Evidence for regional catecholamine uptake and storage sites in the transplanted human heart by positron emission tomography.

Positron emission tomography in combination with the newly introduced catecholamine analogue [11C]hydroxyephedrine ([11C]HED) enables the noninvasive delineation of sympathetic nerve terminals of the heart. To address the ongoing controversy over possible reinnervation of the human transplant, 5 healthy control subjects and 11 patients were studied after cardiac transplant by this imaging approach. Regional [11C]HED retention was compared to regional blood flow as assessed by rubidium-82. Transplant patients were divided into two groups. Group I had recent (less than 1 yr, 4.4 +/- 2.3 mo) surgery, while group II patients underwent cardiac transplantation more than 2 yr before imaging (3.5 +/- 1.3 yr). [11C]HED retention paralleled blood flow in normals, but was homogeneously reduced in group I. In contrast, group II patients revealed heterogeneous [11C]HED retention, with increased uptake in the proximal anterior and septal wall. Quantitative evaluation of [11C]HED retention revealed a 70% reduction in group I and 59% reduction in group II patients (P less than 0.001). In group II patients, [11C]HED retention reached 60% of normal in the proximal anterior wall. These data suggest the presence of neuronal tissue in the transplanted human heart, which may reflect regional sympathetic reinnervation.

Clinical outcome of patients with advanced coronary artery disease after viability studies with positron emission tomography.

OBJECTIVE: The aim of this study was to determine the prognostic significance of perfusion-metabolism imaging in patients undergoing positron emission tomography for myocardial viability assessment. BACKGROUND: Positron emission tomography using nitrogen-13 ammonia and 18fluorodeoxyglucose to assess myocardial blood flow and metabolism has been shown to predict improvement in wall motion after coronary artery revascularization. The prognostic implications of metabolic imaging in patients with advanced coronary artery disease have not been investigated. METHODS: Eighty-two patients with advanced coronary artery disease and impaired left ventricular function underwent positron emission tomographic imaging between August 1988 and March 1990 to assess myocardial viability before coronary artery revascularization. RESULTS: Forty patients underwent successful revascularization. Patients who exhibited evidence of metabolically compromised myocardium by positron emission tomography (decreased blood flow with preserved metabolism) who did not undergo subsequent revascularization were more likely to experience a myocardial infarction, death, cardiac arrest or late revascularization due to development of new symptoms than were the other patient groups (p less than 0.01). Concordantly decreased flow and metabolism in segments of previous infarction did not affect outcome in patients with or without subsequent revascularization. Those with a compromised myocardium who did undergo revascularization were more likely to experience an improvement in functional class than were patients with preoperative positron emission tomographic findings of concordant decrease in flow and metabolism. CONCLUSIONS: Positron emission tomographic myocardial viability imaging appears to identify patients at increased risk of having an adverse cardiac event or death. Patients with impaired left ventricular function and positron emission tomographic evidence for jeopardized myocardium appear to have the most benefit from a revascularization procedure.

P450 3A activity and cyclosporine dosing in kidney and heart transplant recipients.

Interpatient differences in the kinetics of cyclosporine appear to result in part from interindividual differences in the catalytic activity of an enzyme termed P450 3A. We investigated the relationship between P450 3A activity, as measured by the erythromycin breath test (ERMBT), and the appropriate stable daily dose of cyclosporine as currently determined by physicians at our institution. The ERMBT was administered to kidney and heart allograft recipients who had attended at least two monthly clinic visits without having their daily cyclosporine dose changed. There was a significant positive correlation between the ERMBT result and the daily cyclosporine doses (in milligrams per kilogram) in both the heart (r = 0.68; p = 0.04; n = 9) and kidney (r = 0.68; p = 0.03; n = 10) recipients. To confirm our findings, we prospectively administered the ERMBT on multiple occasions to 20 patients who were undergoing kidney transplantation. Although the transplant physicians were blinded to the ERMBT results, the test predicted the stable daily doses of cyclosporine that they ultimately prescribed to the patients (r = 0.54; p = 0.015). When data from all 39 patients were pooled and subjected to multiple regression analysis, the ERMBT was the only variable examined that significantly correlated with the stable daily cyclosporine dose (r = 0.63; p < 0.001; n = 39). In the 20 patients prospectively studied, the prescribed daily dose of cyclosporine generally decreased during the months after surgery and the percentage changes in cyclosporine daily dose correlated with changes in P450 3A activity during this period (r = 0.47; p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

A randomized prospective comparison of MALG with OKT3 for rescue therapy of acute myocardial rejection.

