Cost-effectiveness of Liple (LipoPGE1) for arteriosclerosis obliterans patients in Japan: an economic evaluation using the EQ-5D instrument.

AIM: This study was conducted to evaluate the health-related quality of life (HRQOL) and cost-effectiveness of LipoPGE(1) when added to the conventional treatment of arteriosclerosis obliterans (ASO) patients. The research design consisted of a before and after-treatment study without comparison groups. We collected data from May 1999 through July 2001 at 473 institutions located throughout Japan. The subjects were ASO patients who experienced pain at rest or had ulcers of the extremities. METHODS: The observation period was a 2-month period that commenced with the start of administration of LipoPGE1. The HRQOL score (utility value) was obtained from the EQ-5D instrument, and the incremental cost-effectiveness ratio was calculated on the basis of quality-adjusted life years (QALYs). RESULTS: The mean utility value for the 2 months after the start of the administration of LipoPGE(1) was 0.672, and it was a significantly higher (P<0.0001) than the 0.616 before administration of LipoPGE(1). The incremental cost-effectiveness ratio was 18,807 US dollar/QALY assuming that drug efficacy persisted for 1 year after the end of LipoPGE1 therapy, and 75,227 dollar/QALY assuming a duration of just 3 months. CONCLUSIONS: We concluded that when LipoPGE1 is added to the conventional treatment of ASO patients, the HRQOL of the patient improves, and it is highly cost-effective.

Alterations in cardiac sarcoplasmic reticulum Ca2+ regulatory proteins in the atrial tissue of patients with chronic atrial fibrillation.

OBJECTIVES: Our purpose was to determine whether atrial fibrillation (AF) patients have alterations in sarcoplasmic reticulum (SR) Ca2+ regulatory proteins in the atrial myocardium. BACKGROUND: Clinically, AF is the most frequently encountered arrhythmia. Recent studies indicate that an inability to maintain intracellular Ca2+ homeostasis with a consequent increase in membrane-triggered activity could be the primary initiating factor in some circumstances, and that cytosolic Ca2+ abnormalities are an important mediator of sustained AF. METHODS: We measured the maximum number of [3H]ryanodine binding sites (Bmax) and the expression levels of ryanodine receptor (RyR) mRNA and calcium-adenosine triphosphatase (Ca2+-ATPase) mRNA in atrial myocardial tissue from 13 patients with AF due to mitral valvular disease (MVD) and 9 patients with normal sinus rhythm (NSR). RESULTS: In AF patients, 1) Bmax was significantly lower in each atrium (0.21+/-0.03 pmol/mg [right], 0.16+/-0.04 pmol/mg [left]) than in the right atrium (0.26+/-0.08 pmol/mg) of NSR patients; 2) Bmax was significantly lower in the left atrium than in the right atrium; 3) Bmax in the left atrium was significantly lower at higher levels of pulmonary capillary wedge pressure; 4) the expression level of RyR mRNA was significantly lower in both the left (1.24 x 10(-2)+/-1.28 x 10(-2)) and right (1.70 x 10(-2)+/-1.78 x 10(-2)) atrium than in the right atrium of NSR patients (6.11 x 10(-2)+/-2.79 x 10(-2)); and 5) the expression level of Ca2+-ATPase mRNA was significantly lower in both the left (5.67 x 10(-2)+/-4.01 x 10(-2)) and right (7.71 x 10(-2)+/-3.56 x 10(-2)) atrium than in the right atrium (12.60 x 10(-2)+/-3.92 x 10(-2)) of NSR patients. CONCLUSIONS: These results provide the first direct evidence of abnormalities in the Ca2+ regulatory proteins of the atrial myocardium in chronic AF patients. Conceivably, such abnormalities may be involved in the initiation and/or perpetuation of AF.

Up-regulation of inositol 1,4,5 trisphosphate receptor expression in atrial tissue in patients with chronic atrial fibrillation.

