Predictive Factors of Re-restenosis after Repeated Sirolimus-Eluting Stent Implantation for SES Restenosis and Clinical Outcomes after Percutaneous Coronary Intervention for SES Restenosis

Sirolimus-eluting stent (SES) is established to be effective in reducing restenosis. Repeat revascularization, however, is still required in up to 5–8% of patients. In this study, we analyzed clinical and angiographic variables that might be related with SES re-restenosis and variables related with re-restenosis after repeat SES implantation for SES restenosis. We also assessed clinical outcomes at 2-year follow-up after percutaneous coronary intervention (PCI) for SES restenosis. Repeat revascularization for SES restenosis was performed in 113 patients with 140 lesions. Of the 140 lesions, follow-up coronary angiography (CAG) was performed on 117 lesions (101 patients) and revealed 46 SES re-restenotic and 71 non-re-restenotic lesions. In multivariate analysis, SES-in-SES-strategy and reference diameter before the second PCI were independent predictors of re-restenosis after PCI for SES restenosis. However, the reference diameter was the only independent predictor of re-restenosis after SES-in-SES. Major adverse cardiac events (MACE) at 2 years were found in 44 patients (43.5%), and target lesion revascularization (TLR) was performed in 33.7% of patients after SES restenosis. In conclusion, the incidence of MACE and TLR was relatively high in patients with SES restenosis, but the placement of another SES on larger-diameter vessels may be an effective strategy for the second PCI .     

Role of mucosal microcirculation in gastric lesions induced by lateral hypothalamic lesions in rats

To evaluate the pathophysiology underlying gastric mucosal lesions induced by lateral hypothalamic (LH) lesions, we investigated the changes in acid secretion, gastric mucosal blood flow, gastric mucus and mucosal integrity in the corpus during the 4 h period and 48 h after the production of bilateral electrolytic LH lesions in male Sprague-Dawley rats. Gastric mucosal lesions were macroscopically produced 24 h (63%) and 48 h (83%) after LH lesions, although there were no visible lesions at 7 h. Gastric acid secretion was significantly increased 48 h after LH lesions, compared with that in the control group. Gastric mucosal blood flow and transmucosal potential difference (PD) in the LH lesion group immediately decreased after LH lesions and did not recover during 4 h and at 48 h. On the contrary, in the control group, gastric mucosal blood flow decreased after the brain surgery but soon recovered, and there was no significant change in PD. LH lesions resulted in the reduction of intramucosal mucus to 50% 3 h after LH lesions. Moreover, we exposed the stomach to 10 mmol/L taurocholic acid (TCA) 3 h after LH lesions to examine the disruption in gastric mucosal defensive function in rats with LH lesions. The recovery of the reduced PD by TCA was slow and gastric mucosal lesions were easily formed in the LH lesion group. These results suggest that gastric mucosal ischaemia after lesioning of LH immediately results in the disruption of mucosal defensive function before the formation of visible gastric lesions, and predisposes to the formation of gastric mucosal lesions by a delayed increase in acid secretion.     

Faecal clearance of α1-antitrypsin reflects disease activity and correlates with rapid turnover proteins in chronic inflammatory bowel disease

Faecal clearance of alpha 1-antitrypsin was measured in patients with ulcerative colitis and Crohn's disease and compared with disease activity and markers of protein-calorie malnutrition. Patients with active ulcerative colitis and Crohn's disease showed elevated clearance of alpha 1-antitrypsin and clearance declined in most patients with induction of remission. However, even with inactive disease, elevated protein loss persisted in some patients, presumably reflecting residual inflammation in the intestinal mucosa. There was a significant correlation between clearance of alpha 1-antitrypsin and serum levels of retinol-binding protein and transferrin in patients with ulcerative colitis and with retinol-binding protein in patients with Crohn's disease. Clearance of alpha 1-antitrypsin reflects disease activity in inflammatory bowel disease and correlates with serum levels of rapid-turnover proteins such as retinol-binding protein and transferrin, which are markers for the presence of protein-calorie malnutrition.     

Visualization of the heart and determination of left ventricular mass in rats by echocardiography.

A high-frequency transducer was used to determine the optimal parameters for visualizing the heart in 40 normal Wistar, 15 SHR, and 10 aorta-banded rats. The rats were 5 to 30 weeks old and weighed between 105 and 705 grams. Two-dimensional and M-mode views of the ventricles, atria, valves, and great arteries were obtained by placing the transducer beneath the rats through the left or right parasternal window in either the prone or the right decubitus positions, respectively. Left ventricular (LV) mass was determined on the basis of a spheroid model; these values correlated well with the LV weight for both the Wistar rats (r = 0.94, p less than 0.001) and the rats with cardiac hypertrophy due to pressure load (r = 0.87, p less than 0.001). These results were highly reproducible. This indicates that echocardiography is useful for obtaining quantitative measurements in rats.     

