Report From the American Society of Transplantation Conference on Donor Heart Selection in Adult Cardiac Transplantation in the United States.

Cardiac transplantation remains the only definitive treatment for end-stage heart failure. Transplantation rates are limited by a shortage of donor hearts. This shortage is magnified because many hearts are discarded because of strict selection criteria and concern for regulatory reprimand for less-than-optimal posttransplant outcomes. There is no standardized approach to donor selection despite proposals to liberalize acceptance criteria. A donor heart selection conference was organized to facilitate discussion and generate ideas for future research. The event was attended by 66 participants from 41 centers with considerable experience in cardiac donor selection. There were state-of-the-art presentations on donor selection, with subsequent breakout sessions on standardizing the process and increasing utilization of donor hearts. Participants debated misconceptions and established agreement on donor and recipient risk factors for donor selection and identified the components necessary for a future donor risk score. Ideas for future initiatives include modification of regulatory practices to consider extended criteria donors when evaluating outcomes and prospective studies aimed at identifying the factors leading to nonacceptance of available donor hearts. With agreement on the most important donor and recipient risk factors, it is anticipated that a consistent approach to donor selection will improve rates of heart transplantation.

Long-term use of the CentriMag® Ventricular Assist System as a right ventricular assist device: a case report.

Right ventricular failure (RVF) following implantation of a left ventricular assist system (LVAS) is associated with high morbidity and mortality.( 1-4 ) Numerous centers have reported short-term use of the CentriMag (®) Ventricular Assist System (CVAS) (Levitronix LLC, Waltham, MA) for treatment of cardiogenic shock, decompensated heart failure and right ventricular failure (RVF) following LVAS implantation.( 5-9 ) The present report reviews the clinical course of a patient requiring long-term right ventricular support utilizing the CVAS, following a HeartMate (®) II LVAS (Thoratec Corp. Pleasanton, CA) implantation. Elevated cytotoxic antibody levels complicated the patient's treatment plan by precluding orthotropic heart transplantation. The CVAS operated for 304 days without mechanical difficulty until replaced with the HeartWare (®) Ventricular Assist System (HeartWare Inc. Miramar, FL).

A selective cytopheretic inhibitory device for use during cardiopulmonary bypass surgery.

BACKGROUND: Systemic inflammatory response syndrome (SIRS) can occur in association with cardiopulmonary bypass (CPB) surgery, resulting in multiple organ dysfunction (MOD). Activated neutrophils have been implicated as major inciting factors in this process. Neutrophil-depleting filters incorporated within the extracorporeal blood circuit during CPB have been developed and evaluated, with inconsistent clinical results. METHODS: A novel, biomimetic, selective cytopheretic device (SCD) was tested in vitro within a blood circuit to assess safety and interactions with blood components and further evaluated ex vivo in a bovine model of CPB surgery during ventricular assist device implantation. RESULTS: In vitro blood circuit studies demonstrated that the SCD reduces circulating neutrophils while maintaining low rates of hemolysis compared to current leukocyte-reduction filters. In the bovine CPB model, animals without SCD treatment (No SCD) demonstrated an increase in circulating white blood cell (WBC) and neutrophil counts, steadily increasing throughout CPB. SCD with only systemic heparin anticoagulation (SCD-H) acutely reduced neutrophils for the first 2 hrs of CPB, but followed with a greater than 6-fold increase in neutrophil counts. SCD treatment with regional citrate anticoagulation along the SCD circuit (SCD-C) reduced systemic neutrophil counts throughout 4 hrs of CPB despite lower amounts of eluted cells from the SCD. When analyzed for immature neutrophils, the control and SCD-H showed increasing counts at later time-points, not seen in the SCD-C group, suggesting a more complex mechanism of action than simple leukoreduction. CONCLUSIONS: These results suggest that SCD-C therapy may disrupt the systemic leukocyte response during CPB, leading to improved outcomes for CPB-mediated MOD.

Heart and lung transplantation in the United States, 1997-2006.