A randomized prospective trial for rescue therapy from acute myocardial rejection was undertaken utilizing Minnesota antilymphoblastic globulin (n = 15) versus murine monoclonal anti-CD3 antibody therapy (OKT3) (n = 14). Patients included in the study had moderate rejection unresponsive to bolus high-dose steroid therapy, or moderate-to-severe rejection with hemodynamic instability. Analysis was performed using the t test and chi-square, significance was P less than 0.05. Patient age, sex, interval from transplant to treatment, and number of unresponsive patients vs. hemodynamically unstable patients were similar in both groups (P greater than 0.05). Initial resolution occurred in 9/15 MALG- vs. 14/14 OKT3-treated patients (P = 0.017). Secondary resolution following repeat treatment occurred in 5/6 remaining MALG patients, for a final resolution of 14/15 MALG vs. 14/14 OKT3 patients (P = NS). Rebound rejection was not significantly different (1/14 MALG vs. 4/13 OKT3). However, 7/14 OKT3-treated patients developed life-threatening infections (1 CMV pancreatitis, 2 CMV pneumonias, 1 systemic candidiasis, 3 CMV viremia) vs. 1/15 MALG-treated patients (CMV viremia) (P = 0.014). Death occurred in 4/14 OKT3- (infection) vs. 1/14 MALG- (rejection) treated patients (P = NS). There were no significant differences in the rate of resolution, rebound, infection, or outcome between unresponsive or hemodynamically unstable patients within either group. Although initial rescue is significantly better with OKT3, final resolution is the same in both groups. Since there was a significant incidence of life-threatening infections (7/14) leading to 4 deaths with OKT3 treatment, we recommend MALG for rescue therapy of refractory acute myocardial rejection if this immunosuppressive regimen is to be used.

Accuracy of intraoperative transesophageal echocardiography for estimating the severity of functional mitral regurgitation.

Although intraoperative transesophageal echocardiography (TEE) is used to guide mitral valve reconstructive procedures, the effects of hemodynamic alterations accompanying general anesthesia on mitral regurgitation (MR) are unknown. This study was performed to evaluate the effect of general anesthesia on MR jet size using TEE with color Doppler imaging in patients undergoing mitral valve surgery. Matched preoperative TEEs performed with the patient under intravenous conscious sedation, and intraoperative studies performed with the patient under general anesthesia were retrospectively reviewed in 46 patients undergoing mitral valve surgery. Patients were divided into groups based on etiology of MR, including 21 patients with myxomatous degeneration and leaflet flail, 19 patients with structurally normal leaflets and functional regurgitation due to abnormal leaflet coaptation, and 6 patients with rheumatic mitral disease. On both preoperative and intraoperative studies, regurgitation was quantified using maximal jet area and jet diameter at the vena contracta on color flow Doppler. Patients with leaflet flail and patients with functional MR had similar measures of regurgitation severity on preoperative imaging. On intraoperative imaging, regurgitant jet size was unchanged compared with preoperative studies among patients with leaflet flail (jet diameter 1.04 +/- 0.26 vs 1.10 +/- 0.28 cm, area 9.8 +/- 4.5 vs 10.1 +/- 5.2 cm2 on preoperative studies), although jet size decreased significantly in patients with functional MR (jet diameter 0.79 +/- 0.33 vs 1.10 +/- 0.29 cm [p < 0.001], area 5.7 +/- 3.5 vs 10.0 +/- 3.8 cm2 [p < 0.001] on preoperative studies). These findings were not accounted for by variation in heart rate, blood pressures, echocardiographic instrumentation, or Doppler Nyquist limit.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased sarcolemmal glucose transporter abundance in myocardial ischemia.

