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Biomedical subjects

L C Ginns

Publications and source records attributed to L C Ginns.

At least 19 recordsLinked to original sources
PubMed2004

Familial aggregation of FEF(25-75) and FEF(25-75)/FVC in families with severe, early onset COPD.

BACKGROUND: The Boston Early-Onset COPD study showed that current or ex-smoking first degree relatives of severe early onset COPD probands have significantly lower forced expiratory volume in 1 second (FEV(1)) and FEV(1)/forced vital capacity (FVC) values than current or ex-smoking control subjects, which suggests the existence of genetic risk factors for the development of COPD in response to cigarette smoking. We hypothesised that first degree relatives of early onset COPD probands may also have lower values of spirometric parameters such as forced expiratory flow at the mid-portion of forced vital capacity (FEF(25-75)) and FEF(25-75)/FVC. METHODS: Using generalised estimating equations, FEF(25-75) and FEF(25-75)/FVC were analysed in 333 first degree relatives of probands with severe early onset COPD and 83 population based controls; analyses were also performed on data stratified by smoking status. Narrow sense heritability estimates were calculated using a variance component approach. RESULTS: Significantly lower FEF(25-75) and FEF(25-75)/FVC were observed in smoking (FEF(25-75): beta -0.788 l/s (95% CI -1.118 to -0.457), FEF(25-75)/FVC: beta -20.4% (95% CI -29.3 to -11.6, p<0.0001 for both phenotypes) and non-smoking (FEF(25-75): beta -0.357 l/s (95% CI -0.673 to -0.041, p = 0.0271), FEF(25-75)/FVC: beta -9.5% (95% CI -17.1 to -1.9, p = 0.0145)) first degree relatives of early onset COPD probands. Narrow sense heritability estimates for FEF(25-75) (h(2) = 0.38) and FEF(25-75)/FVC (h(2) = 0.45) were similar to those for FEV(1) and FEV(1)/FVC. CONCLUSION: Lower values of FEF(25-75) and FEF(25-75)/FVC in non-smoking first degree relatives of early onset COPD probands than in controls suggest a genetic susceptibility to develop obstructive lung disease, independent of smoking, which is magnified by exposure to deleterious environments as suggested by the further decrements in FEF(25-75) and FEF(25-75)/FVC seen in smoking first degree relatives. FEF(25-75) and FEF(25-75)/FVC have high heritability and are important intermediate phenotypes for inclusion in genetic epidemiological studies of COPD.

Adolescent↗
PubMed2001

Lung transplantation at the turn of the century.

Lung transplantation has become a viable treatment option for patients with end-stage lung disease. Donor selection and organ allocation must follow specific guidelines. Single, bilateral, and living-donor lobar transplantation have all been performed successfully for a variety of diseases. Complications include reimplantation response and airway complications. Rejection may occur in the hyperacute, acute, or chronic settings and requires judicious management with immunosuppression. Infection and malignancy remain potential complications of the commitment to lifelong systemic immunosuppression. Survival statistics have remained encouraging and continue to improve with experience. Improved exercise tolerance and quality of life have been demonstrated in the years following transplantation. Remaining obstacles include limited donor organ availability, long-term graft function, and patient survival. However, ongoing advances in immune tolerance and standardized training of physicians in the care of transplant patients should carry lung transplant forward in the twenty-first century.

Forecasting↗
PubMed2001

Comparison of the effects of nitric oxide, nitroprusside, and nifedipine on hemodynamics and right ventricular contractility in patients with chronic pulmonary hypertension.