Role of Sympathovagal Balance in the Initiation of Idiopathic Ventricular Tachycardia Originating from Right Ventricular Outflow Tract

VT originating from the right ventricular outflow tract (RVOT) is prone to occur when sympathetic nervous activity is increased. β-Blockade is, therefore, effective in suppressing this VT. The purpose of this study was to determine the role of sympathovagal balance assessed by heart rate variability (HRV) in the spontaneous initiation of repetitive premature ventricular contractions (PVCs) and VT (five or more consecutive PVCs) arising from RVOT in seven patients without structural heart diseases. Frequency-domain measures of HRV were determined by analyzing 24-hour Holter electrocardiographic recording with the maximum entropy method over α 1,280-second period immediately before the onset of 35 single PVCs, 26 episodes of 2-4 consecutive PVCs, and 21 episodes of VT. High frequency component (HF: 0.15–0.40 Hz) was used as an index of parasympathetic activity, and the ratio of low frequency component (LF: 0.04–0.15 Hz) to HF (LF/HF ratio), as an index of sympathovagal balance. NN50(%), a time-domain variable of parasympathetic activity, was also determined. Mean RR interval and any measures of HRV did not change significantly before single PVCs. Mean RR interval shortened and HF decreased prior to repetitive PVCs and VT. The LF/HF ratio, however, increased only before the onset of VT. NN50(%) tended to decrease before repetitive PVCs and decreased significantly before VT. With propranolol (30–60 mg/day), frequency of repetitive PVCs was suppressed from 2,048 ± 1,201 to 746 ± 658/day and VT was totally abolished, but frequency of single PVCs did not change significantly. In conclusion, sympathetic predominance plays an important role in the initiation of repetitive PVCs and VT originating from RVOT in patients without structural heart diseases.     

NF-κB RelA-deficient Lymphocytes: Normal Development of T Cells and B Cells, Impaired Production of IgA and IgG1 and Reduced Proliferative Responses

To investigate the function of NF-κB RelA (p65), we generated mice deficient in this NF-κB family member by homologous recombination. Mice lacking RelA showed liver degeneration and died around embryonic day 14.5. To elucidate the role of RelA in lymphocyte development and function, we transplanted fetal liver cells of 13.5-day embryos from heterozygote matings into irradiated SCID mice. Within 4 weeks, both T and B cells had developed in the SCID mice receiving relA−/− fetal liver transplants, similar to the relA+/+ and +/− cases. T cells were found to mature to Thy-1⁺/TCRαβ⁺/CD3⁺/CD4⁺ or CD8⁺, while B cells had the ability to differentiate to IgM⁺/B220⁺ and to secrete immunoglobulins. However, the secretion of IgG1 and IgA was reduced in RelA-deficient B cells. Furthermore, both T and B cells lacking RelA showed marked reduction in proliferative responses to stimulation with Con A, anti-CD3, anti-CD3+anti-CD28, LPS, anti-IgM, and PMA+calcium ionophore. The results indicate that RelA plays a critical role in production of specific Ig isotypes and also in signal transduction pathways for lymphocyte proliferation.     

Changes in plasma fibronectin levels in patients with thyroid disease and its mechanism

Plasma fibronectin (FN) level was determined in normal subjects and patients with thyroid disease by the Laurell method. In vitro effect of triiodothyronine (T3) on FN synthesis by cultured human fetal skin fibroblasts was also studied. Plasma FN level was 32.2 +/- 5.5 mg/dl (mean +/- SD) in normal adults, and no sex difference was observed. The plasma FN concentrations were increased in patients with hyperthyroidism (63.3 +/- 15.2 mg/dl), decreased in patients with hypothyroidism (19.5 +/- 6.5 mg/dl), and in normal range in patients with simple goiter (30.2 +/- 7.0 mg/dl). These FN values have been normalized with a time lag of a short period after their thyroid function became normal. There was a positive correlation between plasma FN concentrations and serum T3 or T4 concentrations, but a inverse correlation between plasma FN concentrations and serum thyroxine binding globulin or cholesterol levels. In vitro studies revealed that the addition of T3 to the incubation medium stimulated FN synthesis by human fetal skin fibroblasts at the concentrations between 10(-8)M and 10(-6)M. These results indicate the usefulness of plasma FN determination in patients with thyroid disease for their management and studying pathophysiology of the disease, and suggest at the fluctuation of plasma FN concentrations in these patients may at least in part due to the effect of thyroid hormone on FN synthesis by the cells.     

Chest compression-induced vertebral fractures

Two cases with chest compression-induced thoracolumbar transvertebral fractures are discussed. This is a previously unreported complication of cardiopulmonary resuscitation. Dorsal kyphosis and osteopenia were present in both of these cases. There was no spinal cord injury documented, though the potential for injury and paraplegia exists. Care should be taken to avoid this complication, especially in the elderly with kyphosis; however, adequate compressions to insure support of circulation should be maintained.