Examination of sex as an independent risk factor for adverse events after carotid endarterectomy

BackgroundThe incidence of adverse events after carotid endarterectomy (CEA) for women compared with men is controversial. This report compares the incidence of perioperative stroke and death in men and women by examining the effect of comorbidities and hospital setting on CEA outcomes.MethodsAll CEAs performed in non-Federal acute-care Virginia hospitals between 1997 and 2001 were reviewed. Patient demographics, comorbidities, and hospital characteristics were compared for possible relationships to perioperative adverse events.ResultsA total of 14,095 CEAs were performed in 34 urban and 28 rural hospitals (9 high-volume and 53 low-volume hospitals); 42% were performed on women, and 58% were performed on men. Women experienced a significantly higher stroke rate (1.23%) than men (0.87%; P = .04) with bivariate analysis. However, logistic regression analysis of comorbidities and hospital settings demonstrated that sex was actually not independently related to adverse outcomes in CEA (P = .08). Preoperative neurologic symptoms could not be evaluated as risk factors for adverse events. Acute coronary ischemia, history of arrhythmia, end-stage renal disease, nonwhite race, advanced age, and low hospital volume were all significantly related to mortality. History of arrhythmia was the only factor that was significantly related to the incidence of stroke.ConclusionsLogistic regression analysis of comorbidities and hospital setting indicated that female sex is not independently associated with higher mortality or a higher stroke rate during CEA. These data indicate that patients with carotid stenosis frequently have multiple medical problems that need to be carefully examined and controlled before any single patient or hospital factor is designated as significantly related to adverse outcomes

Reinitiation of compensatory lung growth after subsequent lung resection

ObjectiveIn experimental animals, pneumonectomy results in rapid, hyperplastic compensatory growth of the remaining lung. The limits of this induced growth are unknown. We tested the hypothesis that compensatory growth can be reinitiated in the same lung after subsequent lung resection.MethodsA left thoracotomy (Sham group) or left pneumonectomy (PNX group) was performed in Sprague–Dawley rats. A third group underwent left pneumonectomy followed 4 weeks later by a bilobectomy of the right upper and middle lobes (PNX+LBX group). Four weeks after bilobectomy in the PNX+LBX group (8 weeks in the Sham and PNX groups), right ventricular pressures were measured by using the open chest technique, and total lung weight and lower plus cardiac lobe weight indices were measured. Lungs were inflation fixed at 25 cm H2O to measure lobe volume index and to perform morphometric measurements on lung sections. Right ventricle/left ventricle plus septum weight index was measured as another index of pulmonary hypertension.ResultsTotal lung weight index was similar in all groups. Pneumonectomy resulted in increased lower plus cardiac lobe weight and volume indices, which were significantly augmented in the PNX+LBX group. The PNX+LBX group underwent a significant increase in total volume of respiratory region, airspace, and tissue and a decrease in alveolar surface density versus the PNX group. The PNX+LBX group also had significantly increased right ventricular systolic pressure and right ventricle/left ventricle plus septum index.ConclusionThese results demonstrate that compensatory growth can be reinitiated in lungs that had previously undergone postpneumonectomy compensatory growth. This subsequent growth, however, is more hypertrophic, and pulmonary hypertension develops despite subsequent compensatory growth

Adenosine A1 receptor activation attenuates lung ischemia–reperfusion injury

ObjectivesIschemia–reperfusion injury contributes significantly to morbidity and mortality in lung transplant patients. Currently, no therapeutic agents are clinically available to prevent ischemia–reperfusion injury, and treatment strategies are limited to maintaining oxygenation and lung function. Adenosine can modulate inflammatory activity and injury by binding to various adenosine receptors; however, the role of the adenosine A1 receptor in ischemia–reperfusion injury and inflammation is not well understood. The present study tested the hypothesis that selective, exogenous activation of the A1 receptor would be anti-inflammatory and attenuate lung ischemia–reperfusion injury.MethodsWild-type and A1 receptor knockout mice underwent 1 hour of left lung ischemia and 2 hours of reperfusion using an in vivo hilar clamp model. An A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine, was administered 5 minutes before ischemia. After reperfusion, lung function was evaluated by measuring airway resistance, pulmonary compliance, and pulmonary artery pressure. The wet/dry weight ratio was used to assess edema. The myeloperoxidase and cytokine levels in bronchoalveolar lavage fluid were measured to determine the presence of neutrophil infiltration and inflammation.ResultsIn the wild-type mice, 2-chloro-N6-cyclopentyladenosine significantly improved lung function and attenuated edema, cytokine expression, and myeloperoxidase levels compared with the vehicle-treated mice after ischemia–reperfusion. The incidence of lung ischemia–reperfusion injury was similar in the A1 receptor knockout and wild-type mice; and 2-chloro-N6-cyclopentyladenosine had no effects in the A1 receptor knockout mice. In vitro treatment of neutrophils with 2-chloro-N6-cyclopentyladenosine significantly reduced chemotaxis.ConclusionsExogenous A1 receptor activation improves lung function and decreases inflammation, edema, and neutrophil chemotaxis after ischemia and reperfusion. These results suggest a potential therapeutic application for A1 receptor agonists for the prevention of lung ischemia–reperfusion injury after transplantation

