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Ann Thorac Surg 1999;68:688-694
© 1999 The Society of Thoracic Surgeons
a Department of Surgery, Columbia Presbyterian Medical Center, New York, New York, USA
b Division of Circulatory Physiology, Columbia Presbyterian Medical Center, New York, New York, USA
Address reprint requests to Dr Sun, Division of Cardiothoracic Surgery, The Milton S. Hershey Medical Center, Hershey, PA 17033;
e-mail: bcsun{at}psghs.edu
Presented at the Fourth International Conference on Circulatory Support Devices for Severe Cardiac Failure, Houston, TX, Oct 35, 1997.
Abstract
Background. The use of left ventricular assist devices (LVADs) as bridge to transplantation is now accepted as a standard of care for a subset of end-stage heart failure patients. Our interim experience with both pneumatically and electrically powered ThermoCardiosystems LVADs is presented to outline the benefits and limitations of device support as well as discuss its potential role as bridge to recovery and as destination therapy.
Methods and Results. Detailed records were kept prospectively for all patients undergoing LVAD insertion. One hundred LVADs were inserted over 7 years into 95 patients, with an overall survival rate of 75% and a transplantation rate of 70%. Four patients underwent device explant for recovered myocardial function. Three patients received LVADs as destination therapy in the ongoing REMATCH (Randomized Evaluation of Mechanical Assist Treatment for Congestive Heart failure) trial. Overall mean patient age was 51 years, and mean duration of support was 108 days. There were 25 device-related infections including the drive line, device pocket, and blood-contacting surfaces. Cerebral vascular accidents and other embolic events occurred in 7 patients with six deaths. There were four device malfunctions and nine graft-related hemorrhages, resulting in six reoperations and three deaths.
Conclusions. The use of long-term implantable LVADs will likely not be limited to bridge to transplantation. The REMATCH trial has commenced to study the role LVADs may have as an alternative to medical management. Furthermore, as the issues of myocardial recovery are examined, the "bridge to recovery" may be an important additional role for these assist devices.
Long-term implantable left ventricular assist devices (LVAD) are currently in use throughout the world with increasing frequency. The current accepted role for these devices is as a bridge to transplantation; however, as experience is gained with use of these devices, other applications may be feasible and desirable. Congestive heart failure (CHF) is a nationwide epidemic with a prevalence of 3 million victims [1] and more than 400,000 new cases per year [2]. Severe heart failure unresponsive to even maximal medical therapy occurs in approximately 60,000 patients per year [3]. Cardiac transplantation as treatment for CHF has been successful, with a 5-year survival in these patients of 60% [4], compared with 20%30% 2-year survival in patients with New York Heart Association (NYHA) class 4 heart failure [1, 5, 6]. However, because of a limited donor organ supply, cardiac transplantation will only treat 2300 patients in the U.S. this year [8]. Approximately 30,000 patients are listed worldwide for cardiac transplantation every year, and only around 3,800 cardiac transplantations are performed [9]. These numbers have not changed since 1989, though older and more "marginal" donors are being accepted [8, 9]. Unless societys perceptions towards organ donation radically change, cardiac transplantation will remain an epidemiologic triviality.
Assist devices used as a bridge to transplantation currently exacerbate this discrepancy, as the destination is still transplantation. Therapies need to be developed not only to prolong life but also to provide quality life, so the paradigm shift can occur and these alternative therapies become destinations. Cardiac assist devices, total artificial hearts, newer pharmacologic therapies, xenotransplantation, ventricular remodeling surgery, and others will likely play important complimentary roles in the future treatment of CHF. Our experience with 100 implants, encompassing both pneumatically and electrically powered ThermoCardiosystems LVADs, is presented to outline the benefits and limitations of device support as potential destination therapy, as well as discuss management strategies for these patients.