OBJECTIVES: We examined whether patients with atrial fibrillation (AF) have alterations in atrial inositol 1,4,5 trisphosphate receptors (IP3 receptors). BACKGROUND: Abnormal intracellular Ca2+ homeostasis occurs in chronic AF. The intracellular Ca2+ concentration is regulated by ryanodine and IP3 receptors. We recently reported alterations in ryanodine receptors in atrial tissue from patients in chronic AF. METHODS: We analyzed IP3 receptor expression in the right atrial myocardium from 13 patients with mitral valvular disease (MVD) with AF (MVD/AF), five patients with MVD who had normal sinus rhythm (MVD/NSR) and eight control patients with NSR (tissue obtained during coronary artery bypass surgery). Hemodynamic and echocardiographic data were obtained preoperatively, and an immunohistochemical study was performed on atrial tissue. RESULTS: The relative expression level of IP3 receptor protein was significantly greater in MVD/AF (0.75 +/- 0.26) than it was in MVD/NSR (0.42 +/- 0.13, p < 0.01), and both were significantly above control (0.14 +/- 0.08). The relative expression level of IP3 receptor messenger RNA was significantly greater in the MVD/AF group (0.028 +/- 0.008) than it was in the control group (0.015 +/- 0.004, p < 0.01), but patients with MVD/AF did not differ from patients with MVD/NSR (0.020 +/- 0.006). The relative expression levels of IP3 receptor protein and messenger RNA were higher in patients with left atrial dimension > or = 40 mm, pulmonary capillary wedge pressure > or = 10 mm Hg and right atrial pressure > or = 5 mm Hg. Inositol 1,4,5 trisphosphate receptors were over-expressed in the cytosol and at the nuclear envelope of atrial myocytes in MVD. CONCLUSIONS: Since chronic mechanical overload of the atrial myocardium increased IP3 receptor expression, especially in patients with chronic AF, up-regulation of IP3 receptors may be important in modulating intracellular Ca2+ homeostasis and initiating or perpetuating AF.

The influence of tumour resection on angiostatin levels and tumour growth--an experimental study in tumour-bearing mice.

The phenomenon of primary neoplasms inhibiting the growth of their metastatic lesions is thought to be related to endogenous angiogenesis inhibitors. The aim of this experiment was to investigate the influence of tumour resection on angiostatin levels and tumour growth using a tumour-bearing mouse model. A primary Lewis lung cancer tumour model was established in C57BL/6 mice and these mice were divided into two groups 10 days after the tumour cells were inoculated. In the surgical resection group (S group) the tumour was resected, but in the control group (C group) a sham operation was performed. The level of angiostatin in the sera was analysed 5 days after the operation by western blotting. To observe tumour growth, four Lewis lung cancer models were established in these mice from both the S and C groups. An immunohistochemical analysis of the tumour tissues was conducted to estimate the proliferation and apoptotic rates of the tumour cells, as well as the amount of neoangiogenesis in the tumours. Angiostatin was observed in the tumour-bearing mice, but disappeared within 5 days after the tumour had been resected. Increased tumour growth was observed in all of the tumour models in the S group compared with the C group and the differences were significant. A significantly higher intratumour vessel density and proliferation cell index, but a significantly lower apoptotic index were also found in the S group compared with the C group. These findings demonstrated that angiostatin was generated directly from the tumour tissue. Furthermore, tumour resection accelerates the growth of other tumours and this is probably related to multiple factors including increased neoangiogenesis, increased tumour cell proliferation, and decreased apoptosis.

Pharmacokinetic differences between rat tumour and lung tissues following isolated lung perfusion with cisplatin.

