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J Thorac Cardiovasc Surg 1998;116:1029-1042
© 1998 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

POWER OUTPUT OF PERICARDIUM-LINED SKELETAL MUSCLE VENTRICLES, LEFT VENTRICULAR APEX TO AORTA CONFIGURATION: UP TO EIGHT MONTHS IN CIRCULATION

Supported by National Institutes of Health grant HL34778.

Read at the Seventy-eighth Annual Meeting of The American Association for Thoracic Surgery, Boston, Mass, May 3-6, 1998.

Received for publication May 7, 1998. Revisions requested June 3, 1998; revisions received July 31, 1998. Accepted for publication Aug 5, 1998. Address for reprints: Frank A. Baciewicz, Jr, MD, Suite 2102 Harper Professional Bldg, 3990 John R St, Detroit, MI 48201-2097.

	Abstract

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 
Objective:The purpose of this experiment was to evaluate the potential for a skeletal muscle ventricle connected to the circulation between the left ventricle and the aorta to provide effective, long-term cardiac assist.
Methods: Skeletal muscle ventricles were constructed from the latissimus muscle in 10 dogs. After conditioning, the skeletal muscle ventricles were connected to the left ventricle and the aorta with 2 valved conduits. The skeletal muscle ventricle was programmed to contract during diastole.
Results: At time of implantation, skeletal muscle ventricles stimulated at 33 Hz and in a 1:2 ratio with the heart significantly decreased left ventricular work by 56% (P < .01) and at 50 Hz by 65% (P < .01). At a 1:2 ratio, the power output of the skeletal muscle ventricles was 59% of left ventricular power output at 33 Hz (P < .01) and 93% at 50 Hz (P < .01). Animals survived 7, 11, 16, 17, 72, 99, 115, 214, and 249 days. Three deaths were directly related to the skeletal muscle ventricle. One animal is alive at 228 days. In the animal that survived 249 days, skeletal muscle ventricle power output at 8 months with a 33 Hz stimulation frequency and a 1:2 contraction ratio was 57% of left ventricular power output and 82% at 50 Hz. At a 1:1 ratio, skeletal muscle ventricle power output was 97% and 173% of the left ventricle at 33 and 50 Hz, respectively.
Conclusions: Left ventricular assist with a skeletal muscle ventricle connected between the left ventricle and the aorta is the most hemodynamically effective configuration we have tested and can maintain significant power output up to 8 months.

	Introduction

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 
We have studied thc use of skeletal muscle for cardiac assist by constructing muscular pouches, which we term skeletal muscle ventricles (SMVs). These SMVs have been connected to the circulation in a variety of ways for both left and right heart assist. ^1-3 When they were attached directly to the descending thoracic aorta and stimulated as aortic counterpulsators, we demonstrated that SMVs can pump blood chronically in the circulation, providing effective augmentation of diastolic blood pressure in a manner similar to the intra-aortic balloon pump. ⁴ In 1 animal, an SMV lined with autogenous pericardium functioned continuously for over 4 years in circulation.

In acute studies, the most effective configuration for skeletal muscle hemodynamic assist that we have tested has been an SMV attached from the left ventricular (LV) apex to the aorta. ⁵ In a recent study ⁶ with this configuration, the longest survival we obtained was 11 weeks in 1 animal, with the others surviving only 10 to 14 days. Because the addition of a pericardial lining to the inner layer of the SMV was important in establishing the aortic counterpulsator model as a reproducible chronic model, the SMVs in our study were lined with autogenous pericardium. The purpose of this study was to develop pericardium-lined SMVs in a LV apex–to–aorta configuration as a chronic model for cardiac assist and to document hemodynamic performance over time.

