and returned to control values with mitral valve replacement (3.8 +/- 0.2). Left ventricular mass significantly increased in both the mitral regurgitation and mitral valve replacement groups compared with control values (121 +/- 10, 120 +/- 5 versus 95 +/- 9 gm, respectively; p < 0.05). Myocyte length increased with mitral regurgitation beyond control values (194 +/- 4 versus 218 +/- 8 microns; p < 0.05) and increased beyond mitral regurgitation values after mitral valve replacement (231 +/- 7 microns; p < 0.05). Myocyte volume with mitral regurgitation increased slightly beyond control values (33.5 +/- 0.7 versus 37.6 +/- 1.3 microns3; p = 0.15) and significantly increased with mitral valve replacement (40.1 +/- 1.2 microns3; p < 0.05). Myocyte myofibril volume significantly declined with mitral regurgitation compared with control values (14.8 +/- 1.5 versus 22.2 +/- 0.7 microns3; p < 0.05) and significantly increased beyond both mitral regurgitation and control values with mitral valve replacement (27.1 +/- 1.1 microns3; p < 0.05). Myocyte nuclear area with mitral regurgitation remained unchanged from control values (1430 +/- 122 versus 1163 +/- 89 microns2) but increased significantly with mitral valve replacement (2209 +/- 250 microns2; p < 0.05). In summary, the left ventricular contractile dysfunction with chronic mitral regurgitation is accompanied by increased myocyte length and reduced myofibril content. In contrast, the left ventricular hypertrophy and improved left ventricular pump function with mitral valve replacement were due to increased myocyte volume and increased contractile protein content.     

Ventricular interaction and venous capacitance modulate left ventricular preload

The concept of left ventricular (LV) 'preload' has seemed simple and straightforward. Similarly, the capacitance function of the veins seemed to be defined, in spite of the fact that 'venous return' might be said to be increased in heart failure when it was obvious that cardiac output was substantially decreased. In studies during the past several years, we have demonstrated that pericardial pressure, as a major modulator of ventricular interaction, must be accounted for before preload, myocardial compliance or contractility can be assessed reliably. Also, using a new conceptual model based on venous pressure-volume relations that explains how changes in venous capacitance modulate ventricular preload, we have defined the comparative capacitance-conductance effects of various vasodilators in a model of heart failure. We conclude that left ventricular preload is significantly modulated by both changes in ventricular interaction and venous capacitance. To optimize the care of patients with heart disease, it is important to understand both these mechanisms.     

Determinants of myocardial performance after blunt chest trauma

OBJECTIVE: This study investigates whether factors that determine myocardial performance (preload, afterload, heart rate, and contractility) are altered after isolated unilateral pulmonary contusion. METHODS: Catheters were placed in the carotid arteries, left ventricles, and pulmonary arteries of anesthetized, ventilated (FiO2=0.5) pigs (31.2+/-0.6 kg; n=26). A unilateral, blunt injury to the right chest was delivered with a captive bolt gun (n=17) followed by tube thoracostomy. To control for anesthesia and instrumentation at FiO2 of 0.5, one group received tube thoracostomy only (sham injury; n=6). To control for effects of hypoxia without chest injury, an additional sham-injury group (n=3) was ventilated with FiO2 of 0.12. To generate cardiac function (i.e., Starling) curves, lactated Ringer's solution was administered in three bolus infusions at serial time points; the slope of stroke index versus ventricular filling pressure defines cardiac contractility. RESULTS: By 4 hours after pulmonary contusion, pulmonary vascular resistance, airway resistance, and dead space ventilation were increased, whereas PaO2 (72+/-6 mm Hg at FiO2=0.5) and dynamic compliance were decreased (all p < 0.05). Despite profound lung injury, arterial blood pressure, heart rate, cardiac filling pressures, and output remained within the normal range, which is inconsistent with direct myocardial contusion. The slope of pulmonary capillary wedge pressure versus left ventricular end-diastolic pressure (LVEDP) regression was reduced by more than 50% from baseline (p < 0.05), but there was no significant change in the slope of the central venous pressure versus LVEDP regression. By 4 hours after contusion, the slope of the stroke index versus LVEDP curve was reduced by more than 80% from baseline (p < 0.05). By the same time after sham injury with FiO2 of 0.12 (PaO2 < 50 mm Hg), the regression had decayed a similar amount, but there was no change in the slope after sham injury with FiO2 of 0.5 (PaO2 > 200 mm Hg). CONCLUSION: After right-side pulmonary contusion, the most often used estimate of cardiac preload (pulmonary capillary wedge pressure) does not accurately estimate LVEDP, probably because of changes in the pulmonary circulation or mechanics. Central venous pressure is a better estimate of filling pressure, at least in these conditions, probably because it is not directly influenced by the pulmonary dysfunction. Also, ventricular performance can be impaired by depressed myocardial contractility and increased right ventricular afterload even with normal left ventricular afterload and preload. It is thus conceivable that occult myocardial dysfunction after pulmonary contusion could have a role in the progression to cardiorespiratory failure even without direct cardiac contusion.     