Many clinical and laboratory studies suggest that an increase in glucose uptake and metabolism by ischemic myocardium helps protect myocardial cells from irreversible injury. We have examined whether increased sarcolemmal abundance of cardiomyocyte glucose transporters plays a role in this adaptive response. We have shown that acute myocardial ischemia in perfused rat hearts results in increased sarcolemmal abundance of the major glucose transporter, GLUT4, by causing translocation of GLUT4 molecules from an intracellular compartment to the sarcolemma. In nonischemic control hearts only 18 +/- 2.8% of GLUT4 molecules were on the sarcolemma whereas in ischemic hearts this increased to 41 +/- 9.3%. Insulin also caused translocation of GLUT4 molecules to the sarcolemma, and resulted in 61 +/- 2.6% of GLUT4 molecules on the sarcolemma. The combination of ischemia and insulin did not result in additive increases in sarcolemmal GLUT4 abundance. In more persistent or chronic ischemia, the other major myocardial glucose transporter, GLUT1, appears to play an important role. The mRNA for this transporter, which is constitutively expressed on cardiomyocyte sarcolemma, was increased 2.0-fold in regions of hibernating myocardium in humans with coronary heart disease as well as in persistently hypoxic rat neonatal cardiomyocytes in primary culture. In neither of these conditions was GLUT4 mRNA expression increased. Thus, acute myocardial ischemia increases sarcolemmal glucose transporter abundance mainly by translocating previously synthesized GLUT4 molecules from an intracellular compartment, whereas more chronic ischemia also increases GLUT1 abundance via enhanced mRNA expression. Increased GLUT1 and GLUT4 abundance may participate in the augmented glucose uptake of ischemic myocardium and therefore may help protect ischemic myocardium from irreversible injury.

Emergent percutaneous cardiopulmonary bypass in patients having cardiovascular collapse in the cardiac catheterization laboratory.

Percutaneous cardiopulmonary bypass (PCB) was instituted in 30 initially stable patients who developed either cardiac arrest refractory to resuscitation (n = 7) or cardiogenic shock (mean arterial blood pressure < 50 mm Hg unresponsive to fluid resuscitation or vasopressors) (n = 23) after a catheterization laboratory complication. Events leading to collapse included abrupt closure during percutaneous transluminal coronary angioplasty (PTCA) (n = 22), complications from diagnostic cardiac catheterization (n = 6), left ventricular perforation during mitral valvuloplasty (n = 1), and right ventricular perforation during pericardiocentesis (n = 1). PCB was initiated within 20 minutes of cardiovascular collapse in 83% of patients (arrest: 21 +/- 13 minutes [range 10 to 50]; and shock: 17 +/- 6 minutes [range 10 to 30]). Mean arterial blood pressure increased on PCB from 0 to 56 mm Hg in patients with cardiac arrest and from 37 to 63 mm Hg in those with cardiogenic shock at mean PCB flow rates of 2.5 to 5.0 liters/min. Subsequent therapy on PCB included emergent cardiac surgery (n = 14), PTCA (n = 13) and medical therapy (n = 3). Six patients (20%) survived to hospital discharge (3 with cardiac surgery, 2 with PTCA, and 1 with medical therapy). All 7 patients with refractory cardiac arrest died despite further interventions on PCB, whereas 6 of 23 (26%) with cardiogenic shock survived to hospital discharge. Thus, in response to cardiovascular collapse in the catheterization laboratory, PCB does not salvage patients who do not regain a stable cardiac rhythm. PCB can stabilize patients who develop cardiogenic shock for further interventions which are lifesaving in only a minority of patients.

Complete atrioventricular block after valvular heart surgery and the timing of pacemaker implantation.

The natural history of patients who developed complete atrioventricular block after valvular heart surgery was investigated to determine the optimal timing for pacemaker implantation. Patients who developed complete atrioventricular block within 24 hours after operation, which then persisted for > 48 hours, were unlikely to recover; such patients could potentially undergo earlier pacemaker implantation if otherwise ready for discharge.

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.