This article highlights trends in heart and lung transplantation between 1997 and 2006, drawing on data from the OPTN and SRTR. The total number of candidates actively awaiting heart transplantation declined by 45% over the last decade, dropping from 2414 patients in 1997 to 1327 patients in 2006. The overall death rates among patients awaiting heart transplantation declined over the same period. The distribution of recipients among the different status groups at the time of heart transplantation changed little between the inception of the new classification system in 1999 and 2005. Deaths in the first year after heart transplantation have steadily decreased. At the end of 2006, 2885 candidates were awaiting a lung transplant, up 10% from the 1997 count. The median time-to-transplant for listed patients decreased by 87% over the decade, dropping from 1053 days in 1997 to 132 days in 2006. Selection for listing and transplantation has shifted toward more urgent patients since the May 2005 implementation of a new lung allocation system based on survival benefit and urgency rather than waiting time. Only 31 heart-lung transplants were performed in 2006, down from a high of 62 in 1997.

Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs.

We used a load-insensitive index of systolic left ventricular (LV) function and an analysis of diastolic pressure-dimension relationships to test the hypothesis that recombinant human (rh) tumor necrosis factor-alpha (TNF alpha) impairs LV function in dogs. Animals were studied 7-10 d after aseptic implantation of instrumentation to monitor cardiac output, external anterior-posterior LV diameter, and LV and pleural pressures. Data were analyzed from seven dogs that received active rhTNF alpha (100 micrograms/kg over 60 min) and from five dogs that received heat-inactivated rhTNF alpha. At 24 h after infusion of active rhTNF alpha, the slope of the LV end-diastolic dimension-stroke work relationship decreased significantly, indicating a decrement in LV systolic contractility. Simultaneously, LV unstressed dimension increased significantly, suggesting diastolic myocardial creep. The end-diastolic relationship between LV transmural pressure and normalized LV dimension (strain) was markedly displaced to the left, suggesting increased diastolic elastic stiffness. Despite these changes in LV performance, cardiac index was maintained by tachycardia. The abnormalities in LV function were resolved by 72 h. We conclude that rhTNF alpha reversibly impairs LV systolic and diastolic function in unanesthetized dogs. Because dysfunction occurs greater than 6 h after the infusion of rhTNF alpha and persists for 24-48 h, the mechanism underlying this phenomenon may involve secondary mediators or a change in myocardial gene expression.

Central nervous system site of action for the respiratory depressant effect of diacetylmorphine (heroin) in the cat.

The purpose of our study was to identify central nervous system sites involved in the respiratory depressant effect of drugs that stimulate opioid receptors. Diacetylmorphine (heroin) was administered into several cerebroventricular regions of chloralose-anesthetized cats, while monitoring pulmonary ventilation with a Fleisch pneumotachograph. Administration of heroin (17, 50, 150, and 450 micrograms) into the forebrain ventricles, which was restricted to these ventricles, resulted in no significant respiratory effects. In contrast, administration of heroin into either the fourth ventricle or the cisterna magna resulted in a significant (P less than 0.05) decrease in respiratory minute volume (VE). In the fourth ventricle this was because of a decrease in frequency (f) and in the cisterna magna, to a decrease in tidal volume (VT). Intravenous administration of heroin in the same dose-range produced a decrease in VE, which was primarily due to a decrease in f. Bilateral application of heroin (70 micrograms/side) to each of three ventral medullary surface sites (Mitchell's, Schlaefke's, and Loeschcke's areas) known to influence respiration elicited a decrease in VE only at Mitchell's area. This decrease was due to decreases in f and VT. The role of this site in the action of intravenously administered heroin was tested by topical application of naloxone to this area in animals with respiratory depression evoked by intravenous heroin. Bilateral application of naloxone (15 micrograms/side) to Mitchell's area restored breathing to normal. These results lead us to suggest that the site of heroin-induced respiratory depression is a specific area (Mitchell's area) on the ventral surface of the medulla.

IL-8 is an angiogenic factor in human coronary atherectomy tissue.