STUDY OBJECTIVES: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricular (RV) contractility were compared with those of nitroprusside and nifedipine in 14 patients with severe chronic pulmonary hypertension. STUDY DESIGN: Micromanometer and balloon-tipped right heart catheterization were performed. Inhaled NO, IV nitroprusside, and sublingual nifedipine were administered sequentially while patients breathed > 90% oxygen. SETTING: Cardiac catheterization laboratory in a tertiary care teaching hospital. PATIENTS: Fourteen patients with severe pulmonary hypertension unrelated to left ventricular dysfunction. MEASUREMENTS AND RESULTS: During NO inhalation, mean systemic arterial pressure (MAP) was unchanged, but pulmonary artery (PA) pressure ([mean +/- SEM] 49 +/- 2 mm Hg vs 44 +/- 2 mm Hg; p < 0.01), pulmonary vascular resistance (PVR; 829 +/- 68 vs 669 +/- 64 dyne x s x cm(-5); p < 0.01) and RV end-diastolic pressure (RVEDP; 12 +/- 1 vs 10 +/- 1 mm Hg; p < 0.01) decreased. Stroke volume index (SVI; 31 +/- 2 vs 35 +/- 3 mL/m(2); p < 0.05) increased, and the first derivative of RV pressure at 15 mm Hg developed pressure (RV +dP/dt at DP15) was unchanged. During nitroprusside administration, MAP decreased (105 +/- 5 vs 76 +/- 5 mm Hg; p < 0.01), PA was unchanged (48 +/- 2 vs 45 +/- 3 mm Hg; p = not significant), and PVR decreased (791 +/- 53 vs 665 +/- 53 dyne x s x cm(-5); p < 0.01). RV +dP/dt at DP15 increased (425 +/- 22 vs 465 +/- 29 mm Hg/s; p < 0.05), but SVI was unchanged. Nifedipine decreased MAP (103 +/- 5 vs 94 +/- 5 mm Hg; p < 0.01), PA and PVR were unchanged, RVEDP increased (12 +/- 1 vs 14 +/- 2 mm Hg; p < 0.01), and RV +dP/dt at DP15 decreased (432 +/- 90 vs 389 +/- 21 mm Hg/s; p < 0.05). CONCLUSIONS: Inhaled NO is a selective pulmonary vasodilator in patients with chronic pulmonary hypertension that improves cardiac performance without altering RV contractility. Nitroprusside caused a similar degree of pulmonary vasodilation. In contrast to inhaled NO, nitroprusside caused systemic hypotension associated with an increase in RV contractility. Acute administration of nifedipine did not cause pulmonary vasodilation, but RVEDP increased and RV contractility decreased.

Administration, Inhalation↗
PubMed2001

Oxygen therapy improves cardiac index and pulmonary vascular resistance in patients with pulmonary hypertension.

STUDY OBJECTIVES: We tested the hypothesis that breathing 100% oxygen could result in selective pulmonary vasodilatation in patients with pulmonary hypertension, including those patients who would not meet current Health Care Finance Administration guidelines for long-term oxygen therapy. DESIGN, SETTING, AND PATIENTS: From 1996 to 1999, 23 adult patients (mean +/- SEM age, 51 +/- 4 years) with pulmonary arterial hypertension without left-heart failure underwent cardiac catheterization in a university teaching hospital while breathing air and then 100% oxygen. MEASUREMENTS AND RESULTS: Treatment with 100% oxygen increased arterial oxygen saturation (91 +/- 1% to 99 +/- 0.1%, p < 0.05) and PaO(2) (64 +/- 3 to 309 +/- 28 mm Hg, p < 0.05). Treatment with 100% oxygen also decreased mean pulmonary artery pressure (56 +/- 3 to 53 +/- 2 mm Hg, p < 0.05) and increased cardiac index (2.1 +/- 0.1 to 2.5 +/- 0.2 L/min/m(2), p < 0.05). Calculated mean pulmonary vascular resistance (PVR) decreased from 14.1 +/- 1.4 to 10.6 +/- 1.0 Wood units (p < 0.05). Vasodilatation with 100% oxygen occurred preferentially in the pulmonary circulation (PVR/systemic vascular resistance, 0.53 +/- 0.04 to 0.48 +/- 0.03; p < 0.05). The magnitude of the PVR response to oxygen therapy was correlated only with decreasing patient age (r = 0.45, p < 0.05). CONCLUSIONS: Treatment with 100% oxygen is a selective pulmonary vasodilator in patients with pulmonary hypertension, regardless of primary diagnosis, baseline oxygenation, or right ventricular function. Development of disease-specific oxygen prescription guidelines warrants consideration.

Adult↗
PubMed2000

Gender-related differences in severe, early-onset chronic obstructive pulmonary disease.