Isolated lung perfusion has been performed for the treatment of unresectable lung tumours; however, the pharmacokinetics of this procedure remain unclear. This study was conducted to investigate the changes in antitumour drug concentrations in tumour and lung tissues after isolated lung perfusion, using different perfusion times and perfusate drug concentrations. Isolated left lungs were perfused for 20, 40 or 60 min with 25, 50 or 100 micrograms/ml of cisplatin after solitary lung tumour nodules were established in rats, and the total platinum concentrations in the perfused lung and tumour tissues were determined by flameless atomic absorption spectroscopy. The oedema in the perfused lung tissues was evaluated by histological examination and by the wet to dry weight ratios of the lungs. The total platinum concentration increased significantly with perfusion time and increasing perfusate cisplatin concentrations in the lung tissue, but it did not change in the tumour tissue. The wet to dry weight ratios of the lung tissues did not differ significantly among the perfusion groups. Oedema of the perfused lung tissue did not change significantly with the perfusion time or perfusate cisplatin concentration. The results of this study indicate the possibility that different pharmacokinetics exist between tumour and lung tissues following isolated lung perfusion with cisplatin, which could be used as a clinical guide for the selection of appropriate perfusion times and perfusate drug concentrations.

Prolonged survival of xenograft fetal cardiomyocytes by adenovirus-mediated CTLA4-Ig expression.

BACKGROUND: Experimental allografting of fetal cardiomyocytes has been performed successfully. In this study, we attempted to transplant rat fetal cardiomyocytes into the hearts of mice by blocking the CD28/B7 costimulatory pathway via CTLA4-Ig gene transfer. METHODS: Fetal cardiomyocytes derived from Dark Agouti rat were infected with CTLA4-Ig-expressing adenovirus vectors (AdCTLA) and injected directly into the normal myocardium of C3H/He mice (n=15). For control, cells infected with beta-Gal-expressing adenovirus vector (AdRL) and cells without infection were injected into additional mice (n=30). Mice were killed at 2 (n=5), 4 (n=5), and 8 (n=5) weeks after xenotransplantation. Transplanted fetal cardiomyocytes were examined for survival by immunostaining with anti-rat atrial natriuretic peptide and anti-CTLA4-Ig antibodies. RESULTS: Fetal cardiomyocytes were successfully infected by AdCTLA and AdRL. The cardiomyocytes infected with AdCTLA expressed CTLA4-Ig and survived to 8 weeks after xenotransplantation in all of these mice. However, cardiomyocytes infected with AdRL and noninfected cells were not detected even 2 weeks after xenotransplantation. CONCLUSION: Survival of xenografted fetal cardiomyocytes is prolonged by adenovirus-mediated CTLA4-Ig expression.

Induction of hyporesponsiveness to fully allogeneic cardiac grafts by intratracheal delivery of alloantigen.

BACKGROUND: Soluble protein delivered through the mucosal surface can induce immunological unresponsiveness. The purpose of this study was to determine if prior exposure to alloantigen via the trachea could modulate the immune response to subsequent cardiac allografts. METHODS: Hearts from C57BL/10(H2b) mice were transplanted into CBA(H2k) recipients. Recipient mice were given donor 1x10(7) splenocytes into the trachea with or without antibody specific for mouse CD80 (1G10) and/or CD86 (GL1) (100 microg each) 7 days before transplantation. RESULTS: All grafts survived in recipients treated with intratracheal delivery of alloantigen for over 35 days (mean survival time [MST], 56 days), whereas naive control mice and mice treated with syngeneic antigen rejected grafts acutely (MST, 8 and 7 days, respectively). Interestingly, when 1G10, GL1, or both of them were combined with the protocol, the majority of grafts were rejected within 21 days after grafting (MST, 7, 15, and 17 days, respectively). CONCLUSION: Intratracheal delivery of alloantigen induced significantly prolonged survival of fully mismatched cardiac allografts and the effect was abrogated by the blockade CD80 and/or CD86 pathway.

Distribution of oxygenated blood in experimental perfusion via the femoral and carotid arteries.

The efficiency of femoral and carotid artery perfusion was compared in 10 dogs. The purpose of our study was to determine under what conditions the femoral artery can be used to perfuse the upper body satisfactorily during prolonged perfusions.