Natural plant enzyme inhibitors: Part II-protease inhibitors of seeds

Systolic time intervals (STI) were recorded in 8 healthy male volunteers before, during, and after 30-s exposures to +3 Gz, +5 Gz, and +7 Gz acceleration. Heart rate (HR) increased at all +Gz levels, as did the HR corrected QSIc interval, left ventricular ejection time (LVETc), preejection period (PEPc) and PEP/LVET. These changes in STI were also proportional to the +Gz level. At the higher +Gz levels, PEPc and PEP/LVET continued to increase early in the recovery period, but HR and all STI returned to control after 60 s of recovery. Although physiological variables other than myocardial contractility, such as preload and afterload may influence STI during +Gz the effects of +Gz on stroke volume (SV) and cardiac output (CO) were estimated using previously described relationships between STI and invasively determined indices of cardiovascular function. In general CO increased as SV decreased. During recovery, HR and CO fell and CO remained slightly below control levels, primarily because estimated SV remained low. This study demonstrates the feasibility of using STI to estimate noninvasively the transient changes in cardiovascular function during +Gz acceleration.     

Cora valveless pulsatile rotary pump: new design and control

For decades, research for developing a totally implantable artificial ventricle has been carried on. For 4 to 5 years, two devices have been investigated clinically. For many years, we have studied a rotary (but not centrifugal) pump that furnishes pulsatile flow without a valve and does not need external venting or a compliance chamber. It is a hypocycloidal pump based on the principle of the Maillard-Wankel rotary compressor. Currently made of titanium, it is activated by an electrical brushless direct-current motor. The motor-pump unit is totally sealed and implantable, without noise or vibration. This pump was implanted as a left ventricular assist device in calves. The midterm experiments showed good hemodynamic function. The hemolysis was low, but serious problems were encountered: blood components collecting on the gear mechanism inside the rotor jammed the pump. We therefore redesigned the pump to seal the gear mechanism. We used a double system to seal the open end of the rotor cavity with components polished to superfine optical quality. In addition, we developed a control system based on the study of the predicted shape of the motor current. The new design is now underway. We hope to start chronic experiments again in a few months. If the problem of sealing the bearing could be solved, the Cora ventricle could be used as permanent totally implantable left ventricular assist device.     