Material and methods
Device
The TCI Heartmate (ThermoCardiosystems Inc, Woburn, MA), a single pusher-plate device with a maximum stroke volume of 85 cc, can be either pneumatically or electrically actuated and weighs approximately 1 kg. The sintered titanium microspheres on the pump housing and the integrally textured polyurethane on the flexing pusher-plate diaphragm allow formation of a tenacious thrombus that evolves into a stable pseudointimal layer that does not embolize; this reduces the need for systemic anticoagulation [10]. Food and Drug Administration (FDA) approval for the pneumatic version was obtained in November 1994. The electric version received FDA approval in October 1998 [11]. The device is implanted through a median sternotomy with an inflow cannula inserted into the ventricular apex and a woven Dacron outflow graft anastomosed to the ascending aorta. We place the pumping chamber in a preperitoneal position in the left upper quadrant, although other centers advocate intraperitoneal placement. The drive line for the pneumatic device exits through the left lower quadrant.
Drive line exit sites for the vented and electrically powered (VE) device varied through the evolving design changes. The first VE device had two small drive lines, (one for the electrical connections, and one for the air vent), which were tunneled out the left flank. Subsequently, a single drive line device was developed with both components integrated, and facilitated a left lower quadrant exit site. The current VE device allows for a longer subcutaneous tunnel and is now exited in the right lower quadrant.
Patient selection
As in many other treatment modalities, success with LVAD placement hinges on correct patient selection. These devices have often been used in patients as attempted salvage, with predictably poor results. We have developed a screening scale that, employing a scoring system based on criteria obtainable at the time of initial evaluation, is both predictive of successful early outcome and is easy to apply. Oliguria, requirement for ventilatory support, and hepatic dysfunction resulting in coagulopathy are clear endpoints reflecting major end-organ injury and are assigned risk factor scores accordingly. Reoperation and right heart failure present technical limitations during device insertion, and are also assigned risk points.
In our experience, this practical screening scale accurately predicted patients unlikely to survive device insertion and in whom intervention would likely be futile [12]. It is important to emphasize that the physicians at our facility use the scale to guide discussions about the suitability of individual patients, but not as an absolute nor static criterion for device insertion. A previously unsuitable patient may become a suitable implant candidate with adjustments in their management. Most of the later patients in our series (and particularly the survivors) scored less than 5 points on the screening scale.
Implantation technique
An incision from the sternal notch to the umbilicus is made, and sternotomy and pericardial well are created. Before heparinization, a plane is developed in the preperitoneal plane by dividing the linea alba and separating preperitoneal fat and peritoneum from the posterior rectus sheath and the transversalis muscle at its diaphragmatic insertion [13]. Drive lines are tunneled to an exit point appropriate for the type and generation of the device, and the device is brought onto the field. After heparinization, the aorta and right atrium are cannulated, and cardiopulmonary bypass is instituted. We have used the serine protease inhibitor Aprotinin (Miles Incorporated, West Haven, CT) in almost all cases to reduce bleeding and the consequent incidence of transfusion-related right-sided failure [14]. In cases of recent aprotinin therapy, readministration is delayed until arterial access is established to avoid the sequelae of anaphylaxis. Aprotinin is used at one-half Hammarsmith dose during both implant as well as explant/transplantation. A vent is placed through the apex of the left ventricle and, without placing a cross-clamp or administering cardioplegia, device implantation is initiated. The inflow cannula is brought through the diaphragm and secured to a Teflon cuff that has been attached to the ventricular apex with a series of horizontal mattress, Teflon-pledgeted Dacron sutures. The outflow graft is anastomosed to the right lateral aspect of the ascending aorta using a running 4-0 polypropylene suture buttressed with autologous pericardium. As the patient is separated from cardiopulmonary bypass, the device is activated with the patient in a steep Trendelenburg position to reduce the risk of cranial air embolism.
Transesophageal echocardiography is used in all cases to assess for air, to demonstrate adequate inflow attachment and left ventricular decompression, and to identify any anomalous intracardiac connections. A clinically quiescent patent foramen ovale will manifest with desaturation and a large right to left shunt when the left heart becomes unloaded with the LVAD.