BACKGROUND: Interleukin-8 (IL-8), a CXC chemokine that induces the migration and proliferation of endothelial cells and smooth muscle cells, is a potent angiogenic factor that may play a role in atherosclerosis. Previously, IL-8 has been reported in atherosclerotic lesions and circulating macrophages from patients with atherosclerosis. Therefore, we sought to determine whether IL-8 plays a role in mediating angiogenic activity in atherosclerosis. METHODS AND RESULTS: Homogenates from 16 patients undergoing directional coronary atherectomy (DCA) and control samples from the internal mammary artery (IMA) of 7 patients undergoing bypass graft surgery were assessed for IL-8 content by specific ELISA, immunohistochemistry, and in situ hybridization for IL-8 mRNA. The contribution of IL-8 to net angiogenic activity was assessed using the rat cornea micropocket assay and cultured cells. IL-8 expression was significantly elevated in DCA samples compared with IMA samples (1.71+/-0.6 versus 0.05+/-0.03 ng/mg of total protein; P<0.01). Positive immunolocalization of IL-8 was found exclusively in DCA tissue sections, and it correlated with the presence of factor VIII-related antigen. In situ reverse transcriptase polymerase chain reaction revealed the expression of IL-8 mRNA in DCA tissue. Corneal neovascular response, defined by ingrowth of capillary sprouts toward the implant, was markedly positive with DCA pellets, but no constitutive vessel ingrowth was seen with IMA specimens. Neutralizing IL-8 attenuated both the in vivo corneal neovascular response and the in vitro proliferation of cultured cells. CONCLUSIONS: The results suggest that, in human coronary atherosclerosis, IL-8 is an important mediator of angiogenesis and may contribute to plaque formation via its angiogenic properties.

Stress-induced changes in the function of the parasympathetic nervous system are mimicked by blocking GABA in the CNS of the cat.

The purpose of this study was to determine the effect of blockade of receptors for gamma-aminobutyric acid (GABA) in the forebrain, on vagal activity to the stomach and heart. This was done by injecting bicuculline (50 micrograms) into the lateral ventricle of the brain and restricting the drug to the forebrain ventricles by cannulating the cerebral aqueduct. Studies were performed in chloralose-anesthetized cats and gastric motility was monitored using extraluminal force transducers, sutured to the antrum and pylorus. Cardiac vagal activity was determined by noting the sinus bradycardia that developed from activation of the baroreceptor reflex induced by phenylephrine. Administration of bicuculline into the lateral ventricle of 7 animals produced increases in the minute motility index of 5.3 +/- 0.8 (antrum) and 13.9 +/- 2.1 (pylorus). This was associated with inhibition of baroreceptor-induced vagal bradycardia (i.e. -38 +/- 6.4 beats/min before bicuculline and -7.7 +/- 5.7 beats/min after bicuculline). These data indicate that a GABAergic mechanism in the forebrain may be important for controlling vagal outflow to both the stomach and the heart.

Effect of postoperative atrial fibrillation on length of stay after cardiac surgery (The Postoperative Atrial Fibrillation in Cardiac Surgery study [PACS(2)].

Atrial fibrillation (AF) after cardiac surgery is thought to increase length of stay (LOS). A clinical pathway focused on the management of postoperative AF, including prophylaxis with beta blockers, was implemented to assess the effect of AF on LOS after cardiac surgery. Data were obtained on consecutive cardiac surgery patients in preoperative normal sinus rhythm, no prior history of AF, and no chronic antiarrhythmic therapy from January to May 1995 (control) and November 1996 to June 1997 (pathway). Statistical analysis was performed to assess the effect of postoperative AF on the LOS, clinical outcomes, and cost after cardiac surgery. Despite the clinical pathway, the LOS (7 days for both periods; p = 0.12) and incidence of AF (28.9% vs 28.4%; p = 0.92) remained unchanged. Unadjusted direct costs were 15% higher in the pathway period (p <0.001). Increased rates of beta-blocker therapy had a marginal effect on the incidence of postoperative AF, except in the group who only underwent primary coronary artery bypass graft surgery (31.2% vs 25.3%; p = 0.31). Multivariate analysis revealed that AF contributed only 1 to 1.5 days to the LOS. Thus, this investigation represents the most recent analysis of the effects of postoperative AF on LOS, clinical outcomes, and cost after cardiac surgery. Unlike prior studies, the impact of postoperative AF is less prominent in the current era of cardiac surgical care regardless of the presence of a clinical pathway addressing AF.

