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W A Baumgartner

Publications and source records attributed to W A Baumgartner.

At least 37 records · Page 2Linked to original sources
PubMed1999

Nitric oxide mediates neurologic injury after hypothermic circulatory arrest.

BACKGROUND: Prolonged hypothermic circulatory arrest (HCA) causes neurologic injury. However, the mechanism of this injury is unknown. We hypothesized that HCA causes nitric oxide production to result in neuronal necrosis. This study was undertaken to determine whether the neuronal nitric oxide synthase inhibitor 17477AR reduces necrosis after HCA. METHODS: Thirty-two dogs underwent 2 hours of HCA at 18 degrees C. Nitric oxide synthase catalytic assay and intracerebral microdialysis for nitric oxide production were performed in acute nonsurvival experiments (n = 16). Sixteen animals survived for 72 hours after HCA: Group 1 (n = 9) was treated with 17477AR (Astra Arcus), and group 2 (n = 7) received vehicle only. Animals were scored from 0 (normal) to 500 (coma) for neurologic function and from 0 (normal) to 100 (severe) for neuronal necrosis. RESULTS: Administration of 17477AR reduced nitric oxide production in the striatum by 94% (HCA alone), 3.65+/-2.42 micromol/L; HCA and 17477AR, 0.20+/-0.14 micromol/L citrulline). Dogs treated with 17477AR after HCA had superior neurologic function (62.22+/-29.82 for group 1 versus 141.86+/-61.53 for group 2, p = 0.019) and significantly reduced neuronal necrosis (9.33+/-4.67 for group 1 versus 38.14+/-2.23 for group 2, p<0.00001) compared with untreated HCA dogs. CONCLUSIONS: Our results provide evidence that neuronal nitric oxide synthase mediates neuronal necrosis after HCA and plays a significant role in HCA-induced neurotoxicity. Pharmacologic strategies to inhibit neuronal nitric oxide synthase after the ischemic period of HCA may be clinically beneficial.

Amidines↗
PubMed1999

Increased intracerebral excitatory amino acids and nitric oxide after hypothermic circulatory arrest.

BACKGROUND: Prolonged hypothermic circulatory arrest (HCA) results in neurologic injury, but the mechanism of this injury is unknown. This study was undertaken to measure quantitatively intracerebral excitatory amino acids and citrulline, an equal coproduct of nitric oxide, during HCA. We hypothesized that HCA resulted in higher levels of glutamate, aspartate, glycine, causing increased intracellular calcium, and therefore, nitric oxide and citrulline. METHODS: Ten dogs underwent intracerebral microdialysis and 2 hours of HCA at 18 degrees C. Effluent was analyzed by high performance liquid chromatography with electrochemical detection. Five dogs each were sacrificed at 8 and 20 hours after HCA. Neuronal apoptosis was scored from 0 (no injury) to 100 (severe injury). RESULTS: Time course of HCA was divided into six periods. Peak levels of amino acids in each period were compared with those at baseline. Glutamate, coagonist glycine, and citrulline, an equal coproduct of nitric oxide, increased significantly over baseline during HCA, cardiopulmonary bypass, and 2 to 8 hours after HCA. Aspartate increased significantly during HCA and 8 to 20 hours after HCA. Apoptosis score was 65.56 +/- 5.67 at 8 hours and 30.63 +/- 14.96 at 20 hours after HCA. CONCLUSIONS: Our results provide direct evidence that HCA causes increased intracerebral glutamate and aspartate, along with coagonist glycine. We conclude that HCA causes glutamate excitotoxicity with subsequent nitric oxide production resulting in neurologic injury, which begins during arrest and continues until 20 hours after hypothermic circulation arrest. To provide effective cerebral protection, pharmacologic strategies to reduce glutamate excitotoxicity require intervention beyond the initial ischemic insult.

Animals↗
PubMed1999

Operative management of Marfan syndrome: The Johns Hopkins experience.