Men have higher prevalence rates of chronic obstructive pulmonary disease (COPD) than women, which has been attributed to the historically higher rates of cigarette smoking in males. However, the increased rates of cigarette smoking in females within the last several decades have been associated with steadily increasing rates of COPD in women. As part of a study of the genetics of severe, early-onset COPD, we assembled a group of 84 probands with severe, early-onset COPD (without severe alpha(1)-antitrypsin deficiency) and 348 of their first-degree relatives. We found a markedly elevated prevalence (71.4%) of females among the early-onset COPD probands. Among the entire group of first-degree relatives of early-onset COPD probands, univariate analysis demonstrated similar spirometric values and bronchodilator responsiveness in males and females; however, among current or ex-smokers, female first-degree relatives had significantly lower FEV(1)/ FVC (81.4 +/- 17.2% in females versus 87.0 +/- 12.9% in males, p = 0.009) and significantly greater bronchodilator responsiveness (expressed as percentage of baseline FEV(1)) (7.7 +/- 9.4% pred in females versus 4.1 +/- 6.4% pred in males, p = 0.002). Female smoking first-degree relatives were significantly more likely to demonstrate profound reductions in FEV(1) (< 40% pred) than male smoking first-degree relatives (p = 0. 03). Multivariate analysis, performed with generalized estimating equations, demonstrated that current or ex-smoking female first-degree relatives had significantly greater risk of FEV(1) < 80% pred (OR 1.91, 95% CI 1.03- 3.54), FEV(1) < 40% pred (OR 3.56, 95% CI 1.08-11.71), and bronchodilator response greater than 10% of baseline FEV(1) (OR 4.74, 95% CI 1.91-11.75). These results suggest that women may be more susceptible to the development of severe COPD.

Adult↗
PubMed1999

In vivo generation of C4d, Bb, iC3b, and SC5b-9 after OKT3 administration in kidney and lung transplant recipients.

BACKGROUND: OKT3 monoclonal antibody therapy results in an acute clinical syndrome (ACS) associated with the release of tumor necrosis factor and sequestration of neutrophils in the lungs. We have previously shown that inhibition of tumor necrosis factor does not completely eliminate OKT3-ACS, suggesting that other factors also contribute to the ACS. The current studies analyzed complement activation in vivo during the first hour after OKT3 administration. METHODS: Renal (n=4) and lung (n=4) transplant recipients received OKT3 as treatment for rejection and induction therapy, respectively. Complement activation products C4d, Bb, iC3b, and SC5b-9 were measured by ELISA. Hemodynamic parameters were also monitored in the lung transplant recipients. Neutrophil expression of CD11a, CD11b, and CD18 was monitored by flow cytometry. Controls included patients receiving methylprednisolone for rejection (n=4), two adults with adult respiratory distress syndrome who received extracorporeal membrane oxygenation, and normal volunteers (n=5). P values less than 0.05 (*) were considered significant. RESULTS: Increases in the plasma levels of C4d, Bb, iC3b, and SC5b-9 were observed in seven of eight patients after OKT3 administration. Mean values (n=8) at 0, 15, and 60 min (in microg/ml) were as follows-C4d: 1.865, 2.644*, and 2.607*; Bb: 0.245, 0.411, and 0.385; iC3b: 10.881, 17.242*, and 15.145*; and SC5b-9: 0.232, 0.269, and 0.302*. An increase in CD11b and CD18 and a decrease of CD11a on neutrophils in parallel with complement activation was observed. In lung transplant recipients, C3 activation correlated with increases in mean pulmonary and central venous pressures (P<0.05). As compared with extracorporeal membrane oxygenation, which activated classical and alternative pathways, OKT3 predominantly activated complement by the classical pathway. Methylprednisolone pulses did not activate complement. CONCLUSIONS: Complement activation is an early event after OKT3 administration and is associated with the increased expression of adhesion molecules on neutrophils and with pulmonary hemodynamic changes. Effective therapeutic approaches to the control of early monoclonal antibody side effects may require measures that limit complement activation in addition to reducing cytokine activity.

Adult↗
PubMed1999

Induction immunosuppression for lung transplantation with OKT3.

