高压氧对激素性股骨头坏死兔血中IL19、IL20的影响

目的 研究高压氧(HBO)对激素性股骨头坏死(steroid-induced avasculal osteoecrosis of femoral head,SANFH)兔血中白介素19、20(interleukin-19、20,IL19、IL20)的影响.方法 健康新西兰白兔78只,随机分为3组:正常对照组(N组)7只,模型组(M组)41只,HBO组30只.M组又分为造模完成组(M0组)10只,造模2周组(M2组)10只,造模4周组(M4组)10只,造模6周组(M6组)11只.HBO组分为2周HBO组(HBO2组)7只,4周HBO组(HBO4组)11只,6周HBO组(HBO6组)12只.采用注射内毒素加甲基强的松龙的方法对模型组及HBO组动物进行造模处理,HBO 组在造模完成后开始HBO处理,1次/d,于造模2、4、6周分别取静脉血检测IL19、IL20的变化,并于取血后处死动物,取双侧股骨头进行组织形态学观察.结果 IL19表达:M0组明显增高,与N组比较差异有统计学意义(P＜0.05);M2、M4组表达较M0组下降,但M2组比HBO2组、M4组比HBO4组的表达高,差异有统计学意义(P＜0.01或P＜0.05).IL20表达:M0组明显增高,与N组比较差异有统计学意义(P＜0.05);M2组的表达较M0组下降,但比HBO2组表达高,差异具有统计学意义(P＜0.05);M4组与HBO4组比较差异无统计学意义(P＞0.05);M6组表达较M4高,HBO6组继续下降,与M6组比较差异有统计学意义(P＜0.05).病理结果:N组股骨头组织形态学正常;M2、M4组可见不同程度的骨髓腔内脂肪细胞变性及坏死,周围有淋巴细胞为主的炎性细胞浸润;M6组表现为骨髓腔纤维化,成骨表现活跃.HBO治疗2周后,股骨头骨细胞核未见明显固缩,骨小梁间骨髓炎症反应明显减轻,骨母细胞及纤维组织增生,治疗4～6周骨母细胞活跃增生,成骨形成.结论 SANFH时兔血中IL19、IL20含量增高,炎症反应是SANFH的病因之一.HBO治疗可抑制IL19、IL20的释放,减轻炎症反应,从而减轻股骨头坏死的程度.     

高压氧对激素性股骨头坏死兔血中TF、TNF-α的影响

目的 通过研究激素性股骨头坏死(steroid-induced avascular necrosis of the femoral head,SANFH)兔血组织因子(TF)和肿瘤坏死因子(TNF-α)的动态变化及高压氧(hyperbaric oxygen,HBO)对其影响,探讨SANFH发生机制和高压氧治疗的作用机制.方法 健康新西兰白兔78只,按数字随机表法分为3组:正常对照组(N组)7只,模型组(M组)41只,高压氧组(HBO组)30只.模型组又分为造模即刻组(M0组)10只,造模2周组(M2组)10只、造模4周组(M4组)10只、造模6周组(M6组)11只.HBO组分为:2周HBO组(HBO2组)7只、4周HBO组(HBO4组)11只、6周HBO组(HBO6组)12只.采用注射内毒素加甲强龙的方法对模型组及HBO组进行造模处理,HBO组在制模后开始HBO处理,每天1次,并于制模2周、4周、6周分别取静脉血检测TF、TNF-α的变化,于相应取血时间点取血后处死实验动物,取双侧股骨头组织进行组织学观察.结果 M各组TF[M0:(281.42±46.71)pg/ml,M2:(242.25±131.87)pg/ml,M4:(176.39±66.39)pg/ml,M6:(121.32±107.70)pg/ml]、TNF-α[M0:(418.83±75.99)pg/ml,M2:(424.41±57.01)pg/ml,M4:(424.05±136.44)pg/ml,M6:(344.34±112.89)pg/ml]均高于N组[TF:(137.55±21.65)pg/ml,TNF-α:(312.17±31.12)pg/ml],P＜0.05或P＜0.01;而HBO各组与M各组同时间点比较其表达均降低,P＜0.05或P＜0.01;组织学结果:N组股骨头组织形态正常,M组股骨十骺端髓腔内骨髓组织脂肪细胞增多增大、可见变性及片状坏死、炎性细胞浸润、出血、水肿及微小血管血栓、骨髓腔纤维化、造血细胞减少、股骨头萎缩明显;HBO各组脂肪变性、坏死出现率与M组比较明显减少,骨小梁间骨髓炎症反应明显减轻,未见到血栓形成,可见到骨母细胞活跃增生、骨髓纤维化、新生骨形成、股骨头萎缩不明显、骨基质正常.结论 兔SANFH时血中TF、TNF-α含量增高,诱导了体内凝血反应,使股骨头处血栓形成,HBO治疗可抑制实验动物体内TF、TNF-α的释放,从而改善凝血功能的异常,治疗股骨头坏死.

