Low incidence of myocardial recovery after left ventricular assist device implantation in patients with chronic heart failure

BACKGROUND: Mechanical, histological, and biochemical improvement has been described in patients after left ventricular assist device (LVAD) support. Explantation of the LVADs without heart transplantation has been described in selected patients who received this therapy as a bridge to transplantation. METHODS AND RESULTS: A retrospective review of patients receiving a mechanical bridge to transplantation at Columbia Presbyterian Hospital after July 21, 1991, was performed to determine the incidence of patients in whom the device was successfully explanted. From August 1, 1996, to February 1, 1998, we prospectively attempted to identify potential explant candidates by the use of exercise testing. During this time, we recruited 39 consecutive patients after insertion of the Thermo Cardiosystems vented electric device to participate in the following study. Approximately 3 months after device implantation, a maximal exercise test with hemodynamic monitoring and respiratory gas analysis was performed with the LVAD in the automated mode. The electric device was interfaced with a pneumatic console such that the rate could be decreased to 20 cycles/min. Hemodynamic measurements were recorded as the device rate was decreased. A repeat exercise test was then performed if the patient remained hemodynamically stable. A retrospective chart review of 111 LVAD recipients at our institution identified only 5 successful explant patients. Eighteen of the 39 patients were studied. Fifteen patients exercised with maximal device support. At peak exercise, VO2 averaged 14.5+/-3.6 mL. kg-1. min-1; LVAD flow, 8.0+/-1.3 L/min; Fick cardiac output, 11.4+/-3.3 L/min; and pulmonary capillary wedge pressure, 13+/-4 mm Hg. Seven patients remained normotensive and could exercise at a fixed rate of 20 cycles/min. In these patients, peak VO2 declined from 17.3+/-3.9 to 13.0+/-6.1 mL. kg-1. min-1. In one of these patients, the device was explanted. CONCLUSIONS: Significant myocardial recovery after LVAD therapy in patients with end-stage congestive heart failure occurs in a small percentage of patients. Most of these patients have dilated cardiomyopathy. Exercise testing may be a useful modality to identify those patients in whom the device can be explanted.     

Midterm results with the Sorin Monostrut heart valve prosthesis

OBJECTIVE: To monitor the hematological and clinical sequelae of a single tilting disc cardiac valve prosthesis. DESIGN: Prospective nonrandomized trial. SETTING: University teaching hospital. PARTICIPANTS: All patients receiving a single mechanical cardiac valve prosthesis were offered the Sorin Monostrut valve if they met the criteria for valve use. Seventy-five per cent of the patients entered were in New York Heart Association (NYHA) functional class III or IV. One hundred and forty-seven patients were subsequently followed at three months and then yearly after valve implantation for seven years. MAIN OUTCOME MEASURES: At one year, preoperative indexes of hemolysis were compared with three-month and one-year postoperative values. Actuarial curves for survival, freedom from cerebrovascular events and explantation were constructed for the seven-year follow-up period. RESULTS: Hemolysis, as measured by lactate dehydrogenase values, commonly occurs preoperatively, remaining significantly elevated three months and one year following valve implantation. Serum haptoglobin was normal preoperatively but was significantly low at one year. Anemia was uncommon and most patients had normal reticulocyte counts at one year. At three years, 81% of patients were in NYHA functional class I. CONCLUSIONS: Midterm results show that this valve is structurally reliable and meets all current requirements for a safe mechanical valve.     

Use of the Nippon-Zeon pneumatic ventricular assist device as a bridge to cardiac transplantation