	Materials and methods

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 
SMV construction and conditioning
Pericardium-lined SMVs were constructed in 10 mongrel dogs, weighing between 16 and 22 kg, by a technique that has previously been described.⁷ All animals underwent operation in accordance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

In brief, after induction of inhalational anesthesia, the pericardium was harvested from between the phrenic nerves through a right thoracotomy incision. At this time, a transit-time ultrasonic flow probe (A-Series; Transonic Systems, Inc, Ithaca, NY) was placed around the ascending aorta to measure blood flow at that point. The connecting portion of the probe was tunnelled to the mid-dorsal subcutaneous tissue. Next, the left latissimus dorsi muscle was mobilized from the chest wall through a separate flank incision, leaving its humeral insertion intact. A bipolar nerve lead (Medtronic, Inc, Minneapolis, Minn) was placed around the thoracodorsal nerve. The lead was connected to a neurostimulator (Itrel model 7421; Medtronic, Inc), which was placed in the left rectus sheath. The autogenous, fresh pericardium was wrapped around a cylindrical polypropylene mandrel (diameter 3.4 cm, volume 2.5 mL/kg) and secured at the base with 5-0 polypropylene suture to a ring of Dacron felt (USCI, Billerica, Mass). The latissimus muscle was then wrapped circumferentially around the pericardium-lined mandrel from 1.5 to 2 times. The muscle was secured to the sewing ring with polypropylene sutures, and the SMV layers were tacked together with superficially placed polyglactin acid sutures. The wounds were closed in layers with absorbable polyglactin acid sutures.

All animals underwent a 3-week period of vascular delay from the time of SMV construction before conditioning. The neurostimulator was then activated to deliver a 2-Hz single pulse of 1- to 1.5-volt amplitude and 210-µs duration for a period of 6 weeks. This has been shown to induce transformation of the muscle fiber histologic condition from fast-twitch, fatiguable to slow-twitch, fatigue-resistant fibers. ⁸

Connection to the circulation
The configuration of the SMV in relation to its connection to the circulation and the sites of pressure and flow sensors are depicted in Fig. 1. After the conditioning process was complete, the dogs were reanesthetized and the SMV mandrel was removed. The left side of the chest was entered through the fourth intercostal space. A specially constructed valved conduit consisting of a combination of a ringed polytetrafluoroethylene graft^* (12 mm) with an interposed porcine valved Dacron conduit (12 mm, Hancock; Medtronic, Inc) was anastomosed end to side to the descending thoracic aorta. The proximal portion of this conduit was connected to a base-cap of polytetrafluoroethylene cardiovascular patch, which was anastomosed to the SMV. A 10-mm ventriculotome was then used to excise a cylindrical portion of the LV apex. A second specially constructed 12-mm valved conduit, also connected to the SMV base cap, was then anastomosed without cardiopulmonary bypass to the ventricular apex with a right-angled plastic connector (Medtronic, Inc). The connector was secured to the ventricular apex with interrupted, 2-0 pledget-supported polyester sutures. An epicardial sensing electrode (model 6917; Medtronic, Inc) was attached on the left ventricle. The grafts were de-aired, and the nerve stimulator was replaced with a synchronized pulse-train cardiomyostimulator (SP1005; Medtronic, Inc). The stimulator was programmed to deliver a 33-Hz burst train stimulus (each pulse of 210 µs duration), with a delay of 225 to 250 ms from the R wave and a burst train duration of 240 ms. The descending thoracic aorta just distal to the left subclavian artery, but proximal to the aortic anastomosis, was then narrowed approximately 50% with umbilical tape to increase passive flow from the left ventricle through the SMV circuit during cardiac systole. After partial aortic ligation, total cardiac output and LV pressure remained the same; but passive flow through the SMV, which had been minimal, increased to 15% to 35% of the total systemic output.

View larger version (40K): [in this window] [in a new window]   Fig. 1 SMV is connected to the circulation between the LV apex and descending aorta with 2 valved conduits. A constriction was created proximal to the SMV-aortic anastomosis. Pressure was monitored in the left ventricle, SMV, and femoral and carotid arteries. Flow was measured at the aortic root and in the SMV efferent conduit.