Mitral valve reconstruction in elderly, ischemic patients.

The role of mitral valve reconstruction is controversial in elderly patients with concurrent ischemic heart disease owing to technical difficulty, prolonged operative times, high mortality, and possible residual mitral regurgitation. However, mitral reconstruction could be most beneficial in this age group due to preservation of left ventricular function, avoidance of anticoagulation, or repeat operation for bioprosthetic degeneration. We studied the outcome of mitral valve reconstruction in 100 consecutive elderly ischemic patients 65 years or older (mean = 73 years; range, 65 to 86 years) operated on between October 1990 and May 1995. Preoperatively all patients were New York Heart Association (NYHA) class III or IV with an ejection fraction of 32 +/- 2%. All patients underwent primary coronary bypass grafting (2.7 +/- 0.2 grafts) and had a flexible mitral annuloplasty ring inserted. Additionally, 54 patients required further complex mitral repairs. All patients had 4+ mitral regurgitation by transesophageal echocardiography prior to operation. After mitral reconstruction, no patient had more than 1+ regurgitation, while most had none and no systolic anterior leaflet motion was noted. There were 4 early (30 day) deaths (4%) and 6 late deaths (6%) at a mean follow-up of 25 months. Patient morbidity has included episodes of mild congestive heart failure (nine), transient ischemic attack (one), endocarditis (one), and respiratory failure (five). There have been one early and two late reoperations for mitral valve replacement. All remaining patients are in NYHA class I or II. While longer-term follow-up is mandatory, coronary bypass grafting and mitral valve reconstruction in the elderly can be accomplished with acceptable surgical mortality and morbidity, yielding reliable improvement in symptoms and quality of life.

Aortobronchial fistula 13 years following repair of aortic transection.

We describe a 56-year-old man with the new onset of hemoptysis, increasing in frequency and magnitude, initially diagnosed and treated as pulmonary embolism. Bronchoscopy, computed tomography, and thoracic aortography were performed twice before the diagnosis was made. Thirteen years previously, the patient underwent thoracic aortic interposition graft placement for aortic laceration as a result of a motor vehicle accident. The second aortogram demonstrated a small pseudoaneurysm at the expected proximal graft suture line. Aortobronchial fistula, a rare cause of hemoptysis, was diagnosed. The patient underwent successful resection of the graft and placement of a new dacron interposition graft. All cultures, including blood, sputum, and operative specimen cultures, were negative. The patient is alive and well 1 year following surgery.

Regulatory effects of interleukin-10 on lung ischemia-reperfusion injury.

OBJECTIVE: Interleukin-10, a cytokine with antiinflammatory activities, was studied to determine its effects on development of early lung reperfusion injury. METHODS: Adult male rats underwent 90 minutes of left lung ischemia followed by 4 hours of reperfusion. Time-matched sham-operated control rats underwent hilar dissection but not lung ischemia. Lung injury was measured by vascular permeability to bovine serum albumin tagged with iodine 125. To evaluate the effect of exogenous interleukin-10, additional animals received interleukin-10 intravenously before ischemia. To assess the role of endogenous interleukin-10, animals received rabbit antimouse interleukin-10 immunoglobin G (or preimmune rabbit immunoglobin G) before ischemia. RESULTS: Compared with sham control rats, ischemia-reperfusion control rats demonstrated significantly more lung injury. Animals receiving interleukin-10 had significantly less lung injury than did ischemia-reperfusion control rats. Animals receiving antiinterleukin-10 had significantly more lung injury than did animals receiving preimmune immunoglobin G. Alveolar macrophages from animals after 90 minutes of lung ischemia produced more tumor necrosis factor-alpha in culture than did unstimulated macrophages; this production was reduced significantly by the addition of interleukin-10 to the culture medium. CONCLUSION: Endogenous interleukin-10 has a protective effect against early lung reperfusion injury, and interleukin-10 administration can reduce lung reperfusion injury, perhaps in part through its ability to reduce production by alveolar macrophages of tumor necrosis factor-alpha, a known proinflammatory cytokine.

Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy.