The Nippon-Zeon (NZ) ventricular assist device is a sac type, air driven, heterotopic, external pump. Its performance has been evaluated in Japan as a bridge to myocardial recovery. Few data are available on the device as a bridge to heart transplantation. Since 1991, 10 patients (9 men) were bridged to heart transplantation with NZ, all in biventricular support. The mean age was 39 +/- 13 years (range, 21-60 years), mean body weight was 75 +/- 13 kg (range, 51-95 kg). Five patients had a dilated cardiopathy, and five were ischemic (three acute myocardial infarctions). Despite maximal inotropic support, including enoximone in seven, epinephrine in three, and intraaortic balloon pumping in one, eight patients were anuric, three were in acute hepatic failure, and three were intubated. Preoperative hemodynamic and biologic values were: cardiac index, 1.57 +/- 0.4 l/min/m2; pulmonary capillary wedge pressure, 34 +/- 5 mmHg; creatinine, 200 +/- 80 mumol/l; blood urea nitrogen, 17.5 +/- 8 mmol/l; total bilirubin 36 +/- 6 mumol/l; aspartate aminotransferase, 1,000 +/- 2,000 IU/l. In all patients, a biventricular assist device was implanted without the use of cardiopulmonary bypass. Improvement occurred immediately in all but one. Mean left ventricular flow was 4.5 +/- 0.8 l/min. Anticoagulation was maintained with intravenous heparin. Recently for bleeding was required in one case (10%), and two patients had positive blood cultures that were successfully treated. There was no mechanical failure. Hemolysis was not significant (lactate dehydrogenase, 378 +/- 50 IU/l; plasma-free hemoglobin below 10 mg/dl). Each device was free of thrombi and deposits at time of explantation. One patient died while on assist. Nine patients (90%) were transplanted after 11 +/- 8 days (range, 1-32 days). Three died early after transplantation, one of graft failure, two of sepsis. Six patients (66%) could be discharged. The follow-up ranges from 7 to 28 months. NZ is a simple, reliable, pneumatic device driven by a light, silent console; it can be rapidly implanted without cardiopulmonary bypass in patients in desperate condition who are awaiting cardiac transplantation. The difficulty of patient rehabilitation while using this device should limit the duration of support to weeks to allow the patient to be in optimal condition for heart transplantation.     

Cardiomyoplasty after implantation of a pacemaker and cardioverter/defibrillator

Presently, a combination of two surgical methods improves the survival of patients with advanced ventricular dysfunction: implantable cardioverter/defibrillator implantation (which prevents sudden cardiac death) and cardiomyoplasty (which prevents further dilatation of the heart and provides additional cardiac assistance). We report the clinical course of a patient who had cardiomyoplasty after cardioverter/defibrillator implantation and pacemaker insertion. It is a rare case in which three different devices cardioverter/defibrillator, pacemaker, and cardiomyostimulator) are functioning together without crosstalk.     

Hemodynamic and physiologic changes during support with an implantable left ventricular assist device

To evaluate hemodynamic effectiveness and physiologic changes on the HeartMate 1000 IP left ventricular assist device (Thermo Cardiosystems, Inc., Woburn, Mass.), we studied 25 patients undergoing bridge to heart transplantation (35 to 63 years old, mean 50 years). All were receiving inotropic agents before left ventricular assist device implantation, 21 (84%) were supported with a balloon pump, and 7 (28%) were supported by extracorporeal membrane oxygenation. Six patients died, primarily of right ventricular dysfunction and multiple organ failure. Nineteen (76%) were rehabilitated, received a donor heart, and were discharged (100% survival after transplantation). Pretransplantation duration of support averaged 76 days (22 to 153 days). No thromboembolic events occurred in more than 1500 patient-days of support with only antiplatelet medications. Significant hemodynamic improvement was measured (before implantation to before explantation) in cardiac index (1.7 +/- 0.3 to 3.1 +/- 0.8 L/min per square meter; p < 0.001), left atrial pressure (23.7 +/- 7 to 9 +/- 7.5 mm Hg; p < 0.001), pulmonary artery pressure, pulmonary vascular resistance, and right ventricular volumes and ejection fraction. Both creatinine and blood urea nitrogen levels were significantly higher before implantation in patients who died while receiving support. Renal and liver function returned to normal before transplantation. We conclude that support with the HeartMate device improved hemodynamic and subsystem function before transplantation. Long-term support with the HeartMate device has a low risk of thromboemboli and makes a clinical trial of a portable HeartMate device a realistic alternative to medical therapy.     