BACKGROUND: Doctor Antoine Marfan described the first case of Marfan syndrome in 1896. It was over 50 years later that the development of aortic aneurysms and subsequent rupture was appreciated as the most life-threatening component of the syndrome. METHODS: Doctor Vincent Gott, at our institution, performed the first Bentall procedure for an aneurysm of the ascending aorta in 1976. Since that time, the aortic root has been replaced in 231 Marfan patients. Of this group, 218 patients had a composite graft repair, 11 had an aortic root replacement with a homograft, and 2 patients had valve sparing procedures. There were 168 males and 63 females. Of the total 231 patients, 150 were operated on by Dr Gott. The remaining 81 patients were operated on by 10 other Hopkins surgeons. The average diameter of the ascending aorta was 6.8 cm, with a range from 4.5 to 10. The average aortic diameter of 43 patients who had an ascending aortic dissection was 7.3 cm. Fourteen of these patients had dissection with an aortic diameter of 6.5 cm or less. RESULTS: Among the 198 patients who underwent elective repair, there was no 30-day mortality. Thirty-three patients underwent urgent repair with 2 deaths, yielding a 30-day mortality of 6.1%. The mortality for the entire group of patients was 0.9%. Complications associated with this series of patients included 8 with endocarditis, 7 with thromboembolism, and 4 late coronary dehiscences. Actuarial survival was 88% at 5 years, 81% at 10 years, and 75% at 20 years. Multivariate analysis revealed New York Heart Association classification, male gender and urgent surgery as independent risk factors for mortality. CONCLUSION: Marfan patients with aortic aneurysms can undergo elective surgery with a low operative risk and excellent long-term survival with low morbidity. We feel that elective resection of an aneurysm in a Marfan patient should occur when it approaches a diameter of 5.5 cm. It is essential that a timely diagnosis be made in this group of young patients.

Adolescent↗
PubMed1999

Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury?

BACKGROUND: Central nervous system dysfunction continues to produce significant morbidity and associated mortality in patients undergoing cardiac surgery. Using a closed-chest canine cardiopulmonary bypass model, dogs underwent 2 h of hypothermic circulatory arrest (HCA) at 18 degrees C, followed by resuscitation and recovery for 3 days. Animals were assessed functionally by a species-specific behavioral scale, histologically for patterns of selective neuronal necrosis, biochemically by analysis of microdialysis effluent, and by receptor autoradiography for N-methyl-D-aspartate (NMDA) glutamate receptor subtype expression. RESULTS: Using a selective NMDA (glutamate) receptor antagonist (MK801) and an AMPA antagonist (NBQX), glutamate excitotoxicity in the development of HCA-induced brain injury was documented and validated. A microdialysis technique was employed to evaluate the role of nitric oxide (NO) in neuronal cell death. Arginine plus oxygen is converted to NO plus citrulline (CIT) by the action of NO synthase (nNOS). CIT recovery in the cerebrospinal fluid and from canine cortical homogenates increased during HCA and reperfusion. These studies demonstrated that neurotoxicity after HCA involves a significant and early induction of nNOS expression, and neuronal processes leading to widespread augmentation of NO production in the brain. To further investigate the production of excitatory amino acids in the brain, we hypothesized the following scenario: HCA--> increased glutamate, increased aspartate, increased glycine--> increased intracellular Ca2+--> increased NO + CIT. Using the same animal preparation, we demonstrated that HCA caused increased intracerebral glutamate and aspartate that persists up to 20 h post-HCA. HCA also resulted in CIT (NO) production, causing a continued and delayed neurologic injury. Confirmatory evidence of the role of NO was demonstrated by a further experiment using a specific nNOS inhibitor, 7-nitroindazole. Animals underwent 2 h of HCA, and then were evaluated both physiologically and for NO production. 7-Nitroindazole reduced CIT (NO) production by 58.4 +/- 28.3%. In addition, dogs treated with this drug had superior neurologic function compared with untreated HCA controls. CONCLUSIONS: These experiments have documented the role of glutamate excitotoxicity in neurologic injury and have implicated NO as a significant neurotoxin causing necrosis and apoptosis. Continued research into the pathophysiologic mechanisms involved in cerebral injury will eventually yield a safe and reliable neuroprotectant strategy. Specific interventional agents will include glutamate receptor antagonists and specific neuronal NO synthase inhibitors.

Animals↗
PubMed1999

A new optical immunoassay for detection of S-100B protein in whole blood.

