Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment.

BACKGROUND: Myocardial infarction (MI) can directly cause ischemic mitral regurgitation (IMR), which has been touted as an indicator of poor prognosis in acute and early phases after MI. However, in the chronic post-MI phase, prognostic implications of IMR presence and degree are poorly defined. METHODS AND RESULTS: We analyzed 303 patients with previous (>16 days) Q-wave MI by ECG who underwent transthoracic echocardiography: 194 with IMR quantitatively assessed in routine practice and 109 without IMR matched for baseline age (71+/-11 versus 70+/-9 years, P=0.20), sex, and ejection fraction (EF, 33+/-14% versus 34+/-11%, P=0.14). In IMR patients, regurgitant volume (RVol) and effective regurgitant orifice (ERO) area were 36+/-24 mL/beat and 21+/-12 mm(2), respectively. After 5 years, total mortality and cardiac mortality for patients with IMR (62+/-5% and 50+/-6%, respectively) were higher than for those without IMR (39+/-6% and 30+/-5%, respectively) (both P<0.001). In multivariate analysis, independently of all baseline characteristics, particularly age and EF, the adjusted relative risks of total and cardiac mortality associated with the presence of IMR (1.88, P=0.003 and 1.83, P=0.014, respectively) and quantified degree of IMR defined by RVol >/=30 mL (2.05, P=0.002 and 2.01, P=0.009) and by ERO >/=20 mm(2) (2.23, P=0.003 and 2.38, P=0.004) were high. CONCLUSIONS: In the chronic phase after MI, IMR presence is associated with excess mortality independently of baseline characteristics and degree of ventricular dysfunction. The mortality risk is related directly to the degree of IMR as defined by ERO and RVol. Therefore, IMR detection and quantification provide major information for risk stratification and clinical decision making in the chronic post-MI phase.

Is early anticoagulation with warfarin necessary after bioprosthetic aortic valve replacement?

OBJECTIVES: Freedom from anticoagulation is the principal advantage of bioprosthesis; however, the American Heart Association/American College of Cardiology and the American College of Chest Physicians guidelines recommend early anticoagulation with heparin, followed by warfarin for 3 months after bioprosthetic aortic valve replacement. We examined neurologic events within 90 days of bioprosthetic aortic valve replacement at our institution. METHODS: Between 1993 and 2000, 1151 patients underwent bioprosthetic aortic valve replacement with (641) or without (510) associated coronary artery bypass. By surgeon preference, 624 had early postoperative anticoagulation (AC+) and 527 did not (AC-). In the AC- group, 410 patients (78%) received antiplatelet therapy. Groups were similar with respect to gender (female, 36% AC+ vs 40% AC-, P = .21), hypertension (64% AC+ vs 61%, P = .27), and prior stroke (7.6% AC+ vs 8.5% AC-, P = .54). The AC+ group was slightly younger than the AC- group (median, 76 years vs 78 years, P = .006). RESULTS: Operative mortality was 4.1% with 43 (3.7%) cerebrovascular events within 90 days. Excluding 18 deficits apparent upon emergence from anesthesia, we found that postoperative cerebrovascular accident occurred in 2.4% of AC+ and 1.9% AC- patients. By multivariable analysis, the only predictor of operative mortality was hypertension ( P < .0001). Postoperative cerebrovascular accident was unrelated to warfarin use ( P = .32). The incidence of mediastinal bleeding requiring reexploration was similar (5.0% vs 7.4%), as were other bleeding complications in the first 90 days (1.1% vs 0.8%). No variables were predictive of bleeding by multivariate analysis. CONCLUSIONS: Although these data do not address the role of antiplatelet agents, early anticoagulation with warfarin after bioprosthetic aortic valve replacement did not appear to protect against neurologic events.

Neutrophil adhesion and complement inhibition prolongs survival of cardiac xenografts in discordant species.