Uncontrollable severe mitral regurgitation is a frequent complication of end-stage cardiomyopathy, significantly contributing to heart failure in these patients, and predicts a poor survival. Although elimination of mitral valve regurgitation could be most beneficial in this group, corrective mitral valve surgery has not been routinely undertaken in these very ill patients because of the presumed prohibitive operative mortality. We studied the early outcome of mitral valve reconstruction in 16 consecutive patients with cardiomyopathy and severe, refractory mitral regurgitation operated on between June 1993 and April 1994. There were 11 men and five women, aged 44 to 78 years (64 +/- 8 years) with left ventricular ejection fractions of 9% to 25% (16% +/- 5%). Preoperatively all patients were in New York Heart Association class IV, had severe mitral regurgitation (graded 0 to 4+ according to color flow Doppler transesophageal echocardiography) and two were listed for transplantation. Operatively, a flexible annuloplasty ring was implanted in all patients. Four patients also had single coronary bypass grafting for incidental coronary disease. In four patients the operation was performed through a right thoracotomy because of prior coronary bypass grafting, and four patients also underwent tricuspid valve reconstruction for severe tricuspid regurgitation. No patient required support with an intraaortic balloon pump. There were no operative or hospital deaths and mean hospital stay was 10 days. There were three late deaths at 2, 6, and 7 months after mitral valve reconstruction, and the 1-year actuarial survival has been 75%. At a mean follow-up of 8 months, all remaining patients are in New York Heart Association class I or II, with a mean postoperative ejection fraction of 25% +/- 10%. There have been no hospitalizations for congestive heart failure, and a decrease in medications required has been noted. For patients with cardiomyopathy and severe mitral regurgitation, mitral valve reconstruction as opposed to replacement can be accomplished with low operative and early mortality. Although longer term follow-up is mandatory, mitral valve reconstruction may allow new strategies for patients with end-stage cardiomyopathy and severe mitral regurgitation, yielding improvement in symptomatic status and survival.

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.

Diagnosis of unilateral mainstem bronchial obstruction following single-lung transplantation with routine spirometry.

Single-lung transplantation has become a treatment option for many patients with advanced pulmonary disease. Recent advances in surgical technique and refined immunosuppressive regimens have led to improvement in long-term outcomes, but postoperative complications, including airway disorders, remain problematic. Serial spirometry with flow-volume loops is sensitive in detecting early small-airway disease associated with lung allograft rejection or bronchiolitis obliterans, but its role in the diagnosis of large-airway disease in the posttransplantation setting has not been delineated. In this report, we describe a novel alteration in the configuration of the flow-volume loop in a patient who developed unilateral mainstem bronchial obstruction following single-lung transplantation for severe emphysema. Surveillance spirometry performed 6 weeks after transplantation demonstrated a new initial plateau in the maximal expiratory flow-volume curve suggestive of a variable intrathoracic airway obstruction. This unique aberration in the flow-volume curve sheds new insight into the physiologic abnormalities of spirometry in patients receiving lung transplants.

Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity.