BACKGROUND: S-100B is a protein mainly found in astroglial cells and only detected to a low level in blood. Serum levels of S-100B increase in patients with acute brain injuries. The aim of this study was to establish feasibility of a new Optical ImmunoAssay ([OIA], Bio-Star, Inc, Boulder, CO) test for determination of S-100B in blood. METHODS: We have developed a new, rapid, and sensitive OIA test to identify elevated levels of S-100B in whole blood. The OIA test for S-100B combines monoclonal antibodies specific for the B-subunit of S-100 with OIA thin film technology. Each sample was tested for S-100B by the OIA method and a commercially available immunoluminometric assay. Blood samples were drawn serially from 9 patients undergoing coronary artery bypass graft surgery and during the early postoperative period. RESULTS: The OIA test determination of S-100B protein correlated with immunoluminometric assay data (r = 0.8) with a detection limit of 0.25 ng/mL. CONCLUSIONS: The sensitivity and feasibility of this rapid assay may be suitable for rapid evaluation of S-100B in urgent care settings (surgery, intensive care units, or emergency room).

Aged↗
PubMed1998

The role of the monosialoganglioside, GM1 as a neuroprotectant in an experimental model of cardiopulmonary bypass and hypothermic circulatory arrest.

Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 h of HCA at 18 degrees C, and rewarmed to 37 degrees C on closed-chest cardiopulmonary bypass. All animals were mechanically ventilated and monitored for 20 h before extubation and survived for 3 days. Group 1 dogs (n = 6) were pretreated with GM1, 30 mg/kg/24 h for 3 days before HCA, and received continuous infusion of GM1 during the procedure and 30 mg/kg/24 h for 3 days after HCA. Group 2 dogs (n = 6) received vehicle only. With a species-specific behavior scale that yielded a neurodeficit score ranging from 0% (normal) to 100% (brain dead), all animals were neurologically assessed every 12 h by two observers. After death at 72 h, brains were examined by glutamate receptor autoradiography and by histologic examination for patterns of selective neuronal necrosis and were scored blindly from 0 (normal) to 100 (severe injury). These results provide evidence of a role for GE in the development of HCA-induced brain injury and suggest that monosialogangliosides may have a neuroprotective effect in prolonged periods of HCA.

Animals↗
PubMed1998

Conservative management of late rejection after heart transplantation: a 10-year analysis.

OBJECTIVE: Immunosuppressive regimens for rejection after heart transplantation have been modified to reduce infectious complications without diminishing rejection treatment efficacy. A review of a single institutional series was performed to evaluate the influence of conservative management of grade 2 rejection on long-term outcomes after heart transplantation. METHODS: Before 1990, patients with late (>3 months after transplant) grade 2 rejection were treated with supplemental immunosuppressive drugs. Beginning in 1990, patients with late grade 2 rejection were treated conservatively by maintaining the current immunosuppressive regimen without additional therapy. The groups were compared for survival, incidence of subsequent rejection, and incidence of subsequent infection. RESULTS: One hundred twelve patients had one or more episodes of isolated, late grade 2 rejection; 39 (35%) were treated with supplemental immunosuppression (treated group) and 73 (65%) received no additional therapy (nontreated group). The mean time from transplantation to the first episode of isolated grade 2 rejection was 15.6 months in the treated group and 17.8 months in the nontreated group. Graft survival at 5 and 10 years was 69% and 51 %, respectively, in the treated group and 67% and 41 %, respectively, in the nontreated group (p = 0.77). The rates for overall subsequent rejection were 0.031 episodes/patient-month in the treated group and 0.029 episodes/patient-month in the nontreated group (p = 0.64). The rates for early rejection within 6 months of initial grade 2 rejection were 0.044 episodes/patient-month in the treated group and 0.035 episodes/patient-month in the nontreated group (p = 0.56). The rates for overall subsequent infection were 0.018 episodes/patient-month in the treated group and 0.012 episodes/patient-month in the nontreated group (p = 0.05). The rates for early infection within 6 months of initial grade 2 rejection were 0.070 episodes/patient-month in the treated group and 0.032 episodes/patient-month in the nontreated group (p = 0.04). Group comparisons demonstrated a significantly lower incidence of infection in the nontreated group. CONCLUSIONS: Conservative management of late grade 2 rejection neither adversely affects survival nor increases the incidence of subsequent short-term or long-term rejection. This approach lowers the early and late incidence of infection after rejection and may reduce other complications from aggressive supplemental immunosuppression.

Female↗
PubMed1998

Obesity and hypercholesterolemia following heart transplantation.