Intermediate-term outcome of mitral reconstruction in cardiomyopathy.

OBJECTIVE: Severe mitral regurgitation is a frequent complication of end-stage cardiomyopathy that contributes to heart failure and predicts a poor survival. We studied the intermediate-term outcome of mitral reconstruction in 48 patients who had cardiomyopathy with severe mitral regurgitation and were operated on between June 1993 and June 1997. METHODS: Ages ranged from 33 to 79 years (63 +/- 6 years) with left ventricular ejection fractions of 8% to 25% (16% +/- 3%). All patients were receiving maximal drug therapy and were in New York Heart Association class III-IV with severe, refractory 4+ mitral regurgitation. Operatively, all 48 had undersized flexible annuloplasty rings inserted, 7 had coronary bypass grafts for incidental disease, 11 had prior bypass grafts, and 11 also had tricuspid valve repair. RESULTS: One operative death occurred as a result of right ventricular failure. Postoperative transesophageal echocardiography revealed mild mitral regurgitation in 7 patients and no mitral regurgitation in 41. There were 10 late deaths, 2 to 47 months after mitral reconstruction. The 1- and 2-year actuarial survivals have been 82% and 71%. At a mean follow-up of 22 months, the number of hospitalizations for heart failure has decreased, and 1 patient has had heart transplantation. Significantly, New York Heart Association class improved from 3.9 +/- 0.3 before the operation to 2.0 +/- 0.6 after the operation. Twenty-four months after the operation, left ventricular volume and sphericity have decreased, whereas ejection fraction and cardiac output have increased. CONCLUSION: Whether this favorable modification of left ventricular function and geometry will persist remains unknown. However, mitral repair for cardiomyopathy with mitral regurgitation allows new strategies for these patients.

The management of tetralogy of Fallot with pulmonary atresia and diminutive pulmonary arteries.

Since September 1991, 14 consecutive patients with tetralogy of Fallot, pulmonary atresia, and diminutive pulmonary arteries have undergone staged repair. All patients had multiple aortopulmonary collateral arteries and the ductus arteriosus was absent in 11. Mean sizes of the right and left pulmonary arteries were 2.2 +/- 0.7 mm and 1.9 +/- 0.8 mm, respectively (range 0.5 to 3.0 mm). Eight patients (57%) have subsequently received complete repair. Age at initial procedure (shunt, right ventricle-pulmonary artery conduit, or direct aorta-pulmonary artery anastomosis) in this group was 5.3 +/- 6.8 months. The number of operative procedures to achieve complete repair was 2.9 +/- 0.8 per patient (range 2 to 4). Intraoperative postrepair peak right ventricle-left ventricle pressure ratio was 0.57 +/- 0.17. Six of 8 patients (75%) required additional interventional procedures (mean 1.5 +/- 1.2 per patient) for angioplasty of peripheral pulmonary artery stenoses, coil embolization of aortopulmonary collateral arteries, or intra-operative insertion of intravascular pulmonary artery stents. Mean follow-up from complete repair was 8.7 +/- 8.3 months (range 0.5 to 23.8 months) and is complete. There was one in-hospital death at 45 days, and one late cardiac death at 20.3 months. Six patients had initial palliative operations (unifocalization, right ventricle-pulmonary artery conduit, direct aorta-pulmonary artery anastomosis, or transannular outflow patch) but have not undergone complete repair. Age at initial procedure in this group was 27.9 +/- 56.9 months (range 0.27 to 155 months), and mean follow-up from initial procedure was 10.9 +/- 11.2 months (range 0 to 31.4 months). The operative mortality rate was 33% (2 of 6 patients). There was one late noncardiac death at 5.3 months. Three patients are awaiting further intervention or repair. This experience suggests that complete repair is feasible even in patients with extremely diminutive pulmonary arteries (< or = 3.0 mm). Pulmonary artery growth is facilitated by early (3 to 6 month) establishment of central pulmonary artery flow by right ventricle-pulmonary artery conduit (pulmonary arteries > 1.5 mm) or by direct ascending aorta-pulmonary artery anastomosis (pulmonary arteries < 1.5 mm). Subsequent interventional catheterization and operative procedures as required for pulmonary artery stenoses and coil embolization of collateral arteries allow continued recruitment of central pulmonary arteries and may obviate or minimize the need for unifocalization procedures.