Abstract：

Objective To investigate dynamic changes in serum TF and TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head ( SANFH) and also to explore the mechanism of SANFH, as well as effects of hyperbaric oxygen ( HBO) on SANFH. Methods Seventy-eight New Zealand male rabbits were randomly divided into 3 groups:the normal control (group N) (7 animals), the model group (group M) (41 animals) and the HBO group (group H) (30 animals). The model group was subdivided into the immediate model group (the M0 group) (10 animals), the two-week model group (the M2 group) (10 animals), the four-week model group (the M4 group) (10 animals) and the six-week model group (the M6 group) (11 animals). The HBO group was further divided into the 2-week HBO therapy group (HBO2) (7 animals), the 4-week HBO therapy group (HBO4) (11 animals) and the 6-week HBO therapy group (HBO6) (12 animals). Through injection of endotoxin and methyl-prednisolone, rabbits in the group HBO2, HBO4 and HBO6 received HBO therapy 1 hour daily from the second day of the experiment. The durations of HBO therapy were 2 weeks ( HBO2), and 4 weeks respectively. The animals were sacrificed after blood samples were taken at respective blood collection time. Then, levels of TF, TNF-α in the serum were measured and the histological changes in the femoral heads were observed. Results Levels of TF and TNF-α in group M0 increased significantly, when compared with those of group N (P ＜0. 05 or P ＜0.01), while for the HBO subgroups the expression of TF and TNF-α measured at the same time points all decreased, when compared with that of the model subgroups (P＜0. 05 or P ＜0.01). To elaborate, TF levels in group M2 and M4 were much higher than those in group HBO2 and HBO4 ( P＜0. 01 ). TF level in group M6 was higher than that in group HB06 ( P ＜ 0.05). TNF-α in group M0 also increased significantly, when compared with that in group N( P ＜0.01). TNF-α levels in group M2 and M6 were also much higher than those in group HBO2 and HBO6 ( both P ＜0. 01 ). TNF-α in group M4 was higher than that in group HBO4 (P＜0.01). Histological examination revealed that tissues of the femoral heads in group N were normal, osteonecrosis and thrombus could be noted in group M2 and M4, hyperplasia fibrosis could be found in group M6, and osteonecrosis in HBO2 and HB04 groups seemed less severer than that in M2 and M4 groups, no thrombi in HBO2, HBO4 groups were noted, and growth of new bones were detected in HBO4 and HBO6. Conclusions The levels of TF and TNF-α levels increased in the rabbit model of SANFH, inducing blood coagulation. Thrombosis at the femoral heads was one of the causes of SANFH. HBO therapy could inhibit the release of TF and TNF-α, thus improving the abnormality of blood coagulation and enhancing treatment of osteonecrosis.     