Hyperacute rejection results in rapid destruction of a discordant cardiac xenograft and is characterized by antibody deposition, complement activation, and platelet aggregation. The importance of neutrophils is unclear. Complement inhibition prolongs discordant cardiac xenograft survival. The purpose of this experiment was to determine the relative roles of complement and neutrophils. Selective inhibition of complement and neutrophil adhesion was used in a guinea pig-to-Lewis rat cardiac heterotopic xenotransplant model. NPC 15669 (N-[9H-(2,7-dimethylfluorenyl-9-methoxy)carbonyl]-L-leucine), a member of a new class of antiinflammatory agents termed leumedins, specifically prevents recruitment of neutrophils at inflammatory foci by inhibiting upregulation of the CD11b/CD18 adhesion molecule. Soluble complement receptor type 1 (sCR1, BRL 55730) is a potent inhibitor of the alternative and classical complement pathways. Group I (n = 13) received saline vehicle i.v. Group II (n = 15) was treated with NPC 15669 (10 mg/kg i.v. bolus) prior to reperfusion. Group III (n = 13) was treated with sCR1 (20 mg/kg i.v. bolus) prior to reperfusion. Group IV (n = 13) received both NPC 15669 and sCR1. Two xenografts were harvested at each interval time point (Groups I and II, 1, 2, 4, and 6 min; and Groups III and IV, 6, 15, 30, and 60 min). The remainder were followed to cessation of graft function. Graft survival was significantly increased in group IV and group III-375 +/- 13.4 min (mean +/- SD) and 112 +/- 29.4, respectively (P < .05), compared with 9.9 +/- 6.3 in group II and 8.7 +/- 4.9 in group I. Extreme interstitial hemorrhage and edema and contraction band injury were present in group I-III animals at end-stage, and neutrophil infiltration in group III. In group IV grafts, there was a decrease in these parameters despite the longer survival time, and at end-stage rejection the cellular infiltrate was primarily mononuclear. This study demonstrates that complement is an important mediator in early xenograft HYP injury. Combined treatment with NPC 15669 and sCR1 results in reduced histologic injury at all time points and longer graft survival than with sCR1 alone. These results suggest that neutrophil and complement activation play synergistic roles in the pathogenesis of xenograft hyperacute rejection. Neutrophil inhibition may prove to be an important component of multimodality therapy for hyperacute rejection, particularly in less-discordant transplants.

Surgical pathology of nonbacterial thrombotic endocarditis in 30 patients, 1985-2000.

OBJECTIVE: To describe the causes, complications, and histological appearance of nonbacterial thrombotic endocarditis (NBTE) in a surgical population compared with those in previously reported autopsy series. PATIENTS AND METHODS: Cases were identified by reviewing the surgical pathology reports for all cardiac valvular specimens removed at Mayo Clinic, Rochester, Minn., between 1985 and 2000. Archived microscopic slides and medical records were reviewed for each study patient. RESULTS: The study group consisted of 30 patients (20 female and 10 male), with a mean age of 49 years (range, 15-89 years). Of these 30 patients, 28 had single valve involvement (19 mitral, 8 aortic, and 1 tricuspid), and 2 had involvement of both their mitral and aortic valves. An underlying immune-mediated disorder was identified in 18 patients (60%), including primary antiphospholipid syndrome (in 8), rheumatic heart disease (in 6), systemic lupus erythematosus (in 2), and rheumatoid arthritis (in 2), 15 (83%) of whom were women. Of the remaining 12 patients with no autoimmune disease, only 5 (42%) were women. No patient had metastatic malignant disease or disseminated intravascular coagulopathy. Systemic embolization was documented in 10 patients (33%), 8 of whom had cerebral involvement. Valvular vegetations were visualized by echocardiography before surgery in 8 patients and were suspected but not confirmed preoperatively in 1 patient. All vegetations consisted primarily of platelets and fibrin. The site and appearance of vegetations did not vary with the underlying disease state. CONCLUSIONS: In contrast to previously reported autopsy series, NBTE in a surgical population was more commonly associated with autoimmune disorders than malignancy or disseminated intravascular coagulopathy. Women were affected twice as often as men. Systemic embolization, particularly to the brain, was prominent in both surgical and autopsy series. Vegetations had a similar appearance regardless of the specific underlying disease. An antemortem diagnosis of NBTE in a patient with no known risk factors should prompt a search not only for occult malignancy, as suggested by autopsy studies, but also for autoimmune or rheumatic diseases, particularly the antiphospholipid syndrome.

Left ventricular and biventricular pacing in congestive heart failure.