Interactions of regional respiratory mechanics and pulmonary ventilatory impairment in pulmonary emphysema: assessment with dynamic MRI and xenon-133 single-photon emission CT.

STUDY OBJECTIVES: Dynamic MRI and (133)Xe single-photon emission CT (SPECT) were used to directly evaluate the interaction of regional respiratory mechanics and lung ventilatory function in pulmonary emphysema. METHODS: Respiratory diaphragmatic and chest wall (D/CW) motions were analyzed by sequential MRI of fast-gradient echo pulse sequences during two to three respiratory cycles in 28 patients with pulmonary emphysema, including 9 patients undergoing lung volume reduction surgery (LVRS). The extent of air trapping in the regional lung was quantified by the (133)Xe retention index (RI) on three-dimensional (133)Xe SPECT displays. RESULTS: By contrast to healthy subjects (n = 6) with regular, synchronous D/CW motions, pulmonary emphysema patients showed reduced, irregular, or asynchronous motions in the hemithorax or location with greater (133)Xe retention, with significant decreases in the maximal amplitude of D/CW motions (MADM and MACWM; p < 0.0001 and p < 0.05, respectively). The removal of (133)Xe retention sites by LVRS effectively and regionally improved D/CW motions in nine patients, with significant increases in MADM and MACWM (p < 0.01 and p < 0.001, respectively). In a total of 40 studies of the 28 patients including post-LVRS studies, normalized MADM and MACWM correlated with percent predicted FEV(1) (r = 0.881, p < 0.0001; and r = 0.906, p < 0.0001, respectively), and also with (133)Xe RI in each hemithorax (r = -0.871, p < 0 0.0001; and r = -0.901, p < 0 0.0001, respectively.) CONCLUSIONS: This direct comparison of regional respiratory mechanics with lung ventilation demonstrated a close interaction between these impairments in pulmonary emphysema. The present techniques provide additional sensitivity for evaluating pathophysiologic compromises in pulmonary emphysema, and may also be useful for selecting resection targets for LVRS and for monitoring the effects.

Is it possible to differentiate malignant mediastinal nodes from benign nodes by size? Reevaluation by CT, transesophageal echocardiography, and nodal specimen.

STUDY OBJECTIVE: To reevaluate whether it is possible to reliably differentiate malignant mediastinal lymph nodes from benign nodes by size, and to determine the frequency of metastases to normal-sized mediastinal lymph nodes that directly affects the sensitivity for detecting malignant mediastinal lymph nodes (N2 nodes) on CT. DESIGN: Prospective study of patients with non-small cell lung cancer. SETTING: Department of Radiology and First Department of Surgery, Yamaguchi University School of Medicine. PATIENTS: We examined 40 patients with non-small cell lung cancer, who underwent thoracotomy because of operable stage (stage I, II, IIIA) in preoperative staging, using CT and transesophageal echocardiography (TEE). INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Lymph nodes 10 mm or greater in short-axis diameter on CT and TEE were considered abnormal. Furthermore, lymph node size was measured by TEE and nodal specimens in long- and short-axis diameter in each patient. Two hundred eight mediastinal lymph nodes were dissected and N2 nodes were present in 28% of patients (11/40); in 7 of these 11 patients (64%), mediastinal lymph node metastases were misdiagnosed on CT because of normal-sized N2 nodes. Furthermore, in 73% of N2 nodes, nodal size was normal on TEE. There were no significant difference in both diameters between malignant mediastinal lymph nodes and benign nodes on TEE and nodal specimens. CONCLUSIONS: It is not possible to reliably differentiate malignant mediastinal nodes from benign nodes by size alone, and we should be aware of high frequency of normal-sized N2 nodes in patients with operable stage of lung cancer.

Bidirectional blockade of CD4 and major histocompatibility complex class II molecules: an effective immunosuppressive treatment in the mouse heart transplantation model.