高压氧对脑缺血再灌注致线粒体过氧化损伤的保护作用研究

目的 通过观察高压氧(HBO)对局灶性脑缺血再灌注(CI/R)所致脑组织细胞线粒体过氧化损伤及凋亡的影响,探讨HBO对抗CI/R损伤的作用及其机制.方法 将80只SD大鼠按随机数字表法分为4组:假手术对照组(假手术组)8只,CI/R组、CI/R后常压吸氧(CI/R+N)组、CI/R后HBO治疗(CI/R+HBO)组,每组24只.采用大脑中动脉内线栓阻断法(MCAO)制备大鼠局灶性CI/R模型.(假手术组)操作步骤相同,但仅将线栓插入大脑中动脉10 mm后退出.假手术组、CI/R组术后不予任何处理,CI/R+N组术后30 min常压下吸纯氧,CI/R+HBO组术后30 min行常规HBO处理,均为60 min/次,1次/12 h.每组于CI/R术后12、24、48 h各处死8只大鼠,取CI/R损伤灶脑组织,采用比色法检测脑组织内线粒体超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,流式细胞技术检测脑细胞凋亡率.结果 CI/R组术后12、24、48 h SOD活性持续下降,显著低于假手术组[(139.21±11.52与(214.13±13.76)、(127.41±12.36)与(214.13±13.76)、(112.33±11.69)与(214.33±13.76)×10-6U/g)](均P＜0.01);CI/R+N组12、24、48 h SOD活性[(157.16±8.91)、(146.33±9.93)、(133.49±10.21)×10-6 U/g)]明显高于CI/R组(均P＜0.05),CI/R+HBO组12、24、48 h SOD活性[(176.80±12.35)、(169.43±12.41)、(161.56±13.81)×10-6 U/g)]显著高于CI/R组和CI/R+N组(均P＜0.05),显示CI/R后HBO治疗能有效地保护线粒体SOD的活性.CI/R组MDA含量术后持续增高,12、24、48 h显著高于假手术组(均P＜0.01).CI/R+N组MDA含量术后12、24、48 h时均低于CI/R组,但差异均无统计学意义(均P＞0.05);CI/R+HBO组MDA含量术后24、48 h时均显著低于CI/R组(均为P＜0.01)和CI/R+N48 h组(均P＜0.05),显示HBO治疗可有效抑制MDA的产生.CI/R组术后12、24、48 h脑细胞凋亡率持续增高,均显著高于假手术组(均P＜0.01);CI/R+N组术后24、48 h组脑细胞凋亡率均低于CI/R组,但差异无统计学意义(均P＞0.05);CI/R+HBO组术后24、48 h脑细胞凋亡率均显著低于CI/R组(均P＜0.05)和CUR+N 48 h组时(均P＜0.05);显示HBO治疗能有效降低CI/R后脑细胞凋亡率.结论 HBO治疗可明显增强细胞线粒体的稳定性,有效保护CI/R后脑组织线粒体SOD的活性,减轻大鼠CI/R所致线粒体过氧化损伤及脑细胞凋亡,较常压吸氧具有更显著的脑保护作用.     

Effects of hyperbaric oxygen on TF、TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head