Assessment of the role of the renin-angiotensin system in cardiac contractility utilizing the renin inhibitor remikiren

1. The role of the renin-angiotensin system in the regulation of myocardial contractility is still debated. In order to investigate whether renin inhibition affects myocardial contractility and whether this action depends on intracardiac rather than circulating angiotensin II, the regional myocardial effects of systemic (i.v.) and intracoronary (i.c.) infusions of the renin inhibitor remikiren, were compared and related to the effects on systemic haemodynamics and circulating angiotensin II in open-chest anaesthetized pigs (25-30 kg). The specificity of the remikiren-induced effects was tested (1) by studying its i.c. effects after administration of the AT1-receptor antagonist L-158,809 and (2) by measuring its effects on contractile force of porcine isolated cardiac trabeculae. 2. Consecutive 10 min i.v. infusions of remikiren were given at 2, 5, 10 and 20 mg min-1. Mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), systemic vascular resistance (SVR), myocardial oxygen consumption (MVO2) and left ventricular (LV) dP/dtmax were not affected by remikiren at 2 and 5 mg min-1, and were lowered at higher doses. At the highest dose, MAP decreased by 48%, CO by 13%, HR by 14%, SVR by 40%, MVO2 by 28% and LV dp/dtmax by 52% (mean values; P < 0.05 for difference from baseline, n = 5). The decrease in MVO2 was accompanied by a decrease in myocardial work (MAP x CO), but the larger decline in work (55% vs. 28%; P < 0.05) implies a reduced myocardial efficiency ((MAP x CO)/MVO2). 3. Consecutive 10 min i.c. infusions of remikiren were given at 0.2, 0.5, 1, 2, 5 and 10 mg min-1. MAP, CO, MVO2 and LV dP/dtmax were not affected by remikiren at 0.2, 0.5 and 1 mg min-1, and were reduced at higher doses. At the highest dose, MAP decreased by 31%, CO by 26%, MVO2 by 46% and LV dP/dtmax by 43% (mean values; P < 0.05 for difference from baseline, n = 6). HR and SVR did not change at any dose. 4. Thirty minutes after a 10 min i.v. infusion of the AT1 receptor antagonist, L-158,809 at 1 mg min-1, consecutive 10 min i.c. infusions (n = 5) of remikiren at 2, 5 and 10 mg min-1 no longer affected CO and MVO2, and decreased LV dP/dtmax by maximally 27% (P < 0.05) and MAP by 14% (P < 0.05), which was less than without AT1-receptor blockade (P < 0.05). HR and SVR remained unaffected. 5. Plasma renin activity and angiotensin I and II were reduced to levels at or below the detection limit at doses of remikiren that were not high enough to affect systemic haemodynamics or regional myocardial function, both after i.v. and i.c. infusion. 6. Remikiren (10(-10) to 10(-4) M) did not affect contractile force of porcine isolated cardiac trabeculae precontracted with noradrenaline. In trabeculae that were not precontracted no decrease in baseline contractility was observed with remikiren in concentrations up to 10(-5) M, whereas at 10(-4) M baseline contractility decreased by 19% (P < 0.05). 7. Results show that with remikiren i.v., at the doses we used, blood pressure was lowered primarily by vasodilation and with remikiren i.c. by cardiac depression. The blood levels of remikiren required for its vasodilator action are lower than the levels affecting cardiac contractile function. A decrease in circulating angiotensin II does not appear to be the sole explanation for these haemodynamic responses. Data support the contention that myocardial contractility is increased by renin-dependent angiotensin II formation in the heart.     

Left ventricular support with the implantable AB-180 centrifugal pump in sheep with acute myocardial infarction