The effects of cocaine preexposure on the acquisition of cocaine-induced taste aversions

OBJECTIVES: This study investigated the role of programmed ventricular stimulation (PVS) for arrhythmia risk prediction in patients with idiopathic dilated cardiomyopathy (IDC) and spontaneous nonsustained ventricular tachycardia (VT). BACKGROUND: Nonsustained VT in patients with IDC has been associated with a high incidence of sudden cardiac death. METHODS: Over the course of 4 years, 34 patients with IDC, a left ventricular (LV) ejection fraction < or = 35%, and spontaneous nonsustained VT underwent PVS. All patients were prospectively followed for 24+/-13 months. RESULTS: Sustained ventricular arrhythmias were induced in 13 patients (38%). Sustained monomorphic VT was induced in three patients (9%), and polymorphic VT or ventricular fibrillation (VF) in another 10 patients (29%). No sustained ventricular arrhythmia could be induced in 21 study patients (62%). Prophylactic implantation of third-generation defibrillators (ICDs) with electrogram storage capability was performed in all 13 patients with inducible sustained VT or VF, and in nine of 21 patients (43%) without inducible sustained VT or VF. There were no significant differences between the additional use of amiodarone, d,I-sotalol, and beta-blocker therapy during follow-up in patients with and without inducible VT or VF. During 24+/-13 months of follow-up, arrhythmic events were observed in nine patients (26%) including sudden cardiac deaths in two patients and ICD shocks for rapid VT or VF in seven patients. Arrhythmic events during follow-up occurred in four of 13 patients with inducible ventricular arrhythmias compared with five of 21 patients without inducible ventricular arrhythmias at PVS (31% vs. 24%, p=NS). CONCLUSION: PVS does not appear to be helpful for arrhythmia risk stratification in patients with IDC, a left ventricular ejection fraction < or =35%, and spontaneous nonsustained VT. Due to the limited number of patients, however, the power of this study is too small to exclude moderately large differences in outcome between patients with IDC with and without inducible VT or VF.     

Catheter ablation of incessant ventricular tachycardia: acute and long-term results

SUBJECTS: Seventeen patients with incessant ventricular tachycardia refractory to anti-arrhythmic therapy underwent catheter ablation between 1987 and 1993. Fifteen patients had coronary heart disease and two had dilated cardiomyopathy. The mean age of the patients was 65 +/- 8 and the mean left ventricular ejection fraction was 31 +/- 9%. METHODS: Ablation sites were selected on the basis of endocardial activation mapping, concealed entrainment or bundle branch mapping. Catheter ablation was performed with direct current in nine patients and with radiofrequency energy in eight patients. Incessant ventricular tachycardia was terminated by catheter ablation in all 17 patients. RESULTS: One patient died after the ablation procedure due to pericardial tamponade. During electrophysiological testing 5-14 days later, 7 of 16 patients (44%) had inducible sustained or non-sustained ventricular tachycardia. Five of them underwent implantation of an automatic cardioverter/defibrillator, and three of these experienced discharges of the device during a mean follow-up of 30 +/- 12 months. another patient underwent implantation of a cardioverter/defibrillator after spontaneous recurrence of ventricular tachycardia. Out of the nine patients without inducible ventricular tachycardia, one died as a result of sudden cardiac death, and another had spontaneous ventricular tachycardia. Thus, ventricular tachycardia recurred clinically in 6 of 16 patients (38%), in whom ventricular tachycardia with the same morphology as that of the ablated ventricular tachycardia could be determined only in one patient. CONCLUSION: Catheter ablation is the method of choice for the emergency treatment of patients with incessant ventricular tachycardia. Due to the high risk of recurrence, additional anti-arrhythmic management, such as the implantation of a cardioverter/defibrillator, has to be considered.     