Hypothermic circulatory arrest has become an accepted technique for a variety of cardiac and complex aortic operations. However, prolonged periods (> 45 min) of hypothermic circulatory arrest in older patients is associated with marginal cerebral protection and an increased incidence of adverse neurologic events. In an effort to minimize such morbidity, we used a technique of retrograde cerebral perfusion with continuous monitoring of cerebral hemoglobin oxygen saturation during hypothermic circulatory arrest in 35 patients who underwent thoracic aortic operations or resection of intracardiac tumor. There were 27 men and 8 women (mean age 60 years, range 21 to 83 years). Sixteen patients had acute dissection, 6 had contained rupture of a thoracic aortic aneurysm, 10 had either a chronic dissection or aneurysm, and 3 had hypernephromas extending into the heart. Six patients underwent root replacement by means of an open technique for their distal anastomosis, 7 underwent root and partial arch replacement, 12 had root and total arch replacement, 7 had total arch replacement, and 3 had resection of tumor in the heart and retrohepatic vena cava. Seven patients had simultaneous coronary artery bypass grafting, 3 had replacement of one of the arch vessels, and 2 patients had a cesarean section. Sixteen cases were emergency, 6 urgent, and 13 elective. Nine (26%) were reoperations. Thirty-four patients underwent the procedure via a median sternotomy and one patient through a posterolateral thoracotomy. The mean retrograde cerebral perfusion time was 63 minutes (range 35 to 128 minutes), with 30 (86%) patients having more than 45 minutes, 12 (34%) having more than 65 minutes, and 4 (11%) having more than 90 minutes. There was 1 operative death caused by a preoperative myocardial infarction from an aortic dissection, and there were 2 late deaths (multiple organ failure and ruptured total aortic aneurysm). One patient had a stroke with a residual right hemiplegia and a pronounced aphasia. There were no other significant neurologic events or reoperations for bleeding. The average length of stay for patients having elective operations was 11 days and for those having emergency operations, 27 days. At a mean follow-up of 6 months all surviving patients (91%) are well. Hypothermic circulatory arrest is a relatively simple technique that provides a bloodless field and good visualization without the need for aortic crossclamps. Moreover, retrograde cerebral perfusion with continuous monitoring of cerebral oxygen saturation extends the "safe" time for hypothermic circulatory arrest, allowing ample opportunity to perform complicated cardiac and aortic operations with reduced risk of adverse neurologic events.

Cardiopulmonary exercise testing following allogeneic lung transplantation for different underlying disease states.

OBJECTIVES: To assess the exercise response to single lung transplantation in chronic airflow obstruction (CAO), idiopathic pulmonary fibrosis (IPF), and pulmonary vascular disease (PVD) vs double lung transplantation at well-defined time points after transplantation, and to define the change in exercise response in SLT and DLT over the first year after transplantation. DESIGN: Prospective study. SETTING: Tertiary referral hospital. PATIENTS: Fourteen stable SLT recipients (6 with CAO, 4 with IPF, 4 with PVD) and 11 stable DLT recipients. MEASUREMENTS: Spirometry, lung volumes, diffusion lung capacity for carbon monoxide (DLco) and MVV measured prior to exercise at 3 months (n = 25) then at 3-month intervals up to a maximum of 12 months post-transplantation (n = 18 [12 SLT and 6 DLT]). Symptom-limited cardiopulmonary exercise tests at same time points (n = 25 at 3 months, n = 18 [12 SLT and 6 DLT] at 3-month intervals up to 12 months). Breathlessness was estimated by visual analogue scale prior to exercise and at peak exercise. RESULTS: At 3 months, FEV1 percent predicted was lower for SLT-CAO and SLT-IPF vs DLT (p < or = 0.05). Mean FEV1/FVC was lower for SLT-CAO vs all other groups (p < or = 0.05). The FVC, MVV, and DLco/VA were similar for all groups. The TLC and RV were higher for the SLT-CAO group compared with all others. The TLC was lower for SLT-PVD compared with DLT. Exercise responses were similar in all groups studied without a statistically significant difference in achieved VO2, work rate, O2 pulse, anaerobic threshold, heart rate response, respiratory rate, VE/MVV, and VT/VC. The change in O2 saturation during exercise was the least in recipients of DLT. Maximal achieved VO2 rose from 3 to 6 months after SLT but dropped by 9 to 12 months after transplantation. Maximal achieved VO2 trended up from 3 to 6 months after DLT but dropped by 9 to 12 months after transplantation. Maximal achieved work rate rose in both SLT and DLT from 3 to 9 to 12 months after transplantation. There was no significant difference in breathlessness at rest and peak exercise measured between recipients of SLT or DLT. CONCLUSIONS: Minor differences in pulmonary function and change in O2 saturation occur between recipients of SLT and DLT during the first posttransplant year. These differences are most pronounced when comparing SLT-CAO with DLT. However, there is no significant difference in exercise capacity between SLT for CAO, IPF, PVD, and DLT. The rise in maximum achieved VO2 over the first 6 months after transplantation may reflect the effects of exercise training and should be taken into account when examining aerobic response after transplantation.

The artificial heart in human subjects.