Standard sternal closures are used before standard abdominal closures. Gore-Tex patch closure of the abdominal fascia is used in the thin patient to ensure a tension-free closure.
Blood products, if required, are administered through leukocyte filters to reduce antigen exposure of the patient that could complicate later donor organ cross-matching [15]. Inhaled nitric oxide (iNO) is now routinely used to reduce pulmonary hypertension, associated with chronic left ventricular failure that is exacerbated by cardiopulmonary bypass-related generation of thromboxane A2 [16] and transfusion-induced cytokine activation [17]. The ABIOMED BVS 5000 (ABIOMED, Danvers, MA) was used for right ventricular assist in the early postoperative period for patients with severe right-sided circulatory dysfunction [18]. Arginine vasopressin in low doses (0.04 U/min) has been useful in patients with catecholamine-resistant vasodilatory hypotension.
Patients with VE devices were discharged home after extensive rehabilitation and a mandatory (FDA) 30-day postimplant hospital stay. They were followed with weekly outpatient visits. (Patients with pneumatic devices are currently not eligible for home discharge.) Twenty-four-hour access to members of the LVAD team was implemented, and patients carried pagers for notification of impending transplantation.
At explantation, the device pocket is first entered before sternotomy to reassess the position of the outflow graft. The outflow graft is followed to the aorta, which is exposed for cannulation. In emergency situations, the graft itself is easily cannulated for arterial access. The outflow graft is retracted medially and the fibrous rind opened posteriorly to expose the superior vena cava (SVC). Standard bicaval cannulation is performed. The device must be turned off before institution of cardiopulmonary bypass to minimize the risk of air embolism. The device is explanted while awaiting arrival of the donor team or after implant of the new heart. At completion of transplantation, the preperitoneal pocket is drained and closed primarily. The drive line exit site is allowed to close secondarily and is not closed.
Device changes performed for malfunctions included only removal of the device itself through a full sternotomy and cardiopulmonary bypass. The inflow cuff and outflow grafts were not replaced. Device changes for infection involved removal of all foreign material including the inflow cuff, ventricular pledgets, as well as the outflow graft to the aorta. Aprotinin was used for all device changes.
Data collection and analysis
Detailed records were kept prospectively for all patients undergoing LVAD insertion. For purposes of data analysis, a variety of end points were followed. LVAD survival was defined as survival during LVAD support; complications and deaths occurring after transplantation were not included in LVAD morbidity and mortality calculations. Thromboembolic events were defined as clinically verifiable cases of thromboembolism to the coronary, cerebral, or peripheral arterial systems. Right ventricular failure (RVF) was defined as indexed LVAD output below 1.8 L/min/m2 in the setting of elevated central venous pressure (> 20 mm Hg) and a decompressed left ventricle. In addition, patients requiring inotropic support for impaired right ventricular function for greater than 2 weeks were included in the postoperative RVF group.
Results
One hundred TCI Heartmate LVADs were implanted into 95 patients from August 1990 through May 1997: 53 pneumatic devices into 52 patients (one device change), 19 double-lead vented electric devices into 17 patients (two device changes), and 28 single-lead vented electric devices into 26 patients (two device changes) (Table 1).
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Of the 4 patients currently supported, 2 await transplantation and 2 are participants in the device arm of the REMATCH trial (Table 2).
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Fifty portable controllers were changed in the dual-lead system during 2,772 support days, and 30 controllers in the single-lead system during 2,511 support days. The fact that a controller was changed, because of alarming, did not necessarily foreordain a malfunction in the device or in the controller; occasionally, it was an indicator of a physiologic problem that would be subsequently corrected when the physiologic problem was addressed.
Four pump malfunctions occurred, requiring device change or readmission to the hospital. One pneumatic driveline rupture resulted in death. Three malfunctions occurred in patients with dual-lead vented electric devices. Two patients underwent device changes, and all were successfully bridged to transplantation.