Hemodynamic measurements
Initial hemodynamic measurements were made after the SMV was connected to the circulation. In addition to the aortic flow probe that was placed at the time of SMV construction, a second ultrasonic flow probe was placed around the efferent conduit from the SMV. Polyurethane catheters (2.5F) were inserted into the left ventricle, the SMV, and the carotid artery and connected to implantable subcutaneous ports (Vascular-Access Ports; Vascular Access Technologies, Skokie, Ill). They were used for pressure monitoring with fluid-filled tubing connected to transducers. A temporary cannula for pressure monitoring was placed in the femoral artery. Measurements were made not only with the stimulator OFF and ON at the chronic setting of 33 Hz, mode 2, but also at 33-Hz and 50-Hz burst stimulation with the cardiomyostimulator set at both mode 1 (heart rate to SMV ratio l:l when heart rate is less than 120 beats/min; 1:2 when greater than 120 beats/min) and mode 2 (ratio 1:2, heart rate less than 120 beats/min; 1:3 when greater than 120 beats/min). The varying burst frequencies and contraction ratios were tested to show the potential for skeletal muscle to provide increased assistance at these more intense stimulation parameters. Data were collected as hardcopy on a Gould ES 1000B recording and display system (Gould Instruments Systems, Valleyview, Ohio) and digitally on a computer utilizing a data acquisition and analysis program (Windaq; Dataq Instruments, Akron, Ohio). The sampling rate was 400 Hz. The incision was then closed in layers, and the flow probes and 3 pressure monitoring ports were left near the mid-dorsal area of the animals' subcutaneous tissue. The cardiomyostimulator was placed beneath the rectus sheath. The stimulator was set chronically to contract in mode 2, with a 225- to 250-ms delay and 240-ms duration at 33-Hz burst frequency.

Chronic hemodynamic measurements
The animals were allowed to recover after the SMVs were placed in circulation. The pressure monitoring ports were flushed 2 to 3 times weekly to maintain patency with a 500-unit/mL concentration of sodium heparin. Hemodynamic measurements on each animal were then performed at 1 and 2 weeks and 1, 2, and 3 months and roughly every 2 to 3 months thereafter, unless a change in the animal's condition occurred. During a subsequent pressure recording at 2 to 3 months in 4 of the animals, a continuous infusion of intravenous propranolol was given at 1 mg/kg per minute for 1 hour after a 10-mg/kg bolus dose to induce a low cardiac output state, defined as a decrease in aortic blood flow of 50% from control. In 1 dog the infusion was discontinued because of a sudden, precipitous fall in blood pressure. In the remaining 3 dogs, data under low output conditions were recorded after 1 hour of continuous propranolol infusion.

Data analysis
Hemodynamic recordings were analyzed on a computer using the data acquisition and analysis program (Windaq; Dataq Instruments, Inc). Data were analyzed for each setting for a minimum of 10 SMV beats (total heartbeats 10 to 30, depending on contraction ratio).

Stroke volumes for both the SMV and the left ventricle were determined by integrating the area underneath the SMV and aortic flow traces. SMV stroke volume was defined as the stroke volume only during SMV ejection (Fig. 2B). To calculate the work done by the left ventricle pumping blood through the SMV circuit versus work done by the SMV itself, the flow through the SMV when the SMV was contracting was divided into active and passive components. Passive SMV flow was defined as all the flow through the SMV during the cardiac cycle except for SMV ejection. This definition of passive SMV flow assumes that passive flow is independent of SMV relaxation and likely underestimates the contribution that SMV relaxation adds to the flow through SMV circuit and ascribes it to the left ventricle instead. LV stroke volume was defined as the sum of flow across the aortic valve plus passive SMV flow for a cardiac cycle.

View larger version (81K): [in this window] [in a new window]   Fig. 2A. Pressure recordings made at the time of connection of the SMV to the systemic circulation. Transition from the control state with the SMV OFF to stimulation at 33 Hz, 1:2, can be seen, with corresponding changes in the flow and pressure tracings.

View larger version (91K): [in this window] [in a new window]   Fig. 2B. The SMV is seen contracting at 33 Hz at a 1:2 ratio (the chronic stimulation setting) with the heart; shaded areas in the SMV flow trace indicate SMV stroke volume.

View larger version (79K): [in this window] [in a new window]   Fig. 2C. Pressure recording made after 248 days of pumping blood continuously in the circulation. The SMV is shown contracting at 50 Hz, 1:1 ratio.