Mitral valve repair in heart failure.

Mitral regurgitation (MR) is a frequent complication of end-stage heart failure. Historically, these patients were either managed medically or with mitral valve replacement, both associated with poor outcomes. Mitral valve repair via an 'undersized' annuloplasty repair is safe and effectively corrects MR in heart-failure patients. All of the observed changes contribute to reverse remodeling and restoration of the normal left-ventricular geometric relationship. Mitral valve repair offers a new strategy for patients with MR and end-stage heart failure.

Surgical alternatives for heart failure.

Heart failure is one of the leading causes of hospitalization in the United States. Congestive heart failure is a chronic, progressive disease and its central element is remodeling of the cardiac chamber associated with ventricular dilation. Secondary mitral regurgitation is a complication of end-stage cardiomyopathy and is associated with poor prognosis. Historically, these patients were not considered operative candidates because of their high morbidity and mortality. Heart transplantation is now considered standard treatment for select patients with end-stage heart disease; however, it is applicable only to a small number of patients. In an effort to address this problem, newer and alternative surgical approaches are evolving, including mitral valve annuloplasty, the Batista procedure, and other left ventricular shape changing technologies. Using these operative techniques to alter the shape of the left ventricle, in combination with optimal medical management for heart failure, improves survival, and patients may avoid or postpone transplantation.

Development of anti-major histocompatibility complex class I or II antibodies following left ventricular assist device implantation: effects on subsequent allograft rejection and survival.

BACKGROUND: Previous reports have indicated that antibodies to HLA class I or II antigens develop in approximately 60% of patients following left ventricular assist device (LVAD) implantation, subsequent rates of allograft rejection are higher, and survival is adversely affected. METHODS: We performed an analysis of the incidence of antibody development to HLA class I or II antigens by panel reactive antibody (PRA) screening following implantation of the HeartMate LVAD in 38 patients from October 1, 1996 to March 1, 2000 (6 LVAD deaths excluded from study). The occurrence of vascular or cellular rejection of International Society of Heart and Lung Transplantation grade > or = 3A, as determined by endomyocardial biopsy following heart transplantation (HTX), were compared for patients with (n = 32, LVAD group) or without (n = 68, control group) preoperative LVAD support. RESULTS: After LVAD implantation, 9 patients (28%) in the LVAD group developed IgG antibodies to class I (n = 3), class II (n = 5), or both antigens (n = 1) with PRA > 10%. The remaining 23 patients (72%) had either no detectable IgG antibody development or IgG antibody development with PRA < 10%. At the time of HTX, only 4 patients in the LVAD group had persistent PRA > 10%. Only 3 patients (4%) in the control group had PRA > 10% at the time of HTX. The incidence of patients free from rejection at 6 and 12 months was 62% and 44% for the control group, and 49%, and 40% for the LVAD group, respectively (p not significant). The mean linearized rate plus or minus standard deviation of allograft rejection from 0 to 6 months and 7 to 12 months was 0.13 +/- 0.21 and 0.09 +/- 0.14 episodes a month, respectively, for patients with no LVAD support, and 0.17 +/-.25 and 0.06 +/- 0.1 episodes a month, respectively, for those with LVAD support (p = not significant). Post-transplantation survival at 1 and 2 years was 90% and 90%, respectively, for the control group, and 97% and 92%, respectively, for the LVAD group (p not significant). CONCLUSION: Patients with LVAD support before HTX do not appear to be at increased risk for significant allograft rejection in the first year or for death within the first 2 years after transplantation.

Load-insensitive assessment of myocardial performance after tumor necrosis factor-alpha in dogs.

