Double-chambered right ventricle in adulthood.

Patients with double-chambered right ventricle presenting with symptoms in adulthood are rare. From 1990 to 2004, 4 adults and 9 children with double-chambered right ventricle underwent surgical correction. The surgical results and clinical data of the adults were compared with those of the pediatric patients. All adult patients had dyspnea on exertion, 3 children showed growth delay but the others were asymptomatic. The mean age at operation was 44.5 +/- 6.3 years in adults and 5.2 +/- 1.9 years in children. The mean pressure gradient between the anatomically lower right ventricle and the pulmonary artery was significantly higher in adults than in children (91.8 +/- 14.1 vs. 42.2 +/- 5.9 mm Hg). The pulmonary-to-systemic flow ratio in adults was significantly lower than in pediatric patients (1.2 +/- 0.2 vs. 1.8 +/- 0.3). All adults and 8 of the 9 children survived. There were no late deaths or re-operations, and all survivors were in New York Heart Association functional class I. Surgical correction of double-chambered right ventricle in adults gave satisfactory midterm results although right ventricular outflow tract obstruction and clinical symptoms were severe in these patients.

Transient ischemia-induced paresis and complete paraplegia displayed distinct reactions of microglia and macrophages.

In this study, we perform a detailed analysis of the microglial and macrophage responses in a model of spinal cord ischemia and reperfusion (SCI/R) injury in Wistar rats. The rats underwent occlusion across the descending aorta for 13min, causing paraplegia or paresis of varying severity. They were divided into four groups based on neurological assessment: sham, mild paresis, moderate paresis, and severe (complete) paraplegia. To examine the origin of microglia and macrophages in the ischemic lesion, bone marrow from rats expressing green fluorescent protein (GFP) was transplanted into test subjects one month before performing SCI/R. Many GFP(+)/CD68(+) microglia and macrophages were present 7d after SCI/R. Resident (GFP(-)/Iba1(+)/CD68(-)) microglia and bone marrow-derived macrophages (BMDMs; GFP(+)/Iba1(+)/CD68(+)) colocalized in the mild group 7d after SCI/R. In the moderate group, BMDMs outnumbered resident microglia. A greater accumulation of BMDMs expressing insulin-like growth factor-1 (IGF-1) was observed in lesions in the severe group, relative to the moderate group. BMDMs in the severe group strongly expressed tumor necrosis factor α, interleukin-1ß, and inducible nitric oxide synthase, in addition to IGF-1. A robust accumulation of BMDMs occupying the entire ischemic gray matter was observed only in the severe group. These results demonstrate that the magnitude of the microglial and BMDM responses varies considerably, and that it correlates with the severity of the neurological dysfunction. Remarkably, BMDMs appear to have a beneficial effect on the spinal cord in paresis. In contrast, BMDMs seem to exhibit both beneficial and harmful effects in severe paraplegia.

Combined ablation of atrial fibrillation and minimally invasive mitral valve surgery: a case report.

A partial lower inverted J sternotomy and an extended transseptal incision provide excellent exposure for minimally invasive mitral valve surgery. However, the extended trasnsseptal incision causes dividing the sinus node artery, which may result in conduction system disturbance and need for permanent pacemaker implantation. Therefore, there is a challenge in the patient who requires concomitant ablation for atrial fibrillation because of possible conduction system disturbance caused by extended transseptal incision. We describe a new strategy for combined ablation of atrial fibrillation with minimally invasive cardiac surgery by a transseptal approach to the mitral valve through a partial lower sternotomy incision. Cryoablation was performed using a T-shaped cryoprobe with a lesion set of pulmonary vein isolation and ablation of the left and right isthmus in performing mitral annuloplasty, tricuspid annuloplasty, and atrial septal defect closure through a limited sternotomy incision. This technique might minimize possible conduction system disturbance and provide good surgical result for the patients who undergo mitral valve surgery and ablation of atrial fibrillation.

Off-pump coronary bypass via left thoracotomy resulting from sternoclavicular arthritis.

We report a case of coronary artery bypass grafting through the left thoracotomy in a patient who suffered from sternoclavicular joint infection with methicillin-resistance Staphylococcus aureus. We performed off-pump coronary bypass surgery, using the left internal thoracic artery to the left anterior descending coronary artery and a saphenous vein graft from the aorta to the circumflex artery, with a successful outcome. This approach seems to be safe and effective for coronary bypass grafting in situations where median sternotomy is not favorable, as in the described patient.

Coagulant activity during one year after bioprosthetic aortic valve replacement.

Anticoagulant therapy with warfarin is recommended in the early postoperative period after bioprosthetic aortic valve replacement (bAVR). However, some studies have addressed questions about its necessity. We evaluated postoperative coagulant activity data including prothrombin time-international normalized ratio (PT-INR) and thrombin-antithrombin III complex (TAT), measured every month in 21 bAVR patients during the 1st postoperative year. The results were divided into four time intervals after the operation: 1-3 months (P-1), 4-6 (P-2), 7-9 (P-3), and 10-12 (P-4). Warfarin, which was administrated in the first six months, in combination with aspirin, 100 mg, was started targeting PT-INR of 1.75-2.25. The values of TAT in P-1, P-2, P-3 and P-4 were 1.35+/-1.07 (ng/ml), 0.82+/-0.55, 0.81+/-0.78, and 0.72+/-0.62, respectively, showing significantly high values in P-1. Furthermore, the TAT values of P-1 and P-2 within the range of PT-INR from 1.75 to 2.25 were 1.15+/-0.71 (ng/ml) and 0.79+/-0.52; demonstrating statistical difference between them. The coagulant activity assessments suggest that warfarin administration during the first three months is necessary for bAVR patients to keep the TAT within the normal range.