	Results

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 
Initial hemodynamic data
Data obtained at time of connection of the SMV to the circulation are presented in Tables I and II. The decrease in LV end-diastolic pressure with the pacemaker ON versus OFF, although statistically significant, was only 0.7 mm Hg at 33 Hz and 1.2 mm Hg at 50 Hz. At the chronic stimulation frequency of 33 Hz, 1:2 contraction ratio with the heart, LV peak systolic pressure decreased in the beat following SMV contraction by 19% at 33 Hz and by 22% at 50 Hz. Diastolic blood pressure measured in the SMV during SMV contraction was augmented 36% when compared with the mean diastolic blood pressure with the SMV OFF. At 50 Hz burst frequency, 1:2 ratio, the diastolic augmentation was 50%. During SMV relaxation, the diastolic pressure in the SMV decreased by 60% when compared with the diastolic pressure on unstimulated beats.

The initial hemodynamic data also showed significant reductions in the LV tension time index and LV stroke work (LVSW) and minute work (LVMW) during SMV contractions. The LV tension time index decreased by 29% at 33 Hz and 39% at 50 Hz. At 33 Hz, LVSW decreased by 56% when compared with the LVSW with the cardiomyostimulator OFF. LVSW was decreased by 65% when the SMV was stimulated at 50 Hz. LV power output (LVMW) was decreased by 55% at 33 Hz and 64% at 50 Hz. The SMV itself, when stimulated at 33 Hz, was capable of 51% of the stroke work of the native left ventricle alone with the SMV OFF and 95% of native (unassisted) LVSW at 50-Hz burst stimulation. When SMV stroke work (SMV SW) was compared with the assisted LVSW, SMV SW exceeded that of the assisted left ventricle: at 33 Hz, SMV SW was 115% of LVSW and 271% of LVSW at 50 Hz. At the chronic stimulation setting of 33 HZ and a 1:2 ratio, SMV power output (SMVMW) was 26% of thc native left ventricle and 59% of the assisted LVMW. At the higher burst stimulation frequency of 50 Hz, the SMV power output was 49% of the native LV power output and 136% of the assisted power output of the left ventricle.

Chronic SMV function
The SMVs were assessed over time. Fig 3 depicts both the active flow through the SMV circuit (total flow through SMV during stimulation) and the passive flow (total flow with SMV OFF) through the SMV for the 6 animals that survived 1 month and beyond, for the duration of the experiment. The data on the additional 4 dogs were similar; they were excluded only for clarity of the illustration. There is an initial drop in SMV performance, as measured by SMV flow, that is seen in the 1-week measurement after the initial connection to the circulation. However, during subsequent measurements, the flow through the SMV approaches the value obtained at the time of connection to the circulation. Once returning towards baseline, the function of the SMVs remained relatively stable over time in most dogs.

View larger version (21K): [in this window] [in a new window]   Fig. 3 Blood flow through the SMV circuit at 33 Hz, 1:2 (combined SMV stroke volume plus passive stroke volume), versus passive flow with the SMV OFF for each of the 6 dogs that survived more than 1 month is shown for the duration of the experiment. SMV blood flow is expressed as percent of total systemic blood flow.

View larger version (45K): [in this window] [in a new window]   Fig. 4 SMV blood flow, expressed as percentage of total systemic flow, at varying burst frequencies and contraction ratios before induction of heart failure with propranolol (control; solid bars) and after inducing failure with propranolol (heart failure; shaded bars).

View larger version (84K): [in this window] [in a new window]   Fig. 5 Pressure tracings taken from 1 animal at the time of a low-output study after 78 days in circulation. The pressure recording after 1 hour of continuous low cardiac output was induced by propranolol infusion. The transition from temporarily inhibiting the SMV "OFF" to contraction at 33 Hz, 1:1, is shown. At this setting, almost the entire total systemic output is flowing through the SMV.

View larger version (19K): [in this window] [in a new window]   Fig. 6 Flow measured through the SMV and ascending aorta in 1 animal at several points over time. A, A depiction of the flow with the SMV OFF. There is minimal passive flow through the SMV. B, A depiction of the flow with the SMV contracting at 33 Hz, 1:2. From 78 days in circulation onward, the SMV flow is equal to the flow across the aortic valve. Total blood flow, sum of aortic flow and SMV flow.

View larger version (17K): [in this window] [in a new window]   Fig. 7 Stroke work in the SMV, the native left ventricle (with the SMV OFF), and the left ventricle during SMV contraction at 33 Hz, 1:2 (A) and 50 Hz, l:2 (B), measured in 1 animal over time. At 33 Hz, SMV SW was equivalent to that of the native left ventricle. At 50 Hz, SMV SW generally exceed that of the native left ventricle.