BACKGROUND: Anti-CD4 monoclonal antibodies (mabs) are powerful immunosuppressive agents. However, in experimental models anti-CD4 treatment alone is not always completely effective. Anti-major histocompatibility complex (MHC) class II mabs may have a synergistic effect with anti-CD4 mab therapy by blocking the function of both antigen-presenting cells and T cells. METHODS: C3H/He mice (H-2k: I-Ak, I-Ek) received a vascularized cardiac graft from C57BL/10 (H-2b: I-Ab) or BALB/c (H-2d: I-Ad, I-Ed) mice and were treated with a depleting anti-CD4 or a depleting anti-MHC class II antibody either alone or in combination. RESULTS: Anti-CD4 treatment alone prolonged graft survival in both strain combinations but was only minimally effective when BALB/c donors were used. However, when anti-CD4 and anti-MHC class II mabs were administered together, graft survival was significantly prolonged in both strain combinations. The ratio of interleukin-4 (IL-4)/interferon-gamma (IFN-gamma) expressed in both C57BL/10- and BALB/c-transplanted hearts 7 days after transplantation was significantly higher after combined treatment with anti-CD4 plus anti-MHC class II mabs compared with that found after either treatment alone. Twenty-one days after transplantation, the ratio of IL-4/IFN-gamma in BALB/c hearts after combined mab therapy was significantly lower than at 7 days after transplantation, but in contrast, the cytokine ratio in C57BL/10 hearts remained at an elevated level during the first 21 days after transplantation. CONCLUSIONS: These data demonstrate that bidirectional blockade of the antigen-presenting cell and T-cell interaction by use of anti-CD4 and anti-MHC class II mabs in combination is more effective than either treatment alone. Graft survival in this model seems to correlate with a prolonged elevation of the IL-4/IFN-gamma ratio in the transplanted heart, suggesting that in this model the induction of unresponsiveness may be associated with a shift toward a Th2-type T-cell response.

Prostacyclin analog OP2507 prevents pulmonary arterial and airway constriction during lung preservation and reperfusion.

BACKGROUND: The effects of OP2507 on lung preservation with cold Euro-Collins solution and during the reperfusion period were evaluated. METHODS: For this study, canine lungs were flushed with a 10 micrograms/ml OP2507 solution (n = 7) or saline solution (control group, n = 7) (0.1 ml/kg body weight) and stored in the same solution. Pulmonary arterial pressure, pulmonary vascular resistance, airway pressure, respiratory capacity, and wet to dry weight ratio of the lungs were measured before and after 24 hours of cold preservation and after a 60-minute reperfusion period. RESULTS: Treatment with OP2507 significantly attenuated increases in pulmonary arterial pressure, pulmonary vascular resistance, and airway pressure after preservation and during the reperfusion period. Oxygen tension in outflow blood also was maintained with OP2507 treatment throughout the experimental period, whereas it was depressed during the reperfusion period in the control group. By electron microscopy, there was little evidence of vascular endothelial damage, such as cell swelling, detachment of endothelial cells from the lamina, and attenuation of the cytoplasm, in both groups. However, the tight junctions between cells were observed more clearly in the control group than in the OP2507 group, suggesting more cell membrane damage in the control group. CONCLUSIONS: Pretreatment with OP2507 prevented pulmonary artery and airway constriction after 12 hours of cold lung preservation and a decrease of oxygen tension in outflow blood during a 60-minute reperfusion period.

Effect of a thromboxane synthetase inhibitor on protamine-induced circulatory changes in sheep.