Dual-chamber pacing improved hemodynamics acutely in a subset of patients with left ventricular (LV) dysfunction but conveyed no long-term symptomatic benefit in most. More recently, LV pacing and biventricular (multisite) pacing have been used to improve systolic contractility by altering the electrical and mechanical ventricular activation sequence in patients with severe congestive heart failure (CHF) and intraventricular conduction delay or left bundle branch block (LBBB). Intraventricular conduction delay and LBBB cause dyssynchronous right ventricular and LV contraction and worsen LV dysfunction in cardiomyopathies. Both LV and biventricular cardiac pacing are thought to improve cardiac function in this situation by effecting a more coordinated and efficient ventricular contraction. Short-term hemodynamic studies have shown improvement in LV systolic function, which seems more pronounced with monoventricular LV pacing than with biventricular pacing. Recent clinical studies in limited numbers of patients suggest long-term clinical benefit of biventricular pacing in patients with severe CHF symptoms. Continuing and future studies will demonstrate whether and in which patients LV and biventricular pacing are permanently effective and equivalent and which pacing site within the LV produces the most beneficial hemodynamic results.

Aortic root replacement in a patient with vancomycin-resistant Enterococcus faecium endocarditis and leukemia.

Vancomycin-resistant Enterococcus faecium endocarditis is rare and usually occurs in immunocompromised patients. We describe a patient with hairy-cell leukemia and vancomycin-resistant E faecium endocarditis. The patient presented with severe aortic insufficiency. He underwent aortic root replacement with a cryopreserved aortic homograft and was treated with a combination of quinupristin/dalfopristin, ampicillin, and gentamicin.

Quality of life in octogenarians after open heart surgery.

OBJECTIVES: To determine the quality of life in octogenarians after open heart surgery. BACKGROUND: Despite an increasing number of cardiac operations on octogenarians, the outcome as measured by functional status, independence of living, and psychological parameters of quality of life remain unproved. METHODS: Two groups of octogenarians (group 1, undergoing operation in 1986; group 2 in 1991) were reviewed retrospectively to determine operative mortality and functional results. RESULTS: Group 1 (n = 15, mean age of 83.2 years) and group 2 (n = 53, mean age 83.0 years) were studied. Operations included isolated coronary artery bypass grafting (group 1, 10; group 2, 29) and valve replacements +/- coronary artery bypass grafting +/- other procedures (group 1: 5; group 2, 24). Group 1 had 9% hospital mortality and 53% actuarial survival after a mean follow-up of 6.3 years. Group 2 had 17% hospital mortality and 72% actuarial survival after a mean follow-up of 1.5 years. At follow-up, significant improvements were observed in New York Heart Association (NYHA) angina class, congestive cardiac failure class, number of cardiovascular symptoms, and indices for satisfaction with overall life and general affect in both groups. Further, group 2 also showed significant improvements in independence of living, ease of life, and Karnofsky dependency category, but these improvements were less evident in group 1 after a longer period of follow-up. At follow-up, 75% of group 1 and 84% of group 2 octogenarians would definitely have made the same decision to undergo open heart surgery in retrospect. CONCLUSION: This study demonstrates improved quality of life after open heart surgery in octogenarians.

Clinical introduction of a novel prosthesis for valve-preserving aortic root reconstruction for annuloaortic ectasia.

OBJECTIVE: Most patients with annuloaortic ectasia are young. They are at risk for complications related to a lifetime of anticoagulation when composite grafts containing mechanical valves are used for reconstruction. The majority of patients have near normal valve cusps. Valve-preserving techniques have been developed to maintain valve function and avoid anticoagulation. The eddy currents occurring within the sinuses of Valsalva in the natural aortic root have been shown to be important in the smooth, gradual, and gentle closure of the valve. Compliance of the sinuses is important in reducing stress in the leaflets. A novel ascending aortic prosthesis with "built in" compliant sinuses (Robicsek-Thubrikar graft) was developed for clinical aortic root replacement. METHODS: Woven Dacron tubes were used to make the prostheses. Three precisely measured square pieces were cut to make the expandable, individual sinuses. Sewing the individual neo-sinuses to a scalloped end of the Dacron tube graft created the neo-sinotubular junction and sinotubular ridge. Five patients with annuloaortic ectasia underwent valve-preserving aortic root reconstruction. RESULTS: All intraoperative transesophageal echocardiographic images after the valve-preserving procedure showed a normal appearing root with 10% radial expansion of each sinus in systole. The space between the cusps and neo-sinus wall in systole was normal. No patient has more than mild aortic regurgitation. CONCLUSIONS: Valve-preserving aortic root reconstruction with a novel Dacron prosthesis with compliant "built in" sinuses re-establishes normal aortic root geometry with near normal valve motion. This may enhance the durability of the valve-preserving operation.