Tumor necrosis factor-alpha (TNF alpha) has been implicated as an endogenous mediator of the cardiovascular manifestations of sepsis and septic shock. We studied the acute effects of a single dose (50 or 200 micrograms/kg) of intravenous recombinant human TNF alpha (rhTNF alpha) on myocardial function in halothane-anesthetized dogs. Regional cardiac dimensions were measured by using sonomicrometry. Intracavitary left ventricular, ascending aortic, and pulmonary artery pressures were measured by use of micromanometers. Cardiac index was determined by means of thermodilution. Myocardial performance was analyzed by assessing changes in the slope of the left ventricular end-diastolic length-stroke work relationship obtained by performing transient vena caval occlusions. Animals were resuscitated by means of normal saline solutions to maintain baseline regional end-diastolic length. Over a 3-hour period of observation, rhTNF alpha decreased systemic vascular resistance index, but the cytokine did not compromise intrinsic myocardial performance. The circulatory response to rhTNF alpha was a hyperdynamic state characterized by tachycardia, augmented cardiac index, and increased intrinsic myocardial contractility (leftward shift of the left ventricular end-diastolic length-stroke work relationship). In addition, rhTNF alpha caused systemic acidosis and increased plasma levels of prostacyclin metabolite (6-keto-prostaglandin F1 alpha). After the dose of rhTNF alpha large volumes of fluid were required to maintain baseline end-diastolic length. We conclude that in the acute setting, rhTNF alpha elicits abnormalities in peripheral vascular tone that are not accompanied by depression of myocardial function.

Mitral valve reconstruction in sickle cell disease.

As survival improves in patients with sickle cell anemia, the prospects of performing cardiac surgical procedures on older patients with this genetic defect increase. We describe the successful management of a 52-year-old patient with sickle cell disease (homozygous for hemoglobin S) and a history of multiple sickle crisis undergoing cardiopulmonary bypass for mitral valve repair. Preoperative partial exchange transfusion followed by total exchange transfusion at the time of operation was performed to reduce the level of hemoglobin S to 5.4% during bypass. Other management strategies included high-flow normothermic bypass with aortic crossclamping, topical hypothermia, and cold crystalloid cardioplegia.

The use of extracorporeal life support in adult patients with primary cardiac failure as a bridge to implantable left ventricular assist device.

BACKGROUND: Extracorporeal life support (ECLS) is an effective technique for providing emergent circulatory assistance, and may represent a life-saving option in patients who might not initially be considered a candidate for other forms of circulatory support (extracorporeal or implantable left ventricular assist device [LVAD]). In the setting of cardiac arrest, ECLS represents the only viable method of initiating circulatory support. However, ECLS has a number of disadvantages that include high complication rates (eg, stroke, bleeding) and a limited duration of potential support, which have prevented its widespread acceptance, particularly in the adult population. With the increased successful application of long-term implantable LVADs as a bridge to transplant, the major limitation of ECLS could be overcome by bridging patients to a long-term implantable LVAD ("bridge to bridge"), thereby reducing the reluctance to utilize ECLS when indicated. After acquisition of the HeartMate LVAD (Thermo Cardiosystems, Inc, Woburn, MA) we investigated the use of ECLS as a bridge to an implantable LVAD and subsequent transplantation in selected high-risk patients. METHODS AND RESULTS: From Oct 1, 1996 to Sept 30, 2000, 33 adult patients presenting with cardiac arrest or severe hemodynamic instability were placed on ECLS for the bridge to bridge indication. Of the 33 patients, 10 patients survived to LVAD implant, 1 was bridged directly to transplant, 5 weaned from ECLS, and 16 died on ECLS. Overall, 12 patients survived to discharge. One-year actuarial survival from the initiation of ECLS was 36%. One-year actuarial survival from the time of LVAD implant, conditional on surviving ECLS, was 80%. CONCLUSIONS: The 1-year survival of adult patients placed on ECLS and who subsequently survived to an implantable LVAD was favorable. These data support a strategy of ECLS to implantable LVAD bridge to heart transplant in adult patients who are in need of circulatory support and who are not initially candidates for other forms of mechanical support. The favorable results of this strategy support utilization of ECLS even in situations where myocardial recovery is thought to be unlikely.