An unusual case of cardiac dysfunction after left ventricular reconstruction

This report describes an unusual cause of low cardiac output after coronary artery bypass grafting and left ventricular remodeling. It details left ventricular remodeling techniques and discusses the most recent advances and outcomes. As well, significant attention is paid to the issues surrounding failure to separate from cardiopulmonary bypass

Tissue-derived proinflammatory effect of adenosine A2B receptor in lung ischemia–reperfusion injury

ObjectiveIschemia–reperfusion injury after lung transplantation remains a major source of morbidity and mortality. Adenosine receptors have been implicated in both pro- and anti-inflammatory roles in ischemia–reperfusion injury. This study tests the hypothesis that the adenosine A2B receptor exacerbates the proinflammatory response to lung ischemia–reperfusion injury.MethodsAn in vivo left lung hilar clamp model of ischemia–reperfusion was used in wild-type C57BL6 and adenosine A2B receptor knockout mice, and in chimeras created by bone marrow transplantation between wild-type and adenosine A2B receptor knockout mice. Mice underwent sham surgery or lung ischemia–reperfusion (1 hour ischemia and 2 hours reperfusion). At the end of reperfusion, lung function was assessed using an isolated buffer-perfused lung system. Lung inflammation was assessed by measuring proinflammatory cytokine levels in bronchoalveolar lavage fluid, and neutrophil infiltration was assessed via myeloperoxidase levels in lung tissue.ResultsCompared with wild-type mice, lungs of adenosine A2B receptor knockout mice were significantly protected after ischemia–reperfusion, as evidenced by significantly reduced pulmonary artery pressure, increased lung compliance, decreased myeloperoxidase, and reduced proinflammatory cytokine levels (tumor necrosis factor-α; interleukin-6; keratinocyte chemoattractant; regulated on activation, normal T-cell expressed and secreted; and monocyte chemotactic protein-1). Adenosine A2B receptor knockout→adenosine A2B receptor knockout (donor→recipient) and wild-type→ adenosine A2B receptor knockout, but not adenosine A2B receptor knockout→wild-type, chimeras showed significantly improved lung function after ischemia–reperfusion.ConclusionsThese results suggest that the adenosine A2B receptor plays an important role in mediating lung inflammation after ischemia–reperfusion by stimulating cytokine production and neutrophil chemotaxis. The proinflammatory effects of adenosine A2B receptor seem to be derived by adenosine A2B receptor activation primarily on resident pulmonary cells and not bone marrow-derived cells. Adenosine A2B receptor may provide a therapeutic target for prevention of ischemia–reperfusion-related graft dysfunction in lung transplant recipients

Use of a regional wall motion score to enhance risk stratification of patients receiving an implantable cardioverter-defibrillator