One patient had a diaphragmatic separation from the motor and was temporarily supported pneumatically until device change. Two patients had premature bearing wear, both manifesting in increased voltage draw and accelerated battery depletion. Low-level controller alarming preceded identification of the malfunction. One patient elected not to have the device changed and was supported pneumatically for 161 days until transplantation. The other patient underwent device change and was also successfully supported to transplantation.
Myocardial recovery
Four patients demonstrated myocardial recovery and underwent device explant without transplantation. One patient was explanted secondary to device fungal sepsis. He had demonstrated echographic as well as hemodynamic evidence of myocardial recovery and was explanted without immediate donor heart availability.
Three other patients were explanted during a planned heart transplant when a donor heart was en route. With the heart dissected and the patient heparinized and cannulated, the LVAD was turned off. The heart was assessed by transesophageal echocardiography (TEE) as well as hemodynamically. In these patients, the estimated ejection fractions were around 45% with normal cardiac chamber sizes and pressures, low heart rate, and cardiac outputs > 4.0 L without inotropic support. After discussions with family and cardiology, the device was explanted. The arriving hearts were transplanted in other status-one patients. A donor heart has not been lost from these explants.
Heart failure medications had not been given before explantation in these patients but were instituted after LVAD explantation.
Embolic events and cerebral vascular accidents
There were 6 patients with embolic events and 1 patient with hypotensive cerebral vascular accident (CVA) (total 7%), during 340.4 patient-months of support, with an event rate of 0.021 per patient-month. These events resulted in 6 deaths. One case of retinal microembolization, which would appear to be a titanium microsphere, associated with partial monocular visual loss and subsequent recovery. Three CVAs in patients with LVAD endocarditis occurred in patients with overwhelming sepsis, resulting in deaths. In 1 of these patients, the CVA occurred immediately after venting the pneumatic device in a patient who had also undergone aortic valve resuspension for aortic insufficiency at LVAD implant.
One massive air embolism occurring at implantation resulted in unabated seizures and death. The inflow cuff seal was slightly dislodged when evaluating a lateral wall bleed; the air was immediately visualized by echo.
One CVA occurred in a patient with severe hypotension and decreased cerebral perfusion from hemorrhage, ultimately leading to death. One patient had a massive embolic CVA during his 10th month of support that was presumed from the LVAD, though the device was clean when removed at autopsy.
Graft complications
Graft-related complications were defined as bleeding events at LVAD inflow or outflow sites. They occurred in 9 patients requiring four reoperations with 2 deaths. In 2 cases, aortic rupture at the distal anastomotic site required emergent operation and Gore-Tex patch repair, with 1 subsequent death. Of two outflow graft hemorrhages requiring operative intervention, 1 patient succumbed to complications of an intraoperative neurologic insult. Five patients had intermittent pocket bleeds that were managed conservatively until transplantation/explantation, where two outflow graft tears and three inflow site tears were identified.
Infections
Fifty-one (54%) of the patients developed an infection during support. A preimplant infection placed the patient at risk for a postimplant infection, but not necessarily with the same organism. Twenty-five of these patients had infections that were not directly device related (line sepsis, urinary tract, etc.). Twenty-six (27%) patients had device-related infections; the majority (15) were isolated drive line infections. There were five (9%) drive line infections in the pneumatic implants, one (5%) drive line infection in the dual-lead VE device implants, and nine (32%) drive line infections in the single-lead VE device implants (Table 3).
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Deaths
Twenty-four patients died while on support. Six patients died from CVAs, 5 patients died from sepsis, 4 from right ventricular failure, and 3 from hemorrhage. Other causes were less common. Mortality was broken down as follows:
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a p = NS compared with dual-lead device.
b p = 0.034 compared with dual-lead device; p = 0.0146 compared with pneumatic device (two-sided Fishers exact test).