Successful strategies for avoiding obesity and hypercholesterolemia are difficult to validate because of imprecise problem identification. The purpose of this study was to describe the incidence, severity, and onset of obesity and hypercholesterolemia among heart transplant recipients and identify relationships between demographic variables and weight or cholesterol levels during the first year following transplantation. Data were collected from retrospective chart review. Forty-two patients were randomly selected from 224 patients who were undergoing heart transplantation at the Johns Hopkins Hospital between July 1983 and December 1995. Significant differences were found in weight and cholesterol level during the first 12 months. Patients with ideal body weight less than 110%, compared with greater than 110%, survived longer. Relationships were identified between prednisone dose and weight, cumulative prednisone dose and weight, and weight change and change in total cholesterol level 1 year following transplantation. Multivariate analysis showed cumulative prednisone as an independent predictor of weight. Obesity and hypercholesterolemia were significant problems within 3 months of transplantation. Although prednisone dosage should be adjusted to the lowest possible dose, dietary and lifestyle changes remain the foundation of effective management of these posttransplant complications.

Adult↗
PubMed1998

Monosialoganglioside GM1 inhibits neurotoxicity after hypothermic circulatory arrest.

BACKGROUND: Prolonged hypothermic circulatory arrest (HCA) causes clinical neurologic injury. This injury involves neuronal apoptosis, or programmed cell death. We have previously demonstrated that HCA causes glutamate excitotoxicity, increased nitric oxide (NO) production, and NO-mediated apoptosis. We hypothesized that monosialoganglioside GM1 inhibits NO synthase. The purpose of this study was to determine whether GM1 inhibits NO production and neuronal apoptosis after HCA. METHODS: Fourteen dogs underwent intracerebral microdialysis to measure excitatory amino acids, glutamate, aspartate, and citrulline, an equal coproduct of NO. They underwent 2 hours of HCA at 18 degrees C and were sacrificed 8 hours after HCA. Group 1 (n = 6) was pretreated with GM1, 30 mg/kg intravenously every day for 3 days, as well as before and after HCA. Group 2 control dogs (n = 8) received vehicle only. Apoptosis was scored from 0 (normal) to 100 (severe injury). RESULTS: Excitatory amino acids, aspartate and glutamate, coagonist glycine, and citrulline levels increased significantly over baseline during HCA and after HCA. GM1 pretreatment did not appreciably alter levels of glutamate, aspartate, and glycine; however, it substantially decreased citrulline and therefore NO production throughout the experiment. GM1 significantly inhibited apoptosis (group 1 vs group 2: 15.56 +/- 13.60 vs 62.92 +/- 6.17; P < .001). CONCLUSIONS: Our results provide the first direct evidence that GM1 inhibits NO synthase to reduce NO production and HCA-induced neuronal apoptosis. GM1 did not affect excitatory glutamate or aspartate levels. GM1 has been used in clinical trials of spinal cord injury and may be efficacious in reducing neurologic injury after HCA.

Animals↗
PubMed1997

Cognitive outcome after coronary artery bypass: a one-year prospective study.

BACKGROUND: Cognitive deficits have been reported in patients after coronary artery bypass grafting, but the incidence of these deficits varies widely. We studied prospectively the incidence of cognitive change and whether the changes persisted over time. METHODS: Cognitive testing was done preoperatively and 1 month and 1 year postoperatively in 127 patients undergoing coronary artery bypass grafting. Tests were grouped into eight cognitive domains. A change of 0.5 standard deviation or more at 1 month and 1 year from patient's preoperative Z score was the outcome measure. RESULTS: We identified four main outcomes for each cognitive domain: no decline; decline and improvement; persistent decline; and late decline. Only 12% of patients showed no decline across all domains tested; 82% to 90% of patients had no decline in visual memory, psychomotor speed, motor speed, and executive function; 21% and 26% had decline and improvement in verbal memory and language; approximately 10% had persistent decline in the domains of verbal memory, visual memory, attention, and visuoconstruction; and 24% had late decline (between 1 month and 1 year) in visuoconstruction. CONCLUSIONS: This study establishes that the incidence of cognitive decline varies according to the cognitive domain studied and that some patients have persistent and late cognitive changes in specific domains after coronary artery bypass grafting.

Aged↗
PubMed1997

Clinical markers in CSF for determining neurologic deficits after thoracoabdominal aortic aneurysm repairs.