Objective To investigate dynamic changes in serum TF and TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head ( SANFH) and also to explore the mechanism of SANFH, as well as effects of hyperbaric oxygen ( HBO) on SANFH. Methods Seventy-eight New Zealand male rabbits were randomly divided into 3 groups:the normal control (group N) (7 animals), the model group (group M) (41 animals) and the HBO group (group H) (30 animals). The model group was subdivided into the immediate model group (the M0 group) (10 animals), the two-week model group (the M2 group) (10 animals), the four-week model group (the M4 group) (10 animals) and the six-week model group (the M6 group) (11 animals). The HBO group was further divided into the 2-week HBO therapy group (HBO2) (7 animals), the 4-week HBO therapy group (HBO4) (11 animals) and the 6-week HBO therapy group (HBO6) (12 animals). Through injection of endotoxin and methyl-prednisolone, rabbits in the group HBO2, HBO4 and HBO6 received HBO therapy 1 hour daily from the second day of the experiment. The durations of HBO therapy were 2 weeks ( HBO2), and 4 weeks respectively. The animals were sacrificed after blood samples were taken at respective blood collection time. Then, levels of TF, TNF-α in the serum were measured and the histological changes in the femoral heads were observed. Results Levels of TF and TNF-α in group M0 increased significantly, when compared with those of group N (P ＜0. 05 or P ＜0.01), while for the HBO subgroups the expression of TF and TNF-α measured at the same time points all decreased, when compared with that of the model subgroups (P＜0. 05 or P ＜0.01). To elaborate, TF levels in group M2 and M4 were much higher than those in group HBO2 and HBO4 ( P＜0. 01 ). TF level in group M6 was higher than that in group HB06 ( P ＜ 0.05). TNF-α in group M0 also increased significantly, when compared with that in group N( P ＜0.01). TNF-α levels in group M2 and M6 were also much higher than those in group HBO2 and HBO6 ( both P ＜0. 01 ). TNF-α in group M4 was higher than that in group HBO4 (P＜0.01). Histological examination revealed that tissues of the femoral heads in group N were normal, osteonecrosis and thrombus could be noted in group M2 and M4, hyperplasia fibrosis could be found in group M6, and osteonecrosis in HBO2 and HB04 groups seemed less severer than that in M2 and M4 groups, no thrombi in HBO2, HBO4 groups were noted, and growth of new bones were detected in HBO4 and HBO6. Conclusions The levels of TF and TNF-α levels increased in the rabbit model of SANFH, inducing blood coagulation. Thrombosis at the femoral heads was one of the causes of SANFH. HBO therapy could inhibit the release of TF and TNF-α, thus improving the abnormality of blood coagulation and enhancing treatment of osteonecrosis.     

高压氧早期处理对防治兔激素性股骨头坏死凝血-纤溶系统紊乱的作用

目的 观察激素性股骨头坏死兔在高压氧治疗前后凝血-纤溶系统指标含量的变化,以探讨早期高压氧治疗激素性股骨头坏死的作用机制.方法 建立激素性股骨头坏死的动物模型,各组分别采血测定血浆抗凝血酶Ⅲ(AT-Ⅲ)、血栓调节蛋白(TM)、组织型纤溶酶原激活物(tPA)、纤溶酶原激活物抑制剂-1(PAI-1)的含量.结果 4周和6周时高压氧组AT-Ⅲ含量较模型组升高,差异有统计学意义(P＜0.01);1周时高压氧组TM含量较模型组降低,差异有统计学意义(P＜0.05),4周时升高,差异有统计学意义(P＜0.05);2周时高压氧组tPA含量较模型组升高,差异有统计学意义(P＜0.05);2周时高压氧组PAI-1含量较模型组降低,差异有统计学意义(P＜0.05).结论 早期高压氧治疗可以减轻激素性股骨头坏死模型动物的血管内皮的损伤,促进抗凝因子的合成、释放和纤维蛋白溶解,从而改善机体高凝状态.     

高压氧对兔内毒素血症及其炎性介质的影响

目的 探讨高压氧(HBO)对兔内毒素血症及其炎性介质和肺组织病理学的影响.方法 36只健康新西兰白兔随机分成模型对照组和HBO组,每组18只,经耳缘静脉注射脂多糖(LPS)20μg制成内毒素血症模型,HBO组给予HBO治疗2次,每次60 min,在注射内毒素LPS 2 h期(HBO第1次治疗后)、4 h期(HBO第2次治疗后),2组兔同时从耳动脉采集血样本,分别行动脉血气、肿瘤坏死因子-α(TNF-α)、白介素-8(IL-8)、C-反应蛋白(CRP)、血栓素B2(TXB2)和6-酮-前列腺素Fla(6-ketoPGFla)检测,最后取左肺作炎性病理检查.结果 与模型对照组比较,HBO治疗能显著地改善内毒素血症的动脉血氧分压,降低炎症反应时血循环中TNF-α、IL-8、TXB2的浓度(P＜0.05)和提高血清6-keto-PGF1α和CRP水平(P＜0.05),并显著减轻肺组织多形核细胞(PMN)浸润和水肿.结论 HBO能显著改善兔内毒素血症症状及其炎性介质失衡和肺炎性病理性损伤.     