Comment
Optimization of right-sided circulation is the sine qua non of the early postoperative period. The routine use of iNO at 2040 ppm often will dramatically increase right-sided flow by decreasing PVR and subsequent LVAD flows (12 L/min) without changing the pulmonary artery pressures. Sudden drops in LVAD flows in the early postoperative hours are invariably due to interruption of iNO delivery, and will just as rapidly return with reconnection of the system. The vast majority of patients can be weaned from iNO within 48 hours of surgery. Patients are generally weaned from iNO before extubation, but it may be continued postextubation. Milrinone and/or dobutamine are continued for right-sided support until appropriate fluid balance is achieved.
Arginine vasopressin (AVP) infusions at one-tenth dosages used for variceal bleeding (0.040.1 U/min) are routinely used in our institution to treat high-output vasodilatory shock states. In contradistinction to
agonists, there are no receptors within the pulmonary vascular bed; therefore, the PVR is not increased with increasing dosage. The increase in systemic pressure (and coronary perfusion pressure), without increased PVR, optimizes RV function. Within the kidneys, AVP receptors exist only on the efferent renal arterioles and not on the afferent arterioles, effectively increasing the filtration fraction and urine output [22, 23].
Early in our experience, 8 of the first 55 implants (15%) required RVAD implantation. The routine use of iNO and AVP has markedly improved our postoperative management of these critically ill patients. Only 3 of the past 45 implants (7%) have required RVAD support.
Controller changes from persistent alarming were frequent events in both dual- as well as single-lead VE systems. The causes were multifactorial, including software problems, water immersion, static electricity, cable and connector wear, and physiologic derangements. Though the frequency of controller changes from malfunction is decreasing with updated software and other modifications, physiologic derangements must be evaluated before changing. None of the controller malfunctions lead to any morbidity or mortality.
Pneumatic drive line rupture at its attachment to the implanted device was reported by our group as well as others and resulted in one of our device-related deaths. There is now reinforcement of the connection site and this problem has not recurred in our series.
Accelerated bearing wear, outflow graft bleeding, and inflow valve tears may have been related to kinking of the outflow graft. The elbow to the outflow valve housing carries a 45-degree angle, placing the outflow graft directly underneath the sternum when closed. This configuration made resternotomy for transplantation quite perilous. A mild kink was introduced as the graft exited the outflow valve housing, allowing the graft to lie to the right of the sternum, facilitating resternotomy. This kink likely became hemodynamically significant as the patients increased their activity levels and subsequently increased their outputs, leading to the three sequelae. Constant rubbing of the graft at the fold led to outflow erosion and a cause of late bleeding. The device can generate enormous pressures (> 300 mm Hg) within the pumping chamber in an attempt to maintain adequate patient perfusion across this kink. This can lead to inflow valve tears because of the high transvalvular gradient, as well as premature wear on the device bearings.
The new 22.5-degree-angled outflow elbow appears to address these problems. The graft now lies comfortably to the right of the sternum in a gradual arc, without any folds.
The drive line design is a dynamic issue for the current vented electric device. The single-lead system incorporates both the electrical components and the air vent in a single drive line. Though having a single drive line addresses issues of aesthetics as well as the theoretical benefit of lower infections by having only one transcutaneous line, its large size and stiffness have prevented adequate sealing with the skin in many patients. This allows persistent serous drainage and subsequent drive line infections. Various design changes are being discussed and may be implemented before this publication.
Five device changes were performed. Three changes were for device infections (one pneumatic, two single-lead VE). Two changes were for device malfunctions, one for diaphragm separation, and one for bearing wear (both dual-lead VE). There were no deaths in this group.
Myocardial remodeling after prolonged unloading of the ventricle resulting in device explantation without transplantation has been demonstrated [24]. We have explanted devices on 4 such patients; one died 4 months later with rapidly recurring heart failure. One died 2 years later in his sleep, though his ejection fraction before his death was 50% mutiple gated acquisition [MUGA]. Two other patients are alive and well 17 and 6 months postexplant.