View larger version (25K): [in this window] [in a new window]   Fig. 8 Power output of SMV, native left ventricle (with SMV OFF) and left ventricle during SMV assist at 4 combinations of burst frequency and contraction ratio for 1 animal over time. A, At a 1:2 ratio, SMV power output remained relatively stable. B, Power output at the 1:1 ratio was available for only the initial and 2 latest measurements.

	Discussion

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

In previous acute studies of SMVs, power output, when measured with a mock circulation device, was intermediate between the stroke work of the right and left ventricles. ⁹ In these previous studies, power output of the SMVs was equivalent to that of the right ventricle because of the slower SMV contraction rate but did not approach that of the left ventricle. In the present study, the SMVs were able to generate stroke work varying from approximately one half that of the unassisted left ventricle at a 33-Hz burst frequency stimulation and a 1:2 contraction ratio, to nearly equal to the unassisted LV at 50 Hz, 1:2. While pumping at only one half the rate of the heart rate, the power output of the SMVs was 36% and 45% of unassisted LVMW at 33 and 50 Hz. Power output of the SMVs stimulated at a 1:2 contraction ratio with the heart was maintained over time.

Because the SMVs were preloaded by LV contraction, our use of mean SMV pressure during ejection to determine SMV SW without taking LV preloading into consideration would likely overestimate SMV SW and thereby SMV power output. At the same time, an assumption that SMV relaxation plays no role in determining preload and passive flow through the SMV during assist may have underestimated SMV stroke volume and thereby underestimated SMV SW and power output. Clearly, further studies are needed to determine "true" stroke work of the SMV; a conductance catheter and other methods to derive pressure-volume loops from the SMV will help us more accurately determine stroke work and power output.

Some earlier studies on the feasibility of skeletal muscle for cardiac assist used a left ventricle–to–aorta model. Stevens and colleagues ^10,11 performed acute studies with an unconditioned rectus muscle and demonstrated, before muscle fatigue occurred, skeletal-muscle assist increased total cardiac output during b-blockade–induced heart failure. Brister and coworkers, ¹² in an acute study, used a similar model, but with a single valve in the afferent position. The LV apex–to–aorta connection has been evaluated in a computer model by Platt and colleagues, ¹³ who determined it to be the most efficient form of ventricular assist.

In our previous attempts to establish the LV apex–to–aorta configuration as a chronic model, we initially had early thrombosis of the SMV circuit. ¹⁴ In this previous study, flow through the SMV was dependent on SMV contraction; with chronic stimulation at a 1:2 ratio with the heart, stagnation of blood flow inside the SMV secondary to the lower contraction rate may have encouraged thrombus formation. To promote continuous passive flow through the SMV, a constriction of the aorta proximal to the SMV-aortic anastomosis was created. ⁶ One dog in this previous series survived 76 days, being killed at that time because of an infected indwelling flow probe. The remaining 4 dogs lived only up to 2 weeks, dying of rupture of the SMV or the aortic anastomosis and erosion of a flow probe into the great vessels. We were previously able to develop a chronic model of SMV aortic counterpulsation with pericardium-lined SMVs; pericardium-lined SMVs did not rupture and appeared to exhibit thromboresistance. ⁷ Therefore the present study incorporated the use of autogenous pericardium to line the SMVs and the presence of an aortic constriction to create passive SMV flow.

We have used a propranolol infusion to simulate low cardiac output in a previous study. ⁷ In the previous study, during profound low cardiac output, SMV function, measured as percent augmentation of diastolic blood pressure, improved under heart failure conditions when compared with control. The propranolol infusion did not seem to significantly affect SMV performance. Because of our past experience with this model of heart failure, we used propranolol to simulate severe cardiac dysfunction. In our past experience with this heart failure model, animals that underwent a propranolol study at 2 weeks after the SMV was placed in circulation experienced a high mortality. ⁷In fact, in this current study, 1 animal's infusion had to be terminated because of severe hypotension. For this study, only animals that survived up to 3 months received a propranolol infusion. Unfortunately, not all of the animals that survived this long were measured during propranolol-induced failure. There was a trend toward improvement of blood flow through the SMV compared to total systemic flow for 50 Hz, 1:2, and both 33 and 50 Hz at a 1:1 ratio. There was also an increase in the amount of total systemic flow when compared between the SMV ON at a 1:1 ratio and the SMV OFF. It is likely that these trends did not achieve statistical significance because of the small number of animals that underwent a propranolol study. Future studies must further define the potential for SMVs to provide assistance to a failing ventricle using this or other models of heart failure.