Assessment of an extracorporeal life support to LVAD bridge to heart transplant strategy.

BACKGROUND: Extracorporeal life support (ECLS) is an effective technique for providing emergent circulatory assistance. However, its use in adult patients is associated with poor survival when myocardial function fails to recover. Due to the prolonged waiting times for heart transplantation, ECLS as a bridge to transplant is associated with poor survival. In addition, ECLS has been reported to be a significant risk factor for death after bridging to an implantable left ventricular assist device (LVAD). After acquisition of the HeartMate LVAD (Thermo Cardiosystems, Inc) in October 1996, we began using ECLS as a bridge to an implantable LVAD and subsequently transplantation in selected high-risk patients. METHODS: From October 1, 1996 to December 1, 1999, 60 adult patients presenting with cardiogenic shock were evaluated for circulatory assistance. RESULTS: Twenty-five patients (group 1) with cardiac arrest or severe hemodynamic instability and multiorgan failure were placed on ECLS. Eight patients survived to LVAD implant, 1 was bridged directly to transplant, and 4 weaned from ECLS. Nine patients in group 1 survived to discharge. Thirty patients (group 2) underwent LVAD implant without ECLS. Twenty-three were bridged to transplant, with 22 surviving to discharge. Five patients (group 3) were placed on extracorporeal ventricular assist with 3 bridged to transplant and all surviving to discharge. One-year actuarial survival from the initiation of circulatory support was 36% (group 1), 73% (group 2), and 60% (group 3). One-year actuarial survival from the time of LVAD implant in group 1, conditional on surviving ECLS, was 75% (p = NS compared with group 2). CONCLUSIONS: In selected high-risk patients, LVAD survival after initial ECLS was not different from survival after LVAD support alone. An initial period of resuscitation with ECLS is an effective strategy to salvage patients with cardiac arrest or extreme hemodynamic instability and multiorgan injury.

Mechanical circulatory support for acute heart failure.

Circulatory support devices are frequently required in postcardiotomy shock, postmyocardial infarction shock, and acute myocarditis. A panel of cardiac surgeons addressed the use of these devices in 4 patients. Cardiogenic shock after mitral valve replacement was considered best served by a left ventricular assist device (VAD) with apical rather than atrial cannulation. A left VAD should be placed first and a right VAD only if needed. Acute myocardial infarction shock was considered best treated with a left VAD with left ventricular cannulation to avoid thrombosis. If cardiac transplantation is an option, a long-term device must be considered. Young patients with acute fulminant myocarditis should be implanted with VADs in anticipation of recovery, and transplantation should be delayed. Patients with severe heart failure after coronary bypass grafting were considered best served by an extracorporal membrane oxygenation (ECMO) system or a VAD. Current postcardiotomy survival rates of postcardiotomy patients of 20% to 40% are worthwhile, but can be improved. Temporary devices such as ECMO can be changed to more long-term devices when necessary.

Prophylactic mitral reconstruction for mitral regurgitation.

BACKGROUND: Mitral regurgitation (MR) will produce myocardial dysfunction. The goal of this study was to review outcomes of mitral valve reconstruction in asymptomatic patients with severe MR. METHODS: From 1992 to 2000, 93 asymptomatic patients with degenerative disease and severe MR underwent mitral valve reconstruction. Mean preoperative left ventricular internal diameter diastole was 56 +/- 8 mm and ejection fraction was 60% +/- 6%. Mean age was 47 +/- 10 years and mean follow-up 23 +/- 27 months. All patients underwent complex reconstruction. RESULTS: There were no deaths and two late reoperations. One was for systolic anterior motion of the anterior leaflet of the mitral valve requiring valve replacement and one for hemolysis requiring re-repair. There was one perioperative transient ischemic attack and no late thromboembolic events. At follow-up all but 1 patient remains in NYHA class I and all had no MR except in 2 patients at 63 and 89 months. CONCLUSIONS: Mitral valve reconstruction for "asymptomatic" MR can be performed with no mortality and low morbidity before development of left ventricular dysfunction. Early prophylactic repair is advocated in the presence of severe MR if valve reparability is assured.