BACKGROUND: Spinal cord ischemia is a major cause of morbidity and mortality after thoracoabdominal aortic aneurysm operations. The incidence of paraplegia is high even in experienced institutions. METHODS: We investigated whether neurotransmitter excitotoxicity is associated with neurologic deficits after thoracoabdominal aortic aneurysm operations. We hypothesized that patients with spinal cord injury would manifest elevated levels of excitatory amino acids in their cerebrospinal fluid. Sixteen patients undergoing thoracoabdominal aortic aneurysm operations had cerebrospinal fluid drawn through lumbar spinal drains preoperatively, intraoperatively, and postoperatively. Excitatory amino acid levels (glutamate, aspartate, glycine) were measured using high-performance liquid chromatography. Excitatory amino acid levels were compared in patients who exhibited no neurologic deficits postoperatively (group I; n = 12) with patients who had clinically evident lower extremity and cerebral neurologic deficits (group II; n = 4). RESULTS: Significant elevations in glutamate and aspartate levels from baseline (p < 0.05) were limited to group II. Excitatory amino acid levels in group II were significantly elevated (p < 0.05) compared with those observed in group I. Glutamate levels were especially increased during aortic cross-clamping and late reperfusion, whereas aspartate levels were increased only during late reperfusion. CONCLUSIONS: These data suggest that neurotransmitter excitotoxicity plays a significant role in central nervous system injury.

Aged↗
PubMed1997

Neuronal nitric oxide synthase inhibition reduces neuronal apoptosis after hypothermic circulatory arrest.

BACKGROUND: Neurologic injury, including choreoathetosis and learning and memory deficits, occurs after prolonged hypothermic circulatory arrest (HCA). Apoptosis, or programmed cell death, is a possible cause of the neurologic injury seen after HCA. However, the mechanism of apoptosis is unknown. Hypothermic circulatory arrest causes glutamate excitotoxicity, resulting in increased nitric oxide production. We therefore hypothesized that nitric oxide mediates apoptosis. The purpose of this study was to determine if neuronal nitric oxide synthase inhibition reduces neuronal apoptosis in an established canine model of HCA. METHODS: Fourteen male hound dogs (weight, 20 to 27 kg) were placed on closed-chest cardiopulmonary bypass, subjected to 2 hours of HCA at 18 degrees C, rewarmed to normothermia, and sacrificed 8 hours after HCA. Group 1 (n = 7) dogs were treated with the neuronal nitric oxide inhibitor 7-nitroindazole, 25 mg/kg intraperitoneally, before arrest and every 2 hours until sacrifice. Group 2 (n = 7) dogs received vehicle only. The brains were analyzed histopathologically. Apoptosis, identified by hematoxylin-eosin staining, was confirmed by DNA terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling assay and electron microscopy. Apoptosis was scored by a blinded neuropathologist from 0 (normal) to 100 (severe injury). RESULTS: Apoptosis occurred early after HCA in select neuronal populations, including the hippocampus, stria terminalis, neocortex, and entorhinal cortex. Apoptotic neurons showed a characteristic shrunken cytoplasm and nuclear chromatin condensation. 7-Nitroindazole significantly inhibited apoptosis (group 1 versus 2: 19.17 +/- 14.39 versus 61.11 +/- 5.41; p < .001). CONCLUSIONS: Our results provide evidence that apoptosis is associated with the neurologic injury that occurs after HCA and that nitric oxide mediates the apoptosis that occurs after HCA. Strategies for cerebral protection during HCA may include the inhibition of neuronal nitric oxide synthase.

Animals↗
PubMed1997

Predictors of stroke risk in coronary artery bypass patients.

BACKGROUND: Stroke occurs after coronary artery bypass grafting with an incidence ranging between 0.8% and 5.2%. To identify factors associated with stroke, we prospectively examined a study cohort and tested findings in an independent validation sample. METHODS: The study cohort comprised 456 patients undergoing coronary artery bypass grafting only, and the validation sample comprised 1,298 patients. Stroke was detected postoperatively by the study team and confirmed by neurologic consultation and computed tomographic scanning. RESULTS: Five factors taken together were correlated with stroke: previous stroke, presence of carotid bruit, history of hypertension, increasing age, and history of diabetes mellitus. The only significant intraoperative factor was cardiopulmonary bypass time. Probabilities were calculated, and patients were placed into low, medium, and high stroke-risk groups. In the validation sample, this model was able to rank the majority of patients with stroke into the high-risk group. CONCLUSIONS: These five factors taken together can identify the risk of stroke in patients having coronary artery bypass grafting. Recognition of the high-risk group will aid studies on the mechanism and prevention of stroke by modification of surgical procedures or pharmacologic intervention.