Relationship between left ventricular morphology and postoperative cardiac function following valve replacement for mitral stenosis

The left ventricular myocardium excised from 14 patients who had mitral stenosis and who underwent mitral valve replacement was examined, and myocardial fibrosis was quantitated in relation to cardiac function. Conventional mitral valve replacement was performed with cold potassium-induced cardioplegia associated with systemic hypothermia (28 degrees C rectal temperature) and topical cooling. All 14 patients had perivascular fibrosis; the amounts ranged from 16% to 54% of the whole tissue excised. The mean left ventricular end-diastolic volume index (LVEDVI) determined by M-mode echocardiography increased significantly (p less than 0.001) from 66.9 +/- 4.6 ml/m2 preoperatively to 79.0 +/- 2.9 ml/m2 postoperatively. The difference between preoperative and postoperative LVEDVIs was significantly correlated (p less than 0.01) to the percentage of myocardial fibrosis (r = 0.72), in that the index increased postoperatively when myocardial fibrosis was more than 35% and decreased when fibrosis was less than 35%. After mitral valve replacement, the mean ejection fraction increased when fibrosis was less than 35% of whole tissue (+0.12 +/- 0.04) and decreased when fibrosis was greater than 35% (-0.02 +/- 0.02, p less than 0.01). No measured preoperative hemodynamic parameters were predictive of prognosis. These data suggest that the degree of myocardial fibrosis is related to left ventricular performance after mitral valve replacement.     

Identification of two novel 5'' noncoding exons in human MNB/DYRK gene and alternatively spliced transcripts

OBJECTIVES: This study was performed to determine the degree and time course over 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the cardiac allograft in transplanted patients. BACKGROUND: Diastolic dysfunction and to a certain extent systolic dysfunction are common cardiac findings after heart transplantation. The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely contributes to these derangements. METHODS: Cardiomyocyte diameter and percent fibrosis were determined in serial endomyocardial biopsy specimens obtained from 1 month up to 6 years following heart transplantation in 50 patients. Endomyocardial biopsy specimens from 40 patients with primary dilated cardiomyopathy and 11 normal subjects were similarly analyzed for control data. Analyses were performed in a blinded format using a validated computerized image analysis system (Optimas 5.2). RESULTS: Early (1 month) cardiomyocyte enlargement decreased to the smallest diameter 6 months posttransplant, but thereafter progressively increased by 10% to 20% over the subsequent 5- to 6-year period. Although not statistically established, principal stimuli may include a discrepancy in body size (recipient > donor), coronary allograft vasculopathy and posttransplant systemic hypertension. Percent myocardial fibrosis rose early (1 to 2 months) posttransplant and thereafter remained at the same modest level of severity. CONCLUSIONS: Cardiomyocyte diameter of the transplanted heart gradually increases over time, while percent myocardial fibrosis rises early and remains in a modestly elevated plateau after 2 months posttransplant. These histostructural changes likely contribute to the hemodynamic and cardiac functional alterations commonly observed posttransplant.     

Differential regulation of vitamin D receptors in clonal populations of a chronic myelogenous leukemia cell line

BACKGROUND: Both crystalloid and blood cardioplegia result in cardiac dysfunction associated with myocardial edema. This edema is partially due to the lack of myocardial contraction during cardioplegia, which stops myocardial lymph flow. As an alternative, acceptable surgical conditions have been created in patients undergoing coronary artery bypass operations with esmolol-induced minimal myocardial contraction. We hypothesized that minimal myocardial contraction during circulatory support using either standard cardiopulmonary bypass (CPB) or a biventricular assist device would prevent myocardial edema by maintaining cardiac lymphatic function and thus prevent cardiac dysfunction. METHODS: We placed 6 dogs on CPB and 6 dogs on a biventricular assist device and serially measured myocardial lymph flow rate and myocardial water content in both groups and preload recruitable stroke work only in the CPB dogs. In all dogs we minimized heart rate with esmolol for 1 hour during total circulatory support. RESULTS: Although myocardial lymph flow remained at baseline level during CPB and increased during biventricular assistance, myocardial water accumulation still occurred during circulatory support. However, as edema resolved rapidly after separation from circulatory support, myocardial water content was only slightly increased after CPB and biventricular assistance, and preload recruitable stroke work was normal. CONCLUSIONS: Our data suggest that minimal myocardial contraction during both CPB and biventricular assistance supports myocardial lymphatic function, resulting in minimal myocardial edema formation associated with normal left ventricular performance after circulatory support. The concept of minimal myocardial contraction may be a useful alternative for myocardial protection, especially in high-risk patients with compromised left ventricular function.     