When examining the data over time, we noted decreases in SMV performance during the first 2 weeks after placement of the SMV into circulation. We have noted similar decreases empirically in other studies. Although electrical stimulation at 2 Hz has been shown to change the fiber type, it is possible that the muscle may not be fully adapted to perform chronically under loaded conditions. However, after this 2-week period, SMV flow returned toward baseline and remained stable thereafter in most dogs.

The aortic constriction was performed with the SMV pumping at the chronic stimulation parameters of 33 Hz, 1:2 ratio. The constrictions were adjusted to cause one third to one half of the total systemic flow to go through the SMV when the cardiomyostimulator was programmed at the chronic settings. Because there are 2 potential outflow tracts from the left ventricle in this model, the aortic constriction does not appreciably increase afterload when compared with the normal heart with a single LV outflow tract through the aortic valve. The aortic constriction merely redistributes a portion of blood through the alternative outflow tract to help prevent SMV thrombus formation. In reviewing the resulting passive SMV flow over time in circulation for each animal plus each animal's fate, no obvious correlation was found between absolute amount of passive flow or percent passive flow of total systemic flow and number of days in circulation with the presence or absence of clot in the SMV. Further experiments may help to determine what degree of aortic constriction, if any, is necessary for this model. Additionally, it is unknown when performed on an animal with a failing heart, whether similar aortic constrictions will result in a decreased incidence of SMV thrombi.

This study demonstrates conclusively that SMVs in an LV apex–to–aorta configuration can effectively and efficiently provide chronic cardiac assistance for up to 8 months in the circulation. Before SMVs in an LV apex–to–aorta configuration can be considered for clinical trials, further refinement is necessary to eliminate the significant attrition that occurred during this study. SMVs will also need to be tested in a chronic heart failure model. Once a reliable, low mortality model has been achieved, clinical evaluation should proceed.

	Appendix: Discussion

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 
Dr Juan C. Chachques (Paris, France). I saw in your pictures that you are still using direct nerve pacing. Do you have any problems with direct nerve stimulation? We use intramuscular electrodes because we believe that direct nerve stimulation can induce fibrosis and nerve injury.

Do you have a histologic control of the pericardium that you use inside this SMV, and what is the adaptation of the pericardium to this new function? Is this pericardium fresh or treated with glutaraldehyde?

Do you plan to use this configuration for the right heart? Perhaps for the first clinical use it would be interesting to test your SMVs for right ventricular support.

Dr Baciewicz. First, regarding muscle stimulation as compared with nerve stimulation, we have always used the nerve stimulation to stimulate the latissimus dorsi and have not had a problem. I really do not have any experience with a myostimulator.

Second, in terms of how we treat the pericardium, we simply harvest it from phrenic nerve to phrenic nerve, place it in saline solution, and then place it around the mandrel. We do not have any special treatment for it.

Third, at this point we have not used this particular model in a right ventricle situation.

Mr John H. Kennedy (Cambridge, England). I compliment you on your determination in carrying along with what is basically often a fraught project. What was the effect on baroreceptor activity in the presence of a 50% constriction of the proximal thoracic aorta? Normally in a waveform, one would see that in an elevation of diastole, which we were not privileged to see in your slides, and, of course, that would be dependent on the synchrony in terms of radians of the pump versus the natural heart.

Dr Baciewicz. I did not have room on the slides to show you the carotid flow tracing, but essentially it is no different from the femoral tracing.

Mr John R. Pepper (London, England). Do you have any evidence of thromboembolism inside the SMV? Did you do autopsies on the animals and look particularly at the kidneys?