Aged↗
PubMed1997

Hair analysis for drugs of abuse. XVII. Simultaneous detection of PCP, PCHP, and PCPdiol in human hair for confirmation of PCP use.

The paper reports the simultaneous detection hair of phencyclidine (PCP) and its two major metabolites, 1-(1-phenylcyclohexyl)-4-hydroxypiperidine (PCHP) and trans-1-(1-phenyl-4-hydroxycyclohexyl)-4'-hydroxypiperidine (t-PCPdiol) in human hair. The detection of these metabolites provides definitive evidence that a positive hair analysis result is due to active PCP use and not due to external contamination of the hair specimen. Hair (5 mg) from known PCP users was washed three times with 0.1% sodium dodecyl sulfate for 1 min before analysis. Three extraction methods were compared: methanol-5N HCl (20:1) (Method A), 10% HCl (Method B), and 2N sodium hydroxide digestion (Method C). PCP-d5 and PCHP-d5 were used as internal standards. Extracts were purified by Bond Elut Certify solid-phase extraction procedures. Samples were derivatized with N,O-bis-trimethylsilyl acetamide and analyzed by gas chromatography-mass spectrometry. Compared with Method A, the extraction efficiencies of Methods B and C for PCP were 83-89%; however, the extraction efficiencies of Methods B and C for the two metabolites were only half or less than that of Method A. Method A was therefore selected for the analysis of clinical hair specimens from eight PCP users. The coefficients of variation of this method (n = 5) for PCP at 4 ng/mg and for PCHP and t-PCPdiol at 0.2 ng/mg were 2.13, 6.09, and 9.38%, respectively. In the eight hair specimens, PCP values ranged between 0.33 and 14 ng/mg. PCHP between 0.02 and 0.12 ng/mg, and trans-PCPdiol between 0.09 and 0.45 ng/mg. It was found that t-PCPdiol was the major metabolite in the PCP users' hair specimens, although t-PCPdiol was a minor metabolite in the hair specimens of rats intoxicated with PCP.

Animals↗
PubMed1997

Aortic valve replacement in the elderly. Risk factors and long-term results.

OBJECTIVE: The current study was undertaken to determine long-term results of aortic valve replacement (AVR) in the elderly, to ascertain predictors of poor outcome, and to assess quality of life. SUMMARY BACKGROUND DATA: Aortic valve replacement is the procedure of choice for elderly patients with aortic valve disease. The number of patients aged 70 and older requiring AVR continues to increase. However, controversy exists as to whether surgery devoted to this subset reflect a cost-effective approach to attaining a meaningful quality of life. METHODS: This study reviews data on 247 patients aged 70 to 89 years who underwent isolated AVR between 1980 and 1995; there were 126 men (51%) and 121 women (49%). Follow-up was 97% complete (239/247 patients) for a total of 974.9 patient-years. Mean age was 76.2 +/- 4.8 years. Operative mortality and actuarial survival were determined. Patient age, gender, symptoms, associated diseases, prior conditions, New York Health Association class congestive heart failure, native valve disease, prosthetic valve type, preoperative catheterization data, and early postoperative conditions were analyzed as possible predictors of outcome. Functional recovery was evaluated using the SF-36 quality assessment tool. RESULTS: Operative mortality was 6.1% (15/247). Multivariate logistic regression showed that poor left ventricular function and preoperative pacemaker insertion were independent predictors of early mortality. After surgery, infection was predictive of early mortality. Overall actuarial survival at 1, 5, and 10 years was 89.5 +/- 2% (198 patients at risk), 69.3 +/- 3.4% (89 patients at risk), and 41.2 +/- 6% (13 patients at risk), respectively. Cox proportional hazards model showed that chronic obstructive pulmonary disease and urgency of operation were independent predictors of poor long-term survival. Postoperative renal failure also was predictive of poor outcome. Using the SF-36 quality assessment tool, elderly patients who underwent AVR scored comparably to their age-matched population norms in seven of eight dimensions of overall health. The exception is mental health. CONCLUSIONS: Aortic valve replacement in the elderly can be performed with acceptable mortality. Significant preoperative risk factors for early mortality include poor left ventricular function and preoperative pacemaker insertion. Predictors of late mortality include chronic obstructive pulmonary disease and urgency of operation. These results stress the importance of operating on the elderly with aortic valve disease; both long-term survival and functional recovery are excellent.

Aged↗