The myocardial fibrosis in patients with dilated cardiomyopathy. The application of image analysis in the myocardial biopsies

BACKGROUND: The aim of our study is to investigate whether myocardial fibrosis measured by image analysis may be considered as an important and accurate index of dilated cardiomyopathy and its prognosis. METHODS: The study group consisted of 24 patients with dilated cardiomyopathy, which was diagnosed by echocardiography, radionuclide ventriculography, cardiac catheterization, and left ventricular endomyocardial biopsy. The patients' overall disability was conventionally expressed with the criteria for functional capacity. Using image analysis, the percentage of fibrosis in a total of 35 myocardial biopsies was accurately measured, followed by a study comparing the percentage of myocardial fibrosis and the clinical parameters (left ventricular ejection fraction and overall functional capacity), showing the degree of each patient's heart failure. RESULTS: A correlation was found among fibrosis, left ventricular ejection fraction, and overall functional capacity. The cases with small values of fibrosis (< 10%) have big values of ejection fraction and belong to Class I of overall functional capacity. The cases with big values of fibrosis (> 10%) belong to Classes III and IV of overall functional capacity and have small values of ejection fraction. The results of the comparative study were graphically presented and considered significant. CONCLUSION: Myocardial fibrosis measured by image analysis might be considered an important prognostic index of dilated cardiomyopathy.     

Comparison of clinical and morphologic cardiac findings in patients having cardiac transplantation for ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, and dilated hypertrophic cardiomyopathy

This article compares intergroup and intragroup clinical and morphologic findings in patients with ischemic cardiomyopathy (IC), idiopathic dilated cardiomyopathy (IDC), and dilated hypertrophic cardiomyopathy (HC) undergoing cardiac transplantation (CT). Few previous publications have described findings in native hearts explanted at the time of CT. The explanted heart in 92 patients having CT was examined in uniform manner with particular attention to the sizes of the ventricular cavities and the presence of and extent of ventricular scarring. Of the 92 hearts examined, 47 had IC, 35 had IDC, and 10 had dilated HC. Although considerable degrees of intragroup variation occurred, the mean degree of left ventricular dilatation was similar among the patients with IC, IDC, and dilated HC. All patients with IC had left ventricular free wall scarring more extensive than that involving the ventricular septum, but the intragroup variation in the amounts of scarring was considerable. Nine of the 10 patients with dilated HC also had ventricular wall scarring, but it was more extensive in the ventricular septum than in the left ventricular free wall and involvement of the right ventricular wall also was present. Eight (23%) of the 35 IDC patients also had grossly visible ventricular scars but they were small and only 1 of the 8 had coronary narrowing and that was not in the distribution of the scarring. Narrowing of 1 or more epicardial coronary arteries >75% in cross-sectional area by plaque was present in all 47 IC patients, in 8 of the 35 IDC patients (7 had no ventricular scars), and in none of the 10 dilated HC patients. Coronary angiography was the major clinical tool allowing separation of the IC, IDC, and HC patients. Coronary angiography did not detect narrowing in any of the 8 patients with IDC who were found to have coronary narrowing on anatomic study. Thus, among patients with IC, IDC, and dilated HC having CT, distinctive anatomic features allow separation of patients with IC, IDC, and dilated HC, but within each group considerable variation in left ventricular cavity size and extent of ventricular scarring occurs.     

Spironolactone: renaissance of anti-aldosterone therapy in heart failure?