Dr Baciewicz. In fact, there were several sudden deaths within 1 month in the study; but essentially in all the animals that survived long term, our problem was peripheral emboli. Two of the animals died of iliac emboli and 1 of renal failure from renal emboli. However, on all the autopsies, we did not notice any clot or thrombus in the SMV itself. Of course, there are a lot of places in this model where thrombus could develop: we have indwelling SMV catheters; there is a relative constriction in the thoracic aorta, and the animals were given only 85 mg of aspirin per day. But that has been our downfall in terms of keeping the animal alive long term.

Dr Thierry G. Mesana (Marseille, France). It is fascinating to see a real biologic implantable device. But to be biologic means to have less thromboemboli. Do you think that your valves inside your ventricle are really necessary to assist the heart? What is the role of these valves in the thromboemboli that you saw?

Dr Baciewicz. We do think the valves are necessary. We did have earlier models where the valve conduits that we used had been sort of discards or had been on the shelf for multiple years; there was a number of emboli and thrombi on some of these valved conduits. We are now having the conduits made specifically for us; we have not noted a problem with this.

	Acknowledgments

 
We thank Elaine Hockman, PhD, for her assistance with statistical analysis, and Janet Schofding, LVT, Lee Andrus, LVT, Cynthia Cameron, LVT, and Elizabeth Dawe, DVM, for their care of the animals used in this experiment.

	Footnotes

 
*Gore-Tex graft, registered trade name of WL Gore & Associates, Inc, Flagstaff, Ariz.

	References

Top Abstract Introduction Materials and methods Results Discussion Appendix: Discussion References

 

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3. Hooper TL, Niinami H, Hammond RL, et al. Skeletal muscle ventricles as left atrial–aortic pumps: short-term studies. Ann Thorac Surg 1992;54:316-22. [Abstract]
   
4. Thomas GA, Isoda S, Hammond RL, et al. Pericardium-lined skeletal muscle ventricles: up to two years' in-circulation experience. Ann Thorac Surg 1996;62:1698-707. [Abstract/Free Full Text]
   
5. Lu H, Fietsam R Jr, Hammond RL, et al. Skeletal muscle ventricles, configuration left ventricular apex to aorta: acute in circulation studies. Ann Thorac Surg 1993;55:78-85. [Abstract]
   
6. Greer KA, Lu H, Spanta AD, Hammond RL, Stephenson LW. Skeletal muscle ventricles, left ventricular apex–to–aorta configuration: 1 to 11 weeks in circulation. Circulation 1997;95:497-502. [Abstract/Free Full Text]
   
7. Thomas GA, Lu H, Isoda S, et al. Pericardium-lined skeletal muscle ventricles in circulation up to 589 days. Ann Thorac Surg 1994;58:978-88. [Abstract]
   
8. Mannion JD, Bitto T, Hammond RL, Rubinstein N, Stephenson LW. Histochemical and fatigue characteristics of conditioned latissimus dorsi muscle. Circ Res 1986;58:298-304. [Abstract/Free Full Text]
   
9. Mannion JD, Acker MA, Hammond RL, Faltemeyer W, Duckett S, Stephenson LW. Power output of skeletal muscle ventricles in circulation: short-term studies. Circulation 1987;76:155-62. [Abstract/Free Full Text]
   
10. Stevens L, Brown J. Can noncardiac muscle provide useful cardiac assistance? Am Surg 1986;52:423-7. [Medline]
    
11. Stevens L, Badylak SF, Janas W, Gray MH, Geddes LA, Voorhees WD III. A skeletal muscle ventricle made from rectus abdominis muscle in the dog. J Surg Res 1989;46:84-9. [Medline]
    
12. Brister SJ, Fradet G, Dewar M, Wittnich C, Lough J, Chiu R. Transforming skeletal muscle ventricle made from the rectus abdominis muscle for myocardial assist: a feasibility study. Can J Surg 1985;4:341-4.
    
13. Platt KL, Moore TW, Barnea O. Performance optimization of left ventricular assistance: a computer model study. ASAIO J 1993;39:29-38. [Medline]
    
14. Lu H, Thomas GA, Hammond RL, et al. Intrathoracic and extrathoracic skeletal muscle ventricles in circulation: left ventricular apex to aorta configuration. J Card Surg 1994;9:332-42. [Medline]
    

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