Effectiveness of the Cobra aortic catheter for dual-temperature management during adult cardiac surgery.

OBJECTIVES: In animals the Cardeon Cobra catheter (Cardeon Corp, Cupertino, Calif) allows independent control of aortic arch and descending aortic temperatures and profoundly reduces cerebral embolization during bypass. This investigation describes the first clinical use of the device during adult cardiac surgery. The purpose of the study was to confirm that the Cobra catheter delivers adequate cerebral and systemic perfusion while providing simultaneous cerebral hypothermia and systemic normothermia during cardiopulmonary bypass. METHODS: In a prospective multicenter study the Cobra aortic catheter was placed in 20 adults undergoing cardiopulmonary bypass. Arch and corporeal temperatures, bypass flows, and arterial blood pressures were recorded intraoperatively. Jugular bulb and mixed venous oxygen saturation was used to assess the adequacy of cerebral and systemic perfusion. RESULTS: Surgeons at 3 institutions placed the Cobra catheter in patients undergoing coronary artery bypass grafting (n = 13), valve (n = 3), and combined valve-bypass (n = 4) operations. Mean total bypass flows of 2.1 +/- 0.2 L x min(-1) x m(-2) maintained mean arterial pressures in arch and descending aortic circulations of greater than 55 mm Hg. A mean differential of 4.3 degrees C between arch and descending aortic temperatures was established before crossclamp application, and a mean maximum temperature differential of 7 degrees C was established during bypass. A 2.4 degrees C temperature differential was maintained at crossclamp removal. Cerebral and systemic venous oxygen saturation remained greater than 65% during bypass. CONCLUSIONS: The Cobra device met all expectations for an arterial cannula with adequate perfusion to the arch and corporeal circulations. Dual perfusion with the Cobra catheter allows for independent temperature control during cardiopulmonary bypass with simultaneous cerebral hypothermia and systemic normothermia.

Glutamate excitotoxicity: a mechanism of neurologic injury associated with hypothermic circulatory arrest.

Glutamate, the major central nervous system neurotransmitter, may have potent neurotoxic activity under conditions of metabolic stress. By receptor autoradiography, we have demonstrated that brain regions most vulnerable to injury during prolonged hypothermic circulatory arrest have the highest density of glutamate receptors. To test the hypothesis that such injury could be mediated by glutamate excitotoxicity, we used dizocilpine (MK-801), a selective N-methyl-D-aspartate-glutamate receptor antagonist in a canine survival model of hypothermic circulatory arrest. Eighteen male dogs (20 to 25 kg) were supported by closed-chest cardiopulmonary bypass, subjected to 2 hours of hypothermic circulatory arrest at 18 degrees C, and rewarmed on cardiopulmonary bypass. All were mechanically ventilated and monitored for 20 hours before extubation and survived for 3 days. Group A dogs (n = 9) received a prearrest intravenous bolus of dizocilpine (0.75 mg/kg) followed by continuous infusion (75 micrograms/kg per hour), resulting in electroencephalographic silence. Dizocilpine was weaned before extubation. Group B dogs received vehicle only. According to a species-specific behavior scale that yielded a neurologic deficit score ranging from 0 (normal) to 500 (brain dead), all animals were neurologically assessed every 12 hours. After the dogs were killed at 72 hours, brains were examined by receptor autoradiography and histologically for patterns of selective neuronal necrosis; they were scored blindly from 0 (normal) to 100 (severe injury). Group A dogs had better neurologic function than group B (neurologic deficit score 21 +/- 15 versus 192 +/- 40, p < 0.001) and had less neuronal injury (7.3 +/- 3 versus 48.3 +/- 9, p < 0.0001). Densitometric receptor autoradiography revealed preservation of neuronal N-methyl-D-aspartate-glutamate receptor expression in group A only. These results represent the first direct evidence of a role for glutamate excitotoxicity in the development of hypothermic circulatory arrest-induced brain injury and suggest that selective glutamate receptor antagonists may have a neuroprotective capacity in prolonged periods of hypothermic circulatory arrest.

Neutrophil adhesion inhibition prolongs survival of cardiac allografts with hyperacute rejection.