Mortality of patients with severe congestive heart failure (CHF) is still high despite combined treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis. Further therapeutic regimens are needed which include reversal of adverse myocardial remodeling and subsequent ventricular dysfunction. One third of all patients with CHF have diastolic left ventricular (LV) dysfunction with preserved systolic function. In these patients myocardial collagen matrix is the major determinant of myocardial stiffness and therefore diastolic function. Cardiac fibroblasts, expressing mRNA for types I and III collagens which are the major fibrillar proteins of the myocardial collagen network and for matrix metalloproteinase (MMP) 1 which is the key enzyme for interstitial collagen degradation, are controlled by the renin-angiotensin-aldosterone (RAAS) system irrespective of hemodynamics and cardiac myocyte growth. In the rat with primary or secondary hyperaldosteronism, myocardial fibrosis occurs in the pressure overloaded, hypertrophied left and in the normotensive, nonhypertrophic right ventricle. In contrast, no fibrosis is found in either ventricle of rats with infrarenal aortic banding, when the RAAS is not activated, despite comparable systemic hypertension and LV hypertrophy. In cultured cardiac fibroblasts, either effector hormone of the RAAS, angiotensin (Ang) II and aldosterone (Aldo) stimulate collagen synthesis measured by 3H-proline incorporation under serum-free conditions. Aldo is able to stimulate collagen synthesis normalized per total protein synthesis in a dose-dependent manner and at concentrations (10(-9) M) which are comparable to stimulated states in vivo (e.g., CHF). While Aldo does not affect collagen degradation AngII significantly inhibits, MMP 1 activity that would lead to further accumulation of collagen in the myocardium. Specific AngII type I or Aldo receptor antagonists are able to abolish the AngII or Aldo-mediated increase in collagen synthesis, respectively. In vivo in rats with primary or secondary hyperaldosteronism, the Aldo antagonist spironolactone has been shown to prevent myocardial fibrosis in both ventricles irrespective of the development of LV hypertrophy and hypertension. Thus, in vivo and in vitro evidence could be provided that the mineralocorticoid. Aldo, plays a pivotal role in promoting myocardial fibrosis and can be antagonized by its competitive receptor blocker, spironolactone. This may be of particular clinical relevance in treating patients with CHF where the RAAS is activated leading to myocardial fibrosis with subsequent deterioration of myocardial function. Clinical trials are needed to confirm these experimental data. If the ongoing RALES mortality study will prove that survival and/or morbidity of patients with CHF are improved by combined ACE inhibitor/spironolactone treatment a renaissance of anti-aldosterone therapy in patients with CHF would occur.     

Distinction between arrhythmic and nonarrhythmic death after acute myocardial infarction based on heart rate variability, signal-averaged electrocardiogram, ventricular arrhythmias and left ventricular ejection fraction

OBJECTIVES: We investigated whether heart rate variability, the signal-averaged electrocardiogram (ECG), ventricular arrhythmias and left ventricular ejection fraction predict the mechanism of cardiac death after myocardial infarction. BACKGROUND: Postinfarction risk stratification studies have almost exclusively focused on predicting the risk of arrhythmic death. The factors that identify and distinguish persons at risk for arrhythmic and nonarrhythmic death are poorly known. METHODS: Heart rate variability, the signal-averaged ECG, ventricular arrhythmias and left ventricular ejection fraction were assessed in 575 survivors of acute myocardial infarction. The patients were followed up for 2 years; arrhythmic and nonarrhythmic cardiac deaths were used as clinical end points. During the follow-up period, 47 cardiac deaths occurred, 29 (62%) arrhythmic and 18 (38%) nonarrhythmic. RESULTS: All risk factors were associated with cardiac mortality in univariate analysis. With the exception of left ventricular ejection fraction, they were also predictors of arrhythmic death. Depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.001) were related to nonarrhythmic death. In multivariate analysis, depressed heart rate variability (p < 0.001) and runs of ventricular tachycardia (p < 0.05) predicted arrhythmic death. Nonarrhythmic death was associated with depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.01). By selecting patients with depressed heart rate variability, long filtered QRS duration or ventricular arrhythmias and excluding patients with the lowest ejection fraction, we identified a group in which 75% of deaths were arrhythmic. Similarly, by selecting patients with a low ejection fraction and excluding patients with the lowest heart rate variability, we identified a group in which 75% of deaths were nonarrhythmic. CONCLUSIONS: Arrhythmic death was associated predominantly with depressed heart rate variability and ventricular tachycardia runs, and nonarrhythmic death with low ejection fraction, ventricular ectopic beats and depressed heart rate variability. A combination of risk factors identified patient groups in which a majority of deaths were either arrhythmic or nonarrhythmic.     