BACKGROUND: Rapid intravenous administration of protamine after procedures requiring cardiopulmonary bypass is occasionally associated with severe pulmonary hypertension, systemic hypotension, cardiac dysfunction, and lung edema. We hypothesized that the mechanism for these hemodynamic changes after protamine administration is the release of thromboxane. We therefore examined the effect of a thromboxane synthetase inhibitor (OKY-046) on these hemodynamic changes in a sheep model. METHODS: Ten female sheep were prepared with lung lymph fistulas and balloon-tipped pulmonary artery, left atrial, arterial, and venous catheters. After a 5-day recovery period, 2 mg/kg protamine was infused 10 minutes after 200 units/kg heparin, with (n = 5; OKY-046 group) and without (n = 5; heparin/protamine group) OKY-046 (10 mg/kg). RESULTS: In the heparin/protamine group, pulmonary arterial pressure and lung lymphatic flow were significantly increased soon after administration of protamine, from 19 +/- 1 to 51 +/- 2 mm Hg and 5 +/- 1 to 8 +/- 1 ml/hr, respectively. The circulating leukocyte count was significantly reduced, from 3304 +/- 318 to 903 +/- 898 mm3. Cardiac output was also reduced, from 5.8 +/- 0.3 to 3.4 +/- 0.7 L/min/m2. These changes were completely blocked in the OKY-046 group, except for the neutrophil depletion and the increase in lung lymphatic flow. CONCLUSIONS: We conclude that thromboxane plays a significant role in protamine-induced hemodynamic deterioration and pulmonary permeability changes.

End-to-side anastomosis of the mesenteric vein to the inferior vena cava in the treatment of glycogen storage disease: case report.

A 2-year-old boy with Type I glycogen storage disease received an end-to-side anastomosis of the mesenteric vein to the inferior vena cava with marked improvement in his biochemical factors and nutritional status and with shrinkage of the liver. The efficacy and simplicity of this technique and its lack of complications, as evidenced by follow-up studies over a 4 year period, suggest that its further use is warranted.

The induction of angiogenesis by the implantation of autologous bone marrow cells: a novel and simple therapeutic method.

BACKGROUND: Bone marrow contains many kinds of primitive cells that could differentiate to endothelial cells and secrete several growth factors. In the current study, we attempted to induce therapeutic angiogenesis by implanting autologous bone marrow cells (BMCs) and using a rat ischemic hind limb model. METHODS: BMCs were prepared by removing red blood cells. A rat ischemic hind limb model was made by the ligation of the left femoral artery and its branches. BMCs were injected into 7 points of the ischemic muscles. To assess angiogenesis, a microangiogram, laser Doppler, and histologic evaluation were performed after the surgical procedure. RESULTS: A microangiogram and histologic evaluation showed that angiogenesis was significantly induced in the ischemic hind limb by the implantation of BMCs. Laser Doppler imaging analysis showed that blood flow was significantly increased after implantation of BMCs. Some implanted BMCs were stained positively with CD31 and vascular endothelial-cadherin (VE-cadherin), which might have been incorporated into the vasculature. The condition of ischemia caused an elevation in the level of basic fibroblast growth factor in the ischemic muscle and also in interleukin-1beta derived from the implanted BMCs, which might contribute to angiogenesis. CONCLUSION: These findings indicate that autologous bone marrow implantation may be a novel and simple method for inducing therapeutic angiogenesis.

Overexpression of heme oxygenase-1 protects allogeneic thyroid grafts from rejection in naive mice.

BACKGROUND: Endocrine allografts are an option for the treatment of endocrine failure. METHODS: One lobe of the thyroid was transplanted under the kidney capsule. RESULTS: C57BL/10 (H2(b)) thyroids were rejected in naive CBA (H2(k)) mice within 14 days after transplantation. When mice were treated with anti-CD4 monoclonal antibodies (mAb), all grafts survived for more than 60 days. The first grafts still survived after second C57BL/10 or Balb/c (H2(d)) thyroid grafts that were transplanted into the same recipients were rejected acutely, which suggests that the primary grafts were modified under anti-CD4 mAb treatment. To confirm this hypothesis, C57BL/10 thyroid grafts from anti-CD4 mAb-treated mice were retransplanted. All grafts survived in naive mice; this correlated with the overexpression of heme oxygenase-1 (HO-1) in the grafts. Next, an inhibitor of HO-1 (zinc protoporphyrin) or control compound (copper protoporphyrin) was injected intraperitoneally after transplantation of C57BL/10 thyroid grafts into the primary CBA recipients that had been treated with anti-CD4 mAb. The grafts in mice that had been treated with zinc protoporphyrin, but not copper protoporphyrin, were rejected when retransplanted to naive recipients. CONCLUSIONS: Overexpression of HO-1 correlated with the protection of fully allogeneic thyroid grafts from rejection when retransplanted into naive recipients.