Neurologic and other embolic events occur with an acceptably low rate despite the absence of systemic anticoagulation. However, these events precipitated a high 86% mortality. Sepsis is a known predisposing risk factor for thromboembolism. Severe hypotension from hypovolemia and Watershed infarction can occur from massive hemorrhage. Massive air embolism is a technical complication that requires vigilance, but can generally be avoided. These causes for CVAs are device and implant related, and are important in patient risk stratification; but they are not necessarily device specific. Two patients had device specific events, for an event rate of 0.006 per patient-month.
Studies are currently underway to assess the incidence and potential long-term neurocognitive sequelae of asymptomatic microembolic events, which have been shown to be more common in patients during LVAD support than after transplantation [10].
Postimplant infections are an important cause of morbidity in this group. Fifty-one (54%) of the patients developed an infection during support. A preimplant infection placed the patient at risk for a postimplant infection, but not necessarily with the same organism. Preoperative infection may therefore be more of an indicator of the patients ability to address infections and overall immune status and/or an indicator of the severity of their catabolic state. Of the patients that had device-related infections, the majority were isolated drive line infections.
The single-lead systems (pneumatic as well as vented electric) have a higher drive line infection rate than the two-lead vented electric system and are likely related to the difference in sealing at the skin exit site. The larger stiffer single leads do not seal as readily because of their size, as well as the torque that they transmit with movement. The dual-lead VE device had thinner percutaneous leads that incorporate tenaciously and would rarely drain any fluid. The increased incidence of drive line infections from the single-lead VE device as compared with the single-lead pneumatic and the dual-lead VE reached statistical significance (Table 3).
Isolated drive line infections are treated initially with parenteral antibiotics and continued with chronic suppressive oral antibiotics. Topical antibiotics are used on the drive line dressings and are changed according to sensitivities.
Device pocket infections are treated with drainage and closure with muscle flaps as well as chronic suppressive antibiotics. "Device endocarditis" (infection of the blood-contacting surfaces of the device) is often a difficult diagnosis to make. Current imaging techniques are inadequate to evaluate the valves or other structures within the device for vegetations, or other evidence of infection. Patients may only have intermittent constitutional symptoms of infection with a positive blood culture. If a rapid response with antibiotics is seen, these patients can be managed expectantly until transplantation with chronic suppression. An embolic event in the face of clinical infection is best treated by device change.
Postoperative dysrhythmias are common and are rarely catastrophic. Persistent atrial fibrillation was not routinely treated with systemic anticoagulation. Malignant ventricular dysrhythmias are not tolerated well in the early postoperative period, as the RV needs to function to drive blood through the requisite postbypass elevated PVR. However, late malignant ventricular dysrhythmias are tolerated very well hemodynamically as Fontan hemodynamics occurs. Treatment of these dysrhythmias can thus be performed in a less emergent manner [25].
Conversion to high panel reactive antibodies (PRA) is seen in these patients. This may be related to high transfusion rates despite the use of leukocyte-depleted products; however, interest is raised on the cells adherent to the diaphragm as a stimulus for inflammatory and antibody upregulation [26]. Specifically designed combinations of cytolytic agents with plasmapheresis may allow quicker and safer transplantation in this patient population, and are under intense investigation.
The patients quality of life was significantly improved from their moribund preoperative state as they recovered to floor status and were subsequently discharged from the hospital. Of the 35 patients with VE devices who were transferred to floor status, 4 were transplanted early and 24 were discharged home.
Discharged patients were seen weekly and were evaluated for evidence of heart failure as well as device malfunction. Three patients returned to school: 1 to college, 1 to high school, and 1 to middle school. Before return to school, issues of medical support within the school as well as with the local emergency medical services were addressed. The school nurses as well as a companion (classmate or monitor) were instructed on basic operations and troubleshooting of the device as well as use of the hand pump. Five patients returned to work.