BACKGROUND: The use of OKT3, an anti-CD3 monoclonal antibody, for immunosuppressive therapy for lung transplantation has been restricted because of concerns regarding infectious risk and cardiopulmonary instability after its administration. METHODS: Fifty-two patients received OKT3 (5 mg/d intravenously for 10 days) for induction of immunosuppressive therapy, along with azathioprine (1.5 mg x kg(-1) x d(-1) intravenously) and enteral cyclosporine (12 mg x kg(-1) x d(-1)). Maintenance steroid therapy was begun on postoperative day 8. Prophylactic antifungal therapy (fluconazole or amphotericin B) and ganciclovir was used in all patients. Serial transbronchial biopsy and measurements of pulmonary function were used to assess patients for evidence of infection or rejection. Cytomegalovirus infection was diagnosed by biopsy or the presence of cytomegalovirus antigenemia. RESULTS: The 30-day mortality rate was 4%; the in-hospital mortality rate was 8%. Acute graft failure was seen in 6 patients. The median length of intubation was 5 days, and the median hospital stay was 30 days. Systemic and pulmonary artery systolic pressures, cardiac index, and ratio of arterial partial oxygen pressure to fraction of inspired oxygen showed no significant alteration after OKT3 dosage. Gram-negative pulmonary infections were identified in 12 patients. Aspergillus infection was seen in 7 patients. Cytomegalovirus infection in 8 patients responded to ganciclovir and did not affect mortality. Respiratory syncytial viral infection was seen in 7 patients. Acute rejection was never seen during OKT3 administration. No episodes of acute rejection were identified in 14 patients at any time postoperatively. In the remainder, episodes of acute rejection responded to steroid or antithymocyte globulin therapy. At a median length of follow-up of 31 months, freedom from obliterative bronchiolitis was 69%+/-9% at 36 months. The overall survival rate was 88%+/-5% at 12 months, 82%+/-6% at 24 months, and 74%+/-7% at 36 months after transplantation. CONCLUSIONS: OKT3 is a safe and effective agent for induction immunosuppressive therapy in lung transplant recipients that limits the incidence of acute rejection and may decrease the incidence of obliterative bronchiolitis.

Adolescent↗
PubMed1998

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease.

To determine if decreased systemic oxygen (O2) extraction contributes to the exercise limit in severe chronic obstructive pulmonary disease (COPD), 40 consecutive incremental cycle ergometer exercise tests performed by such patients, from which a "log-log" lactate threshold (LT) was identified, were compared to those of 8 patients with left ventricular failure (LVF) and 10 normal controls. Pulmonary gas exchange and minute ventilation were measured continuously and arterial blood gas tensions, pH, and lactate concentrations were sampled each minute. Cardiac output (Qc) was measured by first-pass radionuclide ventriculography. The systemic O2 extraction ratio (O2ER) was calculated as arterial - mixed venous O2 content difference (CaO2 - CvO2)/CaO2. Peak exercise O2 uptake (VO2peak) was markedly reduced in both COPD and LVF [41 (3) and 42 (3)% predicted, respectively], compared to controls [89 (2)% predicted, P < 0.0001 for each]. Similarly, the LT occurred at a low percentage of predicted maximal oxygen consumption in both COPD and LVF [25 (2) and 27 (3)%] compared to normals [46 (3)%, P < 0.0001 for each]. The systemic O2ER at peak exercise was severely reduced in COPD [0.36 (0.02)] compared to the other groups [P < 0.0001 for each], for whom it was nearly identical [0.58 (0.03) vs 0.63 (0.04), LVF vs control, P > 0.05]. In the COPD group, an early LT correlated with reduced systemic O2ER at peak exercise (r = 0.64, P < 0.0001), but not with any index of systemic O2 delivery. These data suggest that lactic acidemia during exercise in patients with severe COPD is better related to abnormal systemic O2 extraction than to its delivery and contributes to the exercise limit.

Acidosis, Lactic↗
PubMed1998

Ventilatory and cardiovascular responses to inspired He-O2 during exercise in chronic obstructive pulmonary disease.

Blunted maximum cardiac output and systemic O2 extraction could constitute primary limits to exercise in severe chronic obstructive pulmonary disease (COPD) or they could simply reflect cessation of exercise because of abnormal pulmonary mechanics. To determine which is the case, eight consecutive patients with severe COPD (FEV1 = 0. 56 +/- 0.04 L, mean +/- SEM), five of whom had alpha1-antiprotease deficiency, performed two incremental cycling tests while breathing N2-O2 or He-O2. Expired gases and V E were measured, and radial and pulmonary arterial blood was simultaneously sampled each minute. Peak exercise V E was higher with He-O2 than with N2-O2 (25.5 +/- 2. 2 versus 19.3 +/- 1.5 L/min, p = 0.002) and PaCO2 was lower (42 +/- 2 versus 46 +/- 2 mm Hg, p = 0.0003). V O2max improved only modestly (594 +/- 75 versus 514 +/- 54 ml/min, p = 0.04), and was accompanied by an increase in peak exercise CaO2 (18.7 +/- 0.9 versus 17.6 +/- 0. 9 ml/dl, p = 0.02). Peak Fick cardiac output was decreased (39 +/- 3% pred) and CvO2 was elevated (130 +/- 10% pred), and neither improved with He-O2 (p > 0.05 for each). Abnormal peak exercise cardiac output and systemic O2 extraction in severe COPD cannot be fully accounted for by limiting pulmonary mechanics and may contribute to exercise intolerance.