Angiogenesis induced by the implantation of self-bone marrow cells: a new material for therapeutic angiogenesis.

Bone marrow, contains various primitive cells that are thought to secrete several angiogenic growth factors and may also differentiate into endothelial cells. The present study was conducted to investigate the possibility that bone marrow cells could be a novel material to induce angiogenesis. The expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rat bone marrow cells was examined by immunohistochemistry. The production of VEGF was compared in tissue culture supernatant under the conditions of normoxia and hypoxia. The process of angiogenesis that occurred following the implantation of bone marrow cells was determined using a rat cornea model. VEGF- and bFGF-positive cells were found in rat bone marrow. The production of VEGF from bone marrow cells was significantly more enhanced by hypoxic conditions than by normoxic conditions. The rat cornea model showed that bone marrow cell implantation created new vessels. The implantation of self-bone marrow cells is a novel and simple method of inducing angiogenesis.

The effect of fluorocarbon emulsion on 24-hour canine heart preservation by coronary perfusion.

This study was designed to evaluate the effects of fluorocarbon emulsion as an oxygen carrier in myocardial preservation. The hearts were preserved for 24 hours by coronary perfusion with either oxygenated crystalloid cardioplegic solution (group C) or crystalloid cardioplegic solution with fluorocarbon added (group FC). The perfusion pressure was kept at 20 mm Hg, and myocardial temperature was maintained at 4 degrees C. Group FC demonstrated better recovery in developed pressure and maximum rate of rise of left ventricular pressure compared with group C. The postpreservation end-diastolic pressure in group C increased significantly compared with the baseline value (value obtained before preservation). On the other hand, group FC showed no significant increase of end-diastolic pressure after preservation. Group FC released a significantly lower level of creatine kinase into its perfusate than did group C. Ultrastructural changes after preservation in group C showed severe ischemic injury, but there was no evidence of ischemic injury in group FC. The use of fluorocarbon emulsion proved beneficial to myocardial protection in long-term preservation of canine hearts.

Clinical trial of nicardipine cardioplegia in pediatric cardiac surgery.

To clarify the effectiveness of nicardipine, one of the dihydropyridine calcium-channel blockers, for myocardial protection during cold potassium cardioplegic arrest in pediatric cardiac surgery, a clinical trial of nicardipine (0.25 mg/L) added to potassium cardioplegic solution was performed in children undergoing surgical repair of congenital heart diseases. Twenty patients were selected to receive nicardipine cardioplegia and 13 patients received a standard potassium cardioplegia, serving as a control group. Nicardipine cardioplegia provided better cardiac performance in the early postoperative period and reduced release of the MB isozyme of creatine kinase, as determined during a 48-hour postoperative period. These results suggest that nicardipine added to cold potassium cardioplegic solution offers additional protection for the myocardium during ischemia and postischemic reperfusion in pediatric cardiac surgery.

Emergency operation for thoracic aortic aneurysm caused by the Ehlers-Danlos syndrome.

Two patients were treated emergently for impending ruptured thoracic aortic aneurysms caused by type IV Ehlers-Danlos syndrome. One patient had typical physical evidence of type IV Ehlers-Danlos syndrome. The other patient had a normal phenotype. Type IV Ehlers-Danlos syndrome was diagnosed by electrophoresis of the collagen extracted from the skin. The clinician must be aware of the variations in presentation of type IV Ehlers-Danlos syndrome.