In preparation for clinical implantation of the Utah J-7 pneumatic artificial heart as a permanent cardiac substitute, the device was implanted into five brain-dead human subjects. This report presents our results and details our two most successful trials. Three different surgical implant techniques were utilized in the five subjects. Because of the unique "no risk" situation of the subjects, the function of the artificial heart could be tested in a manner not advisable in patients, but necessary for clinical preparation. The implantable total artificial heart was able to maintain physiological hemodynamics in two subjects for 41 and 72 hours at which time the trials were electively terminated.

Complement activation during cardiopulmonary bypass. Comparison of bubble and membrane oxygenators.

A prospective randomized trial involving 91 patients undergoing cardiopulmonary bypass compared the effects of bubble oxygenators (with and without methylprednisolone sodium succinate) and membrane oxygenators on complement activation and transpulmonary sequestration of leukocytes. Patients were divided as follows: Group I, 30 patients, bubble oxygenator; Group II, 31 patients, bubble oxygenator and methylprednisolone sodium succinate (30 mg/kg); Group III, 30 patients, membrane oxygenator. In Group I, C3a increased from 323 +/- 171 ng/ml during cardiopulmonary bypass to 1,564 +/- 785 ng/ml at 25 minutes after bypass (p less than 0.0001). A significant decrease in C3a was found in Groups II and III compared to Group I (p less than 0.0001). C5a did not change significantly during cardiopulmonary bypass in any group. Reestablishment of pulmonary circulation at the end of bypass produced significant transpulmonary leukocyte sequestration in Group I; the median cell difference was 1,700/microliter. Transpulmonary sequestration was significantly (p less than 0.0001) less in Group II (median cell difference = 200/microliter) and in Group III (median cell difference = 400/microliter) than in Group I. We conclude that cardiopulmonary bypass with a bubble oxygenator alone initiates significantly (p less than 0.0001) more C3a activation and leukocyte sequestration than when methylprednisolone sodium succinate (30 mg/kg) is given 20 minutes before the start of cardiopulmonary bypass with a bubble oxygenator or when a silicone membrane oxygenator is used.

Implications of increased left ventricular mass index on in-hospital outcomes in patients undergoing aortic valve surgery.

BACKGROUND: Increased left ventricular mass index has been shown to be associated with higher mortality in epidemiologic studies. However, the effect of increased left ventricular mass index on outcomes in patients undergoing aortic valve replacement is unknown. METHODS: We studied 473 consecutive patients undergoing elective aortic valve replacement to assess the influence of left ventricular mass index on outcomes in patients having this procedure. Echocardiographic left ventricular dimensions were used to calculate left ventricular mass index (considered increased if >134 g/m(2) in male patients and >110 g/m(2) in female patients). RESULTS: Left ventricular mass index was increased in 24% of patients undergoing aortic valve replacement. Postprocedural complications (respiratory failure, renal insufficiency, congestive heart failure, and atrial and ventricular arrhythmias), length of stay in the intensive care unit, and in-hospital mortality were increased in patients with increased left ventricular mass index. Multivariable analysis identified prior valve surgery (odds ratio, 4.3; 95% confidence interval, 1.2-15.7; P =.030), left ventricular ejection fraction (odds ratio, 1.07; 95% confidence interval, 1.01-1.14; P =.020), history of hypertension (odds ratio, 8.2; 95% confidence interval, 2.2-30.4; P =.002), history of liver disease (odds ratio, 50.4; 95% confidence interval, 4.2-609.0; P =.002), and increased left ventricular mass index (odds ratio, 38; 95% confidence interval, 9.3-154.1; P <.001) as independent predictors of in-hospital mortality. Furthermore, low output syndrome was identified as the most common mode of death (36%) after aortic valve replacement in patients with increased left ventricular mass index. CONCLUSIONS: Increased left ventricular mass index is associated with increased adverse in-hospital clinical outcomes in patients undergoing aortic valve replacement. Although this finding warrants special modification in perioperative management, further studies are needed to address whether outcomes in asymptomatic patients with aortic valve disease could be improved by earlier aortic valve replacement before a significant increase in left ventricular mass index.