Administration, Inhalation↗
PubMed1998

Respiratory syncytial virus-associated infections in adult recipients of solid organ transplants.

BACKGROUND: Although respiratory syncytial virus (RSV) infection is known to cause severe pulmonary infections in bone marrow transplant recipients, less is known concerning its clinical course, diagnosis, and treatment in solid organ transplant recipients. METHODS: We have conducted a retrospective review of seven cases of RSV infection in adult recipients of solid organ transplants. Four patients received lungs, two received kidneys, and one received a heart. RESULTS: The most common presenting complaints were dyspnea (100%), cough (86%), and purulent sputum (57%). Physical findings included fever (43%), rales (100%), and wheezing (29%). Admission studies were significant for leukocytosis (29%), a left shift in the white blood cell differential (86%), and hypoxemia (mean PaO2 = 64). Chest radiographs were unchanged in 29% and showed infiltrates that were bilateral in 43% and unilateral in 29%. Pulmonary function tests in lung transplant recipients showed a mean fall in forced expiratory volume in 1 second of 26% and a fall in diffusion capacity for carbon monoxide of 24%. Five patients were treated with aerosolized ribavirin. Adverse events associated with treatment included wheezing (80%) and mild dyspnea (20%). The conditions of three of five treated patients were believed by their physicians to have improved 7 days after the initiation of therapy. One of the five treated patients died, and both untreated patients survived. CONCLUSIONS: RSV infection in this population has an extremely variable severity and clinical course, usually dominated by lower respiratory symptoms and obstructive airway disease. Ribavirin therapy is well tolerated, but its efficacy remains unknown.

Adult↗
PubMed1998

Exercise performance in cystic fibrosis before and after bilateral lung transplantation.

BACKGROUND: Lung transplantation improves pulmonary function and quality of life for patients with end-stage cystic fibrosis; however, a systematic evaluation of exercise performance in lung transplant recipients with cystic fibrosis has not been reported. METHODS: Ten patients with end-stage cystic fibrosis performed incremental exercise testing before and after bilateral lung transplantation; their results were compared with those of 10 age-similar healthy volunteers. Breath-by-breath measurements of gas exchange and ventilation were obtained, arterial blood was sampled each minute, and cardiac output determined at rest and peak exercise by radionuclide ventriculography. The arterial-venous O2 content difference was derived by the Fick principle. RESULTS: After transplantation, peak O2 uptake improved (31% +/- 3% vs 45% +/- 4% predicted, P = .03) but was still reduced versus normal (100% +/- 8% predicted, p < .0001). Exercise was limited by pulmonary mechanics in all patients before transplantation but in only 2 after transplantation. Compared with control subjects, the lactate threshold occurred early, both before and after transplantation. Peak exercise cardiac output and arterial O2 content were not different from normal, either before or after transplantation. In contrast, the peak exercise arterial-venous O2 content difference was markedly reduced before and after transplantation versus normal (7.1 +/- 1.2 and 9.3 +/- 0.9 vs 17.1 +/- 1.2 mL/dL, p < or = .0001 for each) and without significant improvement. CONCLUSIONS: Exercise performance in patients with end-stage cystic fibrosis improves after lung transplantation but remains well below normal. Reduced systemic O2 extraction is an important factor limiting exercise in patients with cystic fibrosis after transplantation and may also contribute to the exercise limit before transplantation.

Adolescent↗
PubMed1998

Determinants of abnormal maximum oxygen uptake after lung transplantation for chronic obstructive pulmonary disease.