A small, 257 g centrifugal pump was tested as a left ventricular assist device (LVAD) in sheep given a myocardial infarction. Pump performance, hemolysis, end organ function, weaning, explant procedure, and the incidence of thromboemboli at autopsy were studied over intervals of 1 to 44 days. Twelve sheep were given acute myocardial infarction by ligation of the anterior descending coronary artery and 11 had insertion of the AB-180 Circulatory Support System (CSS). One sheep served as a control for the space occupying effects of the pump in the left chest. Inflow was from the left atrium and outflow was to the descending thoracic aorta. Heparin (57-83 U/ml) in sterile water was infused into the pump at a rate of 10 ml/hr. Pump flows of 1-5.7 L/min were tested. The AB-180 CSS supported 73.5% of the total cardiac output (pump + heart) of 3.89 L/min, with a mean arterial pressure of 86 +/- 7 mmHg at a pump speed of 4,162 +/- 276 rpm immediately after implant. Hemolysis was <10 mg/dl and activated partial thromboplastin time (aPTT) values were in the normal range for sheep (<52 sec) after 48 hr of pumping. Liver enzyme concentrations returned to normal within 2 weeks. There was no evidence of thrombocytopenia. No signs of infection were present during assist and none was found at autopsy. The device was successfully removed three times without the use of pressor agents or blood transfusion. Alarm systems performed appropriately. During the 106 days of cumulative pumping, two sheep showed small (<1.5 cm) renal infarcts. Both were associated with intervals of pump stasis. The AB-180 CSS pump was easily implanted into the left chest without the use of cardiopulmonary bypass. It appears to have a low thromboembolic potential in sheep, without the need for large doses of heparin to elevate aPTT values. This characteristic may ameliorate the excessive bleeding seen clinically with current LVAD systems used for post cardiotomy cardiogenic shock, which require anticoagulation with heparin. The small size and weight of the device permit implantation within the chest and allow chest closure. This may reduce the incidence of infection associated with temporary left ventricular assist and an open sternum.     

Durability testing of components for the Jarvik 2000 completely implantable axial flow left ventricular assist device

A cable-lead tester and real time bearing tester have been developed with provisions to test future implantable electronics, transcutaneous energy transfer system (TETS), and related interconnect cabling designs. The cable/lead tester, used in 1997 to test a previously considered implantable bellows-connector-cabling system, can test up to 10 samples at a time. X-Y-Z-theta motions are applied to the proximal end of the test specimen with its distal end fixed. The real time bearing tester is of a mock loop configuration with the bearings under test housed in a fully functional, Good Manufacturing Practices assembled axial pump. A simulated left ventricular pulsatile preload is applied to the inflow of the axial pump, while its outflow is subjected to an 80 mmHg aortic afterload by pumping into a fixed height tube with no outflow restriction. The heated blood bath saline used in this system is UV sterilized and mechanically filtered by use of a commercial salt water conditioning system attached external to the main preload fluid reservoir. The cable-lead tester and real time bearing tester design include provisions to house a complete Jarvik 2000 left ventricular assist device (Transicoil Medical, Norristown, PA) for in vitro system testing.     

Circulatory support with a left-heart assist device after intracardiac operation: design concepts and management techniques

A simple left-heart assist device was developed to reduce left ventricular preload while simultaneously increasing total systemic blood flow. It consists of special cannulas connected to a simple extracorporeal tubing loop and roller pump, designed to permit bypass of as much as 5 liters of blood per minute from left atrium to ascending aorta. Employed in 15 patients with advanced heart disease who were in low cardiac output following repair, the system was proven effective. An asset of the device is the ability to subsequently separate the patient from the device without need to reenter the thorax or abdomen.     

Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans

This study describes a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic twist in humans and relates this measure to early ventricular filling. LV twist is the counterclockwise rotation of the left ventricle during systole when viewed from the apex. The effect of ventricular twist has been postulated to store potential energy, which ultimately aids in diastolic recoil, leading to ventricular suction. The generated negative early diastolic pressures may augment early ventricular filling. We measured ventricular twist in 40 patients with normal transthoracic echocardiograms. End-systolic twist was determined by measuring rotation of the anterolateral papillary muscle about the center of the ventricle. LV filling was assessed by analysis of transmitral Doppler flow velocities. The mean value obtained was 9 +/- 7 degrees of rotation. Twist measurements were highly reproducible with an intraobserver correlation coefficient of r = 0.881, p <0.001. The magnitude of ventricular twist was strongly correlated positively with acceleration of the mitral E-wave (r = 0.75; p <0.0001) and negatively with the mitral E-wave acceleration time (r = -0.83; p <0.0001).