Hyperacute rejection results in rapid destruction of a cardiac allograft and is characterized by infiltration of neutrophils into the donor organ. We sought to ameliorate this response by using a potent inhibitor of neutrophil adhesion to vascular endothelium, NPC 15669 (N-[9H-(2,7-dimethylfluorenyl-9-methoxy) carbonyl]-L-leucine) and determine its effect on long-term graft survival and histology. This compound specifically prevents recruitment of neutrophils at inflammatory foci by inhibiting upregulation of the CD11b/CD18 adhesion molecule located on the neutrophil surface. Lewis rats were presensitized by three serial ACI rat skin grafts placed 10 days apart. ACI rat hearts were heterotopically transplanted into Lewis recipients 10 to 14 days after the final skin graft. Group I (n = 15) was treated with a 10 mg/kg intravenous bolus of NPC 15669 before reperfusion, followed by 3 mg/kg over 30 minutes. Group II (n = 13) was given saline vehicle intravenously. Two allografts in each group were harvested at 5, 15, 30, and 60 minutes, and the remainder were followed to cessation of graft function. Early 5- to 60-minute allograft histologic findings revealed focal interstitial hemorrhage, edema, and contraction-band necrosis associated with neutrophil infiltration in group II. Group I had significant reduction of all parameters at the earliest time points. Graft survival was significantly increased in group I, 89.2 +/- 20.3 hours (mean +/- SD) compared to 27 +/- 17 hours in group II (p < 0.0001). End-stage rejection was characterized by extensive neutrophil infiltrate and hemorrhage in group II; group I grafts had a predominantly mononuclear cell infiltrate with rare neutrophils.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of theophylline for treatment of prolonged sinus node dysfunction in human orthotopic heart transplantation.

Sinus node dysfunction may complicate heart transplantation in over 50% of cases, leading to prolonged bradyarrhythmias in 20% of recipients. Permanent pacemaker implantation, the standard treatment for such persistent rhythm disturbances, can result in significant complications in this setting. A protocol with theophylline, a methylxanthine known to reverse the sinus node electrophysiologic abnormalities observed in transplant patients, was initiated at our institution in October 1989 to treat posttransplantation bradyarrhythmias and to reduce the need for pacemaker implantation. Patients with sinus or nodal bradycardia or sinus arrest were given theophylline orally; the drug was initiated in 15 of 38 patients (39.5%), 3 to 24 days after transplantation. Mean duration of treatment was 57.4 days (range, 20 to 105 days). Normal sinus rhythm with a rate of more than 90 beats/min was restored in 14 of 15 patients (93.3%). Permanent pacing was required in one patient. Transplant recipients before October 1989 (group 1, n = 112) were compared with subsequent transplant recipients (group 2, n = 38). These groups did not differ significantly in incidence of bradyarrhythmias or potential risk factors for posttransplantation sinus node dysfunction, though a greater preoperative use of amiodarone occurred in group 2. Permanent pacemaker requirement was significantly reduced from 16.1% in group 1 to 2.6% in group 2 (p < 0.05) with the introduction of theophylline. Theophylline is effective treatment for posttransplantation bradyarrhythmias, thereby resulting in a reduced need for pacemaker implantation.

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.

The monosialoganglioside, GM1, reduces neurologic injury associated with hypothermic circulatory arrest.

BACKGROUND: Neurologic injury associated with prolonged hypothermic circulatory arrest (HCA) may be mediated by calcium-dependent glutamate excitotoxicity (GE). The monosialoganglioside GM1 has been shown in vitro to limit GE in conditions of metabolic stress. To test the hypothesis that gangliosides can prevent HCA-induced brain injury, GM1 was used in a canine model of HCA. METHODS: Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 hours of HCA at 18 degrees C, and rewarmed to 36 degrees to 37 degrees C on closed-chest cardiopulmonary bypass. All were mechanically ventilated and monitored for 20 hours before extubation and survived for 3 days. Group 1 dogs (n = 6) were pretreated with GM1, 30 mg/kg/24hr for 3 days before HCA, and received continuous infusion of GM1 during the procedure and 30 mg/kg/24hr 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 hours. After death at 72 hours, 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). RESULTS: Group 1 dogs had better neurologic function compared with group 2 (neurodeficit score, 4.2% +/- 3% vs 38.4% +/- 8%; p < 0.001) and had less neuronal injury (11.3 +/- 3 vs 48.3 +/- 9, p < 0.001). Densitometric receptor autoradiography revealed preservation of neuronal glutamate receptor expression in group 1 only. CONCLUSIONS: 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 capacity in prolonged periods of HCA.

Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass.

It has previously been demonstrated that cardiopulmonary bypass (CPB) causes prolonged pulmonary vascular hyperreactivity (D.P. Nyhan, J.M. Redmond, A.M. Gillinov, K. Nishiwaki, and P.A. Murray. J. Appl. Physiol. 77: 1584-1590, 1994). This study investigated the effects of CPB on endothelium-dependent (acetylcholine and bradykinin) and endothelium-independent (sodium nitroprusside) pulmonary vasodilation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LP-Q) plots were generated in conscious dogs before CPB and again in the same animals 3-4 days post-CPB. The dose of U-46619 used to acutely preconstrict the pulmonary circulation to similar levels pre- and post-CPB was decreased (0.13 +/- 0.01 vs. 0.10 +/- 0.01 mg.kg-1.min-1, P < 0.01) after CPB. Acetylcholine, bradykinin, and sodium nitroprusside all caused dose-dependent pulmonary vasodilation pre-CPB. The pulmonary vasodilator response to acetylcholine was completely abolished post-CPB. For example, at left pulmonary blood flow of 80 ml.kg-1.min-1 acetylcholine (10 micrograms.kg-1.min-1) resulted in 72 +/- 15% reversal (P < 0.01) of U-46619 preconstriction pre-CPB but caused no change post-CPB. However, the responses to bradykinin and sodium nitroprusside were unchanged post-CPB. The impaired pulmonary vasodilator response to acetylcholine, but not to bradykinin, suggests a selective endothelial defect post-CPB. The normal response to sodium nitroprusside indicates that cGMP-mediated vasodilation is unchanged post-CPB.

A case of asymptomatic thoracic aorta mural thrombi.

The natural history, prognostic significance, and optimal therapy of asymptomatic thoracic aorta mural thrombi detected incidentally is not well defined in the literature. We report a case of asymptomatic thoracic aorta mural thrombi in a 42-year-old woman with a history of smoking and steroid use that was conservatively managed with anticoagulation and had a favorable outcome.

Split pectoralis major muscle flap reconstruction after clavicular-manubrial resection.

Resection of the clavicular head and clavicular-manubrial junction is required in cases of chronic osteomyelitis or tumor. This article describes a technique for soft tissue coverage in an infected or irradiated area after resection using a split pectoralis major rotational muscle flap.

Standardized clinical care pathways for major thoracic cases reduce hospital costs.

BACKGROUND: Standardized clinical care pathways have been developed for postoperative management in an attempt to contain costs in an era of rising health care costs and limited resources. The purpose of this study was to assess the effect of these pathways on length of stay, hospital charges, and outcome for major thoracic surgical procedures. METHODS: All anatomic lung (segmentectomy, lobectomy, and pneumonectomy) and partial and complete esophageal resections performed from July 1991 to July 1997 were retrospectively analyzed for length of stay, hospital charges, and outcome. A prospectively developed database was used. Clinical care pathways were introduced in March 1994. Comparisons were made between the procedures performed before (group I) and after (group II) pathway implementation. Common to both pathways are early mobilization and prudent x-ray and laboratory analysis. In addition, the pathway for esophagectomies emphasizes overnight intubation with 24-hour intensive care unit care, and staged diet advancement. The discharge goal was postoperative day 10. For lung resection the emphasis is early postoperative extubation with overnight intensive care unit management. The discharge goal was postoperative day 7. RESULTS: Group I esophagectomies (n = 56) had significantly greater hospital charges compared with group II (n = 96) ($21,977 +/- $13,555 versus $17,919 +/- $5,321; p < 0.04, in actual dollars) and ($29,097 +/- $18,586 versus $19,260 +/- $6,000; p < 0.001, in dollars adjusted for inflation) and greater length of stay (13.6 +/- 6.9 versus 9.5 +/- 2.8 days; p < 0.001). Group I lung resections (n = 185) had a significantly greater length of stay compared with group II (n = 241) (8.0 +/- 6.2 versus 6.4 +/- 3.8 days; p < 0.002); although charges trended downward ($13,113 +/- $10,711 versus $12,404 +/- $7,189; not significant) in actual dollars, charges were significantly less in dollars adjusted for inflation ($17,103 +/- $13,211 versus $13,432 +/- $8,056; p < 0.01). The most significant decreases in charges for esophagectomies were in miscellaneous charges (61% in dollars adjusted for inflation), pharmaceuticals (60%), laboratory (42%) and radiologic (39%) tests, physical therapy charges (35%), and routine charges (34%). For lung resections the greatest savings occurred for pharmaceuticals (38%), supplies (34%), miscellaneous charges (25%), and routine charges (22%). Mortality was similar (esophagectomies: I, 3.6%; II, 0%; lung resections: I, 0.5%; II, 0.8%; not significant). CONCLUSIONS: Introduction of standardized clinical pathways has resulted in a marked reduction of length of stay for all major thoracic surgical procedures. Total charges were reduced for both esophagectomies (34%) and lung resections (21%) with continued quality of outcome.