BACKGROUND: Single lung transplantation for chronic obstructive pulmonary disease relieves a ventilatory limit to incremental exercise, but maximum oxygen uptake remains abnormal. The purpose of this study was to define the relative contributions of Fick principle variables to abnormal aerobic capacity after lung transplantation. METHODS: Twelve paired incremental cardiopulmonary exercise test results obtained before and 3 to 6 months after single lung transplantation for chronic obstructive pulmonary disease were compared. RESULTS: Maximum workload nearly doubled after operation (42.5+/-4.2 vs 25.5+/-4.7 watts, P < .05). Peak exercise minute ventilation increased (32.8+/-3.3 vs 21+/-2.4 L/min, n = 11, P < .05), but maximum oxygen uptake remained markedly abnormal after transplantation (46.6%+/-4.4% vs 32.1%+/-2.9% predicted, P < .05, n = 8). Peak exercise cardiac output was normal (11.0+/-1.4 L/min, 89% predicted), but arterial-mixed venous oxygen content difference at peak exercise was only half of normal (7.2+/-0.61 mL/dL), as a result in part of the failure of mixed venous oxygen saturation to fall normally (peak exercise SvO2 = 49.8%+/-2.8%). CONCLUSIONS: Lung transplantation for chronic obstructive pulmonary disease relieves a ventilatory limit to exercise, but maximum aerobic capacity remains abnormal, in part because of abnormal systemic O2 extraction.

Adult↗
PubMed1997

Relationship between pulmonary artery diameter at computed tomography and pulmonary artery pressures at right-sided heart catheterization. Massachusetts General Hospital Lung Transplantation Program.

RATIONALE AND OBJECTIVES: The purpose of the study was to determine the relationship between pulmonary artery (PA) size at computed tomography (CT) and PA pressures, to develop a noninvasive CT method of PA pressure measurement, and to determine a PA diameter that can enable differentiation of normal subjects from those with pulmonary hypertension. METHODS: PA vessel diameters in 55 candidates for lung and heart-lung transplantation were measured at CT and correlated with PA pressures with both linear and stepwise multiple regression. The multiple regression equations were then tested prospectively in 35 pretransplantation patients. RESULTS: Combined main and left main PA cross-sectional area corrected for body surface area showed the best correlation with mean PA pressure (r = .87). The multiple regression equations helped predict mean PA pressure within 5 mm Hg in 50% of patients with chronic lung disease and in only 8% of patients with pulmonary vascular disease. CONCLUSION: There was a very good correlation between main and left main PA size and mean PA pressure. At present, however, CT has not demonstrated sufficient accuracy to be used clinically.

Adolescent↗
PubMed1997

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

Although lung transplantation improves exercise capacity by removal of a ventilatory limitation, recipients' postoperative maximum oxygen uptake (VO2max) remains markedly abnormal. To determine if abnormal skeletal muscle oxidative capacity contributes to this impaired aerobic capacity, nine lung transplant recipients and eight healthy volunteers performed incremental quadriceps exercise to exhaustion with simultaneous measurements of pulmonary gas exchange, minute ventilation, blood lactate, and quadriceps muscle pH and phosphorylation potential by 31P-magnetic resonance spectroscopy (31P-MRS). Five to 38 mo after lung transplantation, peak VO2 was decreased compared with that of normal control subjects (6.7 +/- 0.4 versus 12.3 +/- 1.0 ml/min/kg, p < 0.001), even after accounting for differences in age and lean body weight. Neither ventilation, arterial O2 saturation nor mild anemia could account for the decrease in aerobic capacity. Quadriceps muscle intracellular pH (pH(i)) was more acidic at rest (7.07 +/- 0.01 versus 7.12 +/- 0.01 units, p < 0.05) and fell during exercise from baseline values at a lower metabolic rate (282 +/- 21 versus 577 +/- 52 ml/min, p < 0.001). Regressions for pH(i) versus VO2, phosphocreatine/inorganic phosphate ratio (PCr/Pi) versus VO2, and blood lactate versus pH(i) were not different. Among transplant recipients, the metabolic rate at which pH(i) fell correlated closely with VO2max (r = 0.87, p < 0.01). The persistent decrease in VO2max after lung transplantation may be related to abnormalities of skeletal muscle oxidative capacity.

Adult↗
PubMed1997

Preoperative predictors of operative morbidity and mortality in COPD patients undergoing bilateral lung volume reduction surgery.