Mechanical circulatory support in children

Nine children (aged 1.2-15 years) have been treated with mechanical circulatory support devices at our institution. Indications for treatment were acute cardiac allograft rejection (n = 4), postcardiotomy cardiogenic shock (n = 4), and bridge to cardiac transplantation (n = 1). Eight patients required left ventricular support, and one required biventricular support. A BioMedicus centrifugal pump was used in eight patients, and a Hemopump intra-aortic axial flow device was used in one patient. In two patients, an intra-aortic balloon pump was in place at the time that circulatory support was instituted. Mechanical support time ranged from 2 to 139 h, and the average flow index was 2.31 l/min per m2. Three patients required hemodialysis during support, and one patient required re-exploration because of mediastinal hemorrhage. Recovery of native ventricular function was assessed by transthoracic or transesophageal echocardiography, and weaning from the device was achieved by gradually decreasing pump flow in increments of 0.1 to 0.5 l/min. Seven patients were successfully weaned from support. Two hospital deaths occurred after circulatory support had been discontinued: one patient died of respiratory failure and the other of gram-negative pneumonia and sepsis. The five surviving patients experienced no significant complications, and their hemodynamic indices were normal at the time of discharge. At a mean follow-up of 28.8 months, these patients are leading active unrestricted lives, with no long-term device-related sequelae. Based on this experience, mechanical circulatory support is feasible in children who experience profound circulatory failure from a variety of causes.     

Complex cases in heart surgery

Between January 1968 and December 1993, 837 patients underwent cardiac operations with were either complex or performed in the presence of a life threatening disease of other vital organs. Of them 74 (8.8%) patients have died within 30 days after the operation. A substantial number of the operations and associated operative death included left ventricular (LV) aneurysmectomy or plication or LV endoaneurysmectomy with coronary artery bypass (CAB) grafts with or without other cardiac procedures, cardiac reoperations, CAB grafts and mitral or aortic valve replacement, combined mitral and aortic valve replacement (MAVR) with or without tricuspid valve replacement and CAB grafts, CAB grafting for an end-stage coronary artery disease (CAD), emergency CAB grafts for an acute myocardial infarction with cardiogenic shock, complex internal thoracic artery (ITA) grafting, and miscellaneous. The best results were achieved in CAB grafts for an end-stage CAD, complex ITA grafting, CAB grafts with mitral or aortic valve replacement, cardiac reoperations. MAVR and miscellaneous. This is probably, related to an intensive treatment of congestive heart failure (CHF) before the operation, pretreatment with the oxygen free radical inhibitor (allopurinol), selective use of an intraaortic balloon assist device and LV venting, routine use of hemoconcentrator (ultrafiltration) during cardiopulmonary bypass in those with CHF, thorough myocardial protection and a complete coronary revascularization.     

Effects of isoflurane on receptor-operated Ca2+ channels in rat aortic smooth muscle

OBJECTIVE: Map-guided procedures have been the accepted standard for ventricular tachycardia surgery. However, promising results of visually guided resections without mapping have been reported. The goal of this study was to evaluate the efficacy of large encircling cryoablation without mapping for ventricular tachycardia after anterior myocardial infarction. METHODS: Between 1985 and 1996, this procedure, along with aneurysmectomy, was performed on 38 patients for malignant ventricular tachycardia. The mean interval between the operation and myocardial infarction was 59.2 months; 7 patients (18.4%) were operated on within 1 month of myocardial infarction. The mean patient age was 62.1 +/-7.3 years and the mean left ventricular ejection fraction was 29.0% +/-7.2%. RESULTS: Hospital mortality was 2.6% (1 patient). The electrical success rate based on postoperative electrophysiologic studies was 94.5%. Overall electrical success rate was 89.1%. Freedom from ventricular tachycardia was 77% (95% CI 61%-94%) at both 5 and 7 years. Freedom from sudden cardiac death was 91% (95% CI 80%-100%) at both 5 and 7 years, with overall actuarial survivals at 5 and 7 years of 63% (95% CI 47%-80%) and 42% (95% CI 22%-63%), respectively. The main cause of late death was congestive heart failure in 62.6% of these patients. CONCLUSIONS: One can achieve good results without intraoperative mapping in the treatment of patients with ventricular tachycardia after anterior myocardial infarction by using large encircling cryoablation.     