Often, patients faced discharge with uncertainty and apprehension. Patients, family members, and close associates were trained in basic operations of the device, and 24-h access to a member of the LVAD team was implemented. Patients carried pagers for notification of impending transplantation. Day trips out of the hospital as well as overnight stays at a local hotel helped with the transition home. Home health agencies as well as outpatient physical therapy were also instructed on device management. Though some patients and family members never resolved their fear and apprehension, most become well adapted and comfortable with their device.
Our interim results with the TCI Heartmate LVADs have shown overall excellent support of this critically ill subgroup of heart failure patients. Early institution of mechanical support should be established to rehabilitate these patients. The subsequent cardiac transplantation is technically more challenging, but the physiologic rehabilitation allows for a more predictable postoperative course.
The "bridge to recovery" is a very intriguing application for this technology. How this translates to long-term function and survival is unknown and is under intense investigation by others and us.
Infection is currently the most important morbidity associated with this device. Modifications to the drive line will likely decrease the incidence of drive line infection; however, a totally implantable LVAD (Penn State/Arrow, Reading, PA) will likely substantially reduce this. Impeller-based devices (TCI-Nimbus [Woburn, MA], Trans Coil [New York, NY]) are close to clinical application and may become the next-generation support system. The use of these devices as destination therapy for a subset of heart failure patients is currently under investigation at our center and others in the REMATCH trial. As device technologies develop, it is clear that mechanical assist will play a greater role in the management of heart failure than its current use as bridge to transplantation. [7]
References
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V. Rao, J. P. Slater, N. M. Edwards, Y. Naka, and M. C. Oz Surgical management of valvular disease in patients requiring left ventricular assist device support Ann. Thorac. Surg., May 1, 2001; 71(5): 1448 - 1453. [Abstract] [Full Text] [PDF] |
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M.H. Yacoub A novel strategy to maximize the efficacy of left ventricular assist devices as a bridge to recovery Eur. Heart J., April 1, 2001; 22(7): 534 - 540. [PDF] |
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M. A. Acker Mechanical circulatory support for patients with acute-fulminant myocarditis Ann. Thorac. Surg., March 1, 2001; 71 (2007): S73 - S76. [Abstract] [Full Text] [PDF] |
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G. S. Kumpati, P. M. McCarthy, and K. J. Hoercher Left ventricular assist device bridge to recovery: a review of the current status Ann. Thorac. Surg., March 1, 2001; 71 (2007): S103 - S108. [Abstract] [Full Text] [PDF] |
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G. M. Wieselthaler, H. Schima, A. M. Lassnigg, M. Dworschak, R. Pacher, M. Grimm, and E. Wolner Lessons learned from the first clinical implants of the DeBakey ventricular assist device axial pump: a single center report Ann. Thorac. Surg., March 1, 2001; 71 (2007): S139 - S143. [Abstract] [Full Text] [PDF] |
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L. W. Stevenson and R. L. Kormos Mechanical cardiac support 2000: current applications and future trial design: June 15-16, 2000 Bethesda, Maryland J. Am. Coll. Cardiol., January 1, 2001; 37(1): 340 - 370. [Full Text] [PDF] |
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D. Marelli, H. Laks, D. Fazio, M. A. Hamilton, G. C. Fonarow, D. A. Meehan, and J. D. Moriguchi Mechanical assist strategy using the BVS 5000i for patients with heart failure Ann. Thorac. Surg., July 1, 2000; 70(1): 59 - 66. [Abstract] [Full Text] [PDF] |
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P. Mohacsi, M. C. Deng, R. Murphy, C.-H. Bergh, E. Gronda, M. Komajda, R. Pacher, J. Spinar, K. Swedberg, and J. F. Cleland Implantable left ventricular assist systems (LVAS): Recent results. A report from a series of meetings sponsored by the Study Group on Advanced Heart Failure of the Working Group on Heart Failure Eur J Heart Fail, March 1, 2000; 2(1): 13 - 18. [Abstract] [Full Text] [PDF] |
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