Bilateral volume reduction surgery (VRS) improves lung function for selected patients with emphysema. However, predictors of outcome are not well defined. We reviewed the preoperative characteristics of the first 47 consecutive patients who underwent bilateral VRS at the Massachusetts General Hospital in order to define potential predictors of unacceptable outcome. Preoperative data included spirometry, plethysmography, diffusion of carbon monoxide (Dco), maximum inspiratory pressure (MIP), maximum expiratory pressure, resting arterial blood gases (ABG), cardiopulmonary exercise testing with ABG and lactate sampling, and radionuclide ventriculography. Prepulmonary and postpulmonary rehabilitation 6-min walk tets (6MWT), and preoperative chest CT scans were also obtained. Twenty-two subjects were male and 17 of the subjects were on the lung transplant list. Patient characteristics included age of 60.5 +/- 7.5 years, FEV1 of 0.67 +/- 0.20 L, total lung capacity of 7.56 +/- 1.7 L, Dco of 7.40 +/- 4.1 mL/min/mm Hg, and PaCO2 of 41.6 +/- 6.4 mm Hg (mean +/- SD). The FEV1, vital capacity, MIP, resting room air PaCO2, prepulmonary and postpulmonary rehabilitation 6MWT, and PaCO2 at maximum oxygen consumption correlated with length of hospitalization (p < 0.05). Based on analysis of 41 of 47 patients for whom there were complete data, the inability to walk more than 200 m on the 6MWT before or after preoperative pulmonary rehabilitation, and resting PaCO2 > or = 45 mm Hg were the best predictors of an unacceptable outcome. If either of these characteristics was present, six of 16 vs zero of 25 died (Fisher's Exact Test, p = 0.0025, one-tailed) and 11 of 16 vs four of 25 had hospital courses > 21 days (p < 0.002). Both the 6MWT < 200 m and resting PaCO2 > or = 45 mm Hg alone correlated with death (p = 0.004 and p = 0.012, respectively) and the resting PaCO2 > or = 45 mm Hg correlated with hospital days > 21 (p = 0.0002). In conclusion, the data suggest that the inability to walk at least 200 m in 6 min before or after pulmonary rehabilitation and a resting room air PaCO2 > or = 45 mm Hg are excellent preoperative predictors of unacceptable postoperative outcomes.

Exercise Test↗
PubMed1996

Complications of lung transplantation.

This article summarizes the complications of lung transplantation. Complications discussed are categorized into (1) complications of the operation itself, including hemorrhage, the reimplantation response, airway anastomotic complications, cardiac and hemodynamic complications, and gastrointestinal complications; (2) complications of transplantation, including acute and chronic rejection; and (3) complications of the immunosuppressive agents used to prevent rejection, including infection, malignancy, and direct toxicities of the medications. This article describes the usual presenting features of these complications and summarizes strategies used by transplant providers for their prevention, early diagnosis, and treatment.

Critical Care↗
PubMed1995

Klippel-Trénaunay syndrome with multiple pulmonary emboli--an unusual cause of progressive pulmonary dysfunction.

A 32-year-old man with progressive dyspnea and congenital lymphedema was transferred to our hospital for evaluation as a lung transplant candidate with the suspected diagnosis of primary pulmonary hypertension. Evaluation revealed the additional history of previous limb-shortening procedures for the left leg, the presence of syndactyly, long-standing bilateral (left to right) lower extremity varices, as well as soft tissue asymmetry with the left leg and arm larger than the right-sided counterparts. A diagnosis of Klippel-Trénaunay syndrome was made on the basis of these findings. Because of the deep venous malformations known to occur in this syndrome, we sought evidence of recurrent pulmonary emboli as an explanation for the patient's progressive dyspnea, despite negative pulmonary arteriography and ventilation-perfusion scanning results at another institution. Repeat pulmonary arteriography demonstrated evidence of chronic and subacute pulmonary emboli. The patient is presently being treated with warfarin anticoagulation, with plans for placement of a caval filter if anticoagulation alone is insufficient to prevent further embolism. Klippel-Trénaunay syndrome is a rare cause of chronic pulmonary emboli, and this entity should be considered when the characteristic historical and physical findings are present. A case report and review of the syndrome, with particular focus on the aspects relevant to the vascular surgeon, are presented.

Adult↗