Intestinal ischemia/reperfusion-induced bacterial translocation and lung injury in atherosclerotic rats with hypoadiponectinemia.

BACKGROUND: Intestinal ischemia/reperfusion causes intestinal mucosal injury, which may result in bacterial translocation (BT) and multiple organ failure. Lung injury is a common complication after intestinal ischemia/reperfusion. Adiponectin is an antiinflammatory adipokine, and it plays an important role in the development of metabolic syndrome in hypoadiponectinemia. In atherosclerosis with hypoadiponectinemia, BT also may aggravate injuries induced by intestinal ischemia/reperfusion. METHODS: Wistar rats were divided into 3 groups: Normal group (normal diet), Chol group (2% high cholesterol diet), and Chol+1400W group (Chol group plus 1400W, an inducible nitric oxide [iNOS] inhibitor, at 1 mg/kg intraperitoneally 30 minutes preoperatively). The serum concentrations of lipids and adiponectin and vascular responses were measured. After midline laparotomy (time, T0), the superior mesenteric artery was occluded with a microvascular clamp for 30 minutes, followed by 360 minutes of reperfusion (T1). Intestinal injury was assessed from microcirculatory flow, histology, serum diamine oxidase activity, and permeability. Lung injury was assessed by histology, pulmonary permeability index (PPI), and wet-to-dry lung weight (W/D) ratio. Intestinal and lung nitric oxide (NO) concentrations were also measured. BT was assessed by serum peptidoglycan (PG) concentration. RESULTS: The Chol and Chol+1400W groups developed hyperlipidemia and hypoadiponectinemia; the 2 groups also had vascular endothelial dysfunction without histological changes, indicating early atherosclerosis. These groups also showed poor recovery of intestinal microcirculatory flow at T1. The serum diamine oxidase activity, histological intestinal damage, and permeability were elevated at T1 in the Chol group; however, these findings were not significant in the Normal and Chol+1400W groups. Histological lung damage and lung PPI and W/D ratio were increased only in the Chol group. Intestinal and lung NO concentrations were significantly elevated at T1 in the Chol group. The serum PG concentration was elevated significantly in the Chol group. CONCLUSION: In atherosclerotic rats with hypoadiponectinemia, intestinal microcirculatory flow does not recover adequately after intestinal ischemia/reperfusion because of endothelial dysfunction. Atherosclerosis with hypoadiponectinemia increased the incidence of BT further by aggravating intestinal mucosal injury and, moreover, it aggravated lung injury. Although inhibition of iNOS does not lead to adequate recovery of intestinal microcirculatory flow, it reduces injury by decreasing the amount of NO derived from high enzymatic iNOS activity in the intestine.

Pitavastatin prevents intestinal ischemia/reperfusion-induced bacterial translocation and lung injury in atherosclerotic rats with hypoadiponectinemia.

BACKGROUND: Atherosclerosis with hypoadiponectinemia can be further aggravated by intestinal ischemia/reperfusion (II/R)-induced injuries, such as bacterial translocation and lung injury. We investigated the effect of statin administration on the risk of II/R-induced injury in atherosclerotic rats with hypoadiponectinemia. METHODS: Wistar rats were divided into 4 groups: (1) the Normal group (normal diet), (2) the Chol group (2% high cholesterol diet), (3) the St-1w group, and (4) the St-2w group (Chol group plus pitavastatin administration for 1 or 2 weeks, respectively). The serum concentrations of lipids and adiponectin were measured preoperatively. After midline laparotomy (time, T0), the superior mesenteric artery was occluded with a microvascular clamp for 30 min, followed by 360 min of reperfusion (T1). Intestinal and lung nitric oxide (NO) concentrations were measured. Intestinal injury was assessed by microcirculatory flow, histology, and permeability. Bacterial translocation was assessed by analysis of serum peptidoglycan concentration. Lung injury was assessed by histologic examination, pulmonary permeability index, and wet/dry lung weight ratio. RESULTS: The 2-week administration of statins with high-cholesterol feeding (St-2w group) improved hypoadiponectinemia to levels similar to those of the Normal group. Intestinal and lung NO concentrations were significantly lower at T1 in the Normal and St-2w groups than in the Chol group. Statin administration improved poor recovery of intestinal microcirculatory flow in the Chol group. At T1, intestinal and lung injuries were significantly aggravated and serum peptidoglycan concentration was significantly elevated in the Chol group compared with the Normal and St-2w groups. The 1-week administration of statins had no significant influence on serum adiponectin levels, tissue NO concentration, or tissue injury. CONCLUSION: Administration of pitavastatin reduces the risk of II/R-induced injury in atherosclerotic rats with hypoadiponectinemia by improving hypoadiponectinemia and inhibiting inducible NO synthase-produced NO. Furthermore, preoperative improvement of hypoadiponectinemia may be important as an index of the protective effect of pitavastatin for II/R-induced injury in atherosclerotic rats with hypoadiponectinemia.