Heparin-coated bypass circuits reduce pulmonary injury.

Heparin coating of the extracorporeal circuit not only reduces heparin requirements during cardiac operations but also may reduce organ injury associated with cardiopulmonary bypass (CPB). To examine this possibility, pulmonary injury and neutrophil adhesion molecule expression after CPB were studied in pigs undergoing CPB with a standard extracorporeal circuit (group S, n = 6) or a heparin-coated CPB circuit (Carmeda BioActive Surface) (group HC, n = 6). Pigs received heparin sodium (300 U/kg intravenously) and then underwent 90 minutes of hypothermic (28 degrees C) CPB using membrane oxygenators, followed by 2 hours of observation. Blood samples were obtained for determination of neutrophil number and expression of the neutrophil adhesion molecule subunit CD18 (by immunofluorescence flow cytometry). The CPB-associated injury was less in group HC. Two hours after CPB, the arterial oxygen tension group was higher in group HC (597.2 +/- 31.2 versus 220.5 +/- 42.3 mm Hg; p < 0.0001), the pulmonary vascular resistance was lower in these animals (408.6 +/- 69.4 versus 1,159.8 +/- 202.4 dyne.s.cm-5; p = 0.02), and the static compliance was higher in group HC (66.4 +/- 5.4 versus 39.8 +/- 5.8 mL/mm Hg; p = 0.004). After 60 minutes of CPB, both groups had similar increases in expression of the neutrophil adhesion molecule subunit CD18 (29.4% +/- 19.5% versus 26.0% +/- 24.4%, group S and group HC, respectively) and similar decreases in neutrophil counts (6,056 +/- 1,285 to 2,453 +/- 979 cells/microL versus 6,010 +/- 1,748 to 3,197 +/- 1,225 cells/microL, group S and group HC, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Neutrophil modulation results in improved pulmonary function after 12 and 24 hours of preservation.

Neutrophils are important mediators of reperfusion injury, and suppression of neutrophil function or numbers can reduce reperfusion injury and improve long-term organ preservation in transplantation. NPC 15669, a leumedin, is a novel compound that prevents recruitment of neutrophils at inflammatory foci by inhibiting CD11b/CD18 adhesion molecule expression. NPC 15669 was used to inhibit neutrophil adhesion during reperfusion of isolated rabbit lungs after 12 and 24 hours of cold storage. Lungs (New Zealand White male rabbits, 2 to 3 kg) were flushed with 4 degrees C Euro-Collins (EC) solution, harvested en bloc, stored under various study conditions, and reperfused for 3 hours with fresh whole blood at 37 degrees C in an isolated perfusion system at constant flow and an inspired oxygen fraction of 1. Four groups (n = 6 each) were studied. Group I underwent immediate whole blood reperfusion. Group II were stored for 12 hours in 4 degrees C EC solution before reperfusion. Group III were stored for 12 hours in 4 degrees C EC solution and reperfused with whole blood containing NPC 15669 (10 mg/kg whole body weight). Group IV were stored for 24 hours in 4 degrees C EC solution and reperfused with whole blood containing NPC 15669 (10 mg/kg). Pulmonary artery and peak airway pressures were significantly lower and compliance higher in groups III and IV lungs after 3 hours of reperfusion (p < 0.05) compared with group I. Group I and III lungs had significantly less edema than group II (p < 0.05). The arterial partial pressure of oxygen was similar in all stored groups (II to IV).(ABSTRACT TRUNCATED AT 250 WORDS)