AbstractObjectives. We postulated that preoperative assessment of both regional wall motion and left ventricular ejection fraction would serve as an accurate prognostic indicator of long-term cardiac mortality and functional outcome in patients treated with an implantable cardioverter-defibrillator.Background. Long-term cardiac mortality has remained high in patients receiving an implantable cardioverter-defibrillator. The ability to risk stratify patients before defibrillator implantation is becoming increasingly important from a medical and economic standpoint.Methods. The hypothesis was retrospectively tested in 74 patients who had received an implantable cardioverterdefibrillator. Left ventricular ejection fraction and regional wall motion score, derived from centerline chord motion analysis, were calculated for each patient from the preoperative right anterior oblique contrast ventriculogram. Wall motion score was the only significant independent predictor of long-term cardiac mortality and functional status by multivariate analysis because of its enhanced prognostic capability in patients with an ejection fraction in the critical range of 30% to 40%.Results. Patients with an ejection fraction >40% had a 3-year cardiac mortality rate of 0% compared with 25% for those with an ejection fraction of 30% to 40% and 48% for those with an ejection fraction <30% (p < 0.05). Similarly, 75% of patients with an ejection fraction >40% were in New York Heart Association functional class I or II during long-term follow-up compared with 59% of those with an ejection fraction 30% to 40% and 29% of those with an ejection fraction <30%. Among patients with an ejection fraction of 30% to 40%, those with a wall motion score >16% had a 3-year cardiac mortality rate of 0% compared with 71% of those with a wall motion score ≤ 16% (p = 0.002). In addition, 86% of patients with a wall motion score >16% were in functional class I or II during long-term follow-up compared with 13% of those with a wall motion score ≤16% (p = 0.001).Conclusions. Long-term cardiac mortality and functional outcome in patients receiving an implantable cardioverterdefibrillator can be predicted if the left ventricular ejection fraction and regional wall motion score are measured preoperatively

Stroke rate is markedly reduced after carotid endarterectomy by avoidance of protamine

AbstractPurpose: Postoperative neurologic injury remains a significant risk of carotid endarterectomy. Mechanisms include embolization of debris and formation of thrombus on the newly endarterectomized surface. We hypothesized that the risk of postoperative neurologic injury would be lower in those patients who did not receive protamine for reversal of heparin anticoagulation.Methods: We reviewed 348 consecutive primary carotid endarterectomies performed since January 1, 1986, to determine the relationship between surgical outcomes and reversal of heparin anticoagulation. Patients undergoing additional simultaneous cardiovascular procedures were excluded. One hundred ninety-three patients received protamine after completion of the endarterectomy. The remaining 155 patients did not receive any protamine.Results: All patients in both groups survived to discharge. There were no strokes in those patients who did not receive any protamine; however, the stroke rate in the protamine group was 2.6% (5 of 193), p < 0.045. The incidence of hematoma requiring reexploration was 1.0% (2 of 193) and 1.9% (3 of 155) in the protamine and no-protamine groups, respectively (p = NS). Intraoperative shunting was used more frequently in the no-protamine group (84% vs 67%, p < 0.001), and patch angioplasty was performed more frequently in the protamine group (35% vs 15%, p < 0.001). However, neither shunting nor patching significantly influenced stroke rates.Conclusions: We conclude that carotid endarterectomy without reversal of heparin anticoagulation is associated with a reduced postoperative stroke rate without a significant increase in morbidity rates. (J VASC SURG 1995;22:264-70.

Hypothermic retrograde venous perfusion with adenosine cools the spinal cord and reduces the risk of paraplegia after thoracic aortic clamping

AbstractObjective: We evaluated the utility of retrograde venous perfusion to cool the spinal cord and protect neurologic function during aortic clamping. We hypothesized that hypothermic adenosine would preserve the spinal cord during ischemia. Methods: Six swine (group I) underwent thoracic aortic occlusion for 30 minutes at normothermia. Group II animals underwent spinal cooling by retrograde perfusion of the paravertebral veins with hypothermic (4°C) saline solution during aortic occlusion. The spinal cords of group III animals were cooled with a hypothermic adenosine solution in a similar fashion. Intrathecal temperature was monitored and somatosensory evoked potentials assessed the functional status of spinal pathways. Results: Spinal cooling without systemic hypothermia significantly improved neurologic Tarlov scores in group III (4.8 ± 0.2) and group II (3.8 ± 0.4) when compared with group I scores (1.3 ± 0.6) (P < .001). Furthermore, 5 of the 6 animals in group III displayed completely normal neurologic function, whereas only one animal in group II and no animals in group I did (P = .005). Somatosensory evoked potentials were lost 10.6 ± 1.4 minutes after ischemia in group I. In contrast, spinal cooling caused rapid cessation of neural transmission with loss of somatosensory evoked potentials at 6.9 ± 1.2 minutes in group II and 7.0 ± 0.8 minutes in group III (P = .06). Somatosensory evoked potential amplitudes returned to 85% of baseline in group III and 90% of baseline in group II compared with only 10% of baseline in group I (P = .01). Conclusions: We conclude that retrograde cooling of the spinal cord is possible and protects against ischemic injury and that adenosine enhances this effect. The efficacy of this method may be at least partly attributed to a more rapid reduction in metabolic and electrical activity of the spinal cord during ischemia. (J Thorac Cardiovasc Surg 2000;119:588-95