Effects of brain death on myocardial function and ischemic tolerance of potential donor hearts

BACKGROUND: An increasing number of experimental and clinical studies reports hemodynamic instability in the donor organism after brain death. However, the relative importance of brain death-related cardiac dysfunction on posttransplantation cardiac function and the reversibility of the observed changes remain controversial. In this study a load-independent analysis of cardiac function after brain death was performed. Special interest was focused on a possible interactive influence of brain death and cardiac preservation on postischemic cardiac function. METHODS: In 12 anesthetized dogs, brain death was induced by inflation of a subdural balloon; 12 sham-operated animals served as control subjects. After a 2-hour observation in situ, the hearts were explanted and perfused parabiotically either immediately or after hypothermic ischemic preservation (4 hours, 4 degrees C). Heart rate, cardiac output, left ventricular pressure, the maximum of left ventricular pressure development and aortic pressure were measured in situ. In addition, the slope of the end-systolic pressure-volume relationship, coronary blood flow, and myocardial oxygen consumption were estimated in the cross-circulated hearts. RESULTS: In spite of a brain death-associated hemodynamic deterioration in situ (expressed as low mean aortic pressure and significant decrease of maximal dP/dt), myocardial function was similar to control after explantation, if assessed ex vivo. Furthermore, after hypothermic ischemic preservation and reperfusion, complete functional recovery of control and brain-dead hearts could be observed. CONCLUSIONS: These data indicate that hemodynamic instability after brain death may rather reflect altered loading conditions than irreversible myocardial damage or primary cardiac dysfunction. Furthermore, there is no evidence for a brain death-related impairment of ischemic tolerance.     

Beta adrenoceptor density in the donor heart: a guide to prognosis?

BACKGROUND: Failure of the donor (graft) heart is the main cause of mortality in the first month after orthotopic cardiac transplantation. In a preliminary study marked downregulation of cardiac beta adrenoceptor density was found in apparently normal donor hearts of recipients who developed severe cardiac failure soon after implantation. Cardiac beta adrenoceptors are an important factor in the development of cardiac failure in the human heart. The aim of this study therefore was to determine whether fatal graft failure in the first month after transplantation is associated with downregulation of beta adrenoceptor density in the donor heart. PATIENTS AND METHODS: Right ventricular endomyocardial biopsy specimens were taken from consecutive adult donor patients immediately before implantation. A previously described radioligand binding method was used to determine beta adrenoceptor density in consecutive patients who developed fatal graft failure and died within 1 month of transplantation and in a group of control donors transplanted during the same period. RESULTS: Perioperative fatal graft failure developed in 13 patients. Forty one specimens from donor hearts that were transplanted into recipients who did not develop fatal graft heart failure formed the control group. There were no systematic differences in donor or recipient characteristics between the graft heart failure and control groups. In particular donor catecholamine requirement and recipient pulmonary vascular resistance did not differ between groups. Total beta adrenoceptor density was reduced in the fatal graft heart failure group compared with that in the controls (13.4 (7) fmol/mg v 21 (7) fmol/mg; P < 0.01). There was a positive correlation between beta adrenoceptor density in the donor heart and time to death in the graft heart failure group (r2 = 0.3, P < 0.05). The beta adrenoceptor binding affinity (Kd) did not differ between the graft failure group and the controls (47 (6) pM v 44 (7) pM). CONCLUSION: The development of perioperative fatal cardiac failure after orthotopic cardiac transplantation is associated with downregulation of beta adrenoceptors in the donor heart before implantation.