高压氧预处理对移植皮瓣大鼠炎性介质基质金属蛋白酶-9及高迁移率蛋白B1的影响

目的 探讨高压氧(HBO)预处理对移植皮瓣大鼠缺血再灌注炎症反应的影响.方法 56只SD大鼠按随机数字表法分为7组:假手术组、缺血再灌注(IR)1、3、5d组、HBO预处理+缺血再灌注(HBO)1、3、5d组,每组8只.建立腹部带蒂移植皮瓣动物模型,并进行HBO预处理,应用ELISA法检测各组大鼠血清炎性介质基质金属蛋白酶-9(MMP-9)及高迁移率蛋白B1(HMGB1)水平.结果 IR1、3d组MMP-9水平、IR 1、3、5d组HMGB1水平显著高于假手术组[(13.74±2.04)μg/L和(11.05±1.35)μg/L](P＜0.01),IR5 d组MMP-9水平[(16.66±2.45)μg/L],高于假手术组(P＜0.05);HBO1、3d组MMP-9、HMGB1水平低于同时间IR组(P＜0.05),HBO 5 d组HMGB1水平显著低于同时间IR组(P＜0.01).结论 HBO预处理可能通过降低移植皮瓣大鼠MMP-9、HMGB1水平而减轻皮瓣移植后缺血再灌注炎症反应.     

高压氧对兔内毒素血症治疗的实验研究

目的 观察高压氧(HBO)治疗对兔内毒素血症系统症状、周围血细胞及肺脏病理变化的影响.方法 46只新西兰兔静脉注射内毒素150μg/kg后,随机分成2组:对照组22只,不给予任何处理;HBO组24只,采用HBO治疗(每8 h 1次,共6次).2组分别于汴射内毒素后2、6、24、48 h采耳动脉血1 ml,检测白细胞和血小板,48 h后处死兔,观察肺组织变化.结果 与注射内毒素前相比,对照组兔白细胞和血小板在实验后2、6、24 h明显下降,48 h仍未恢复正常(P＜ 0.01或＜0.05).HBO组2、24h白细胞和血小板分别高于对照组(P＜0.01,P＜0.05),48 h后几乎完全恢复到实验前水平(P＞0.05).与对照组相比,HBO组兔肺组织内炎症反应较轻,且无微血栓及出血灶,48 h死亡率显著降低(P＜0.05).结论 HBO治疗能够显著减轻兔内毒素血症症状及白细胞、血小板的下降,减轻肺组织的炎症反应与出血,并显著降低死亡率(P＜0.05).     

高压氧治疗对创伤性颅脑损伤大鼠抗氧化能力的影响

目的 观察高压氧(hyperbaric oxygen,HBO)治疗对创伤性颅脑损伤(traumatic brain injury,TBI)模型大鼠抗氧化能力的影响,为临床TBI患者实施HBO治疗提供基础实验依据.方法 80只雄性Wistar大鼠按数字表法随机分为8组,每组10只,第1～4组为脑创伤组,分别于建模后24h内(1组)、第5天(2组)、第10天(3组)、第15天(4组)处死;第5～7组为HBO治疗组,第5组建模当天开始行HBO治疗至第5天处死,第6组建模后第5天开始行HBO治疗至第10天处死,第7组建模后第10天开始行HBO治疗至第15天处死;第8组为空白对照组.采用侧位液压撞击(lateral fluid percussion,LFP)法建立TBI大鼠模型.HBO治疗方案:压力0.2 MPa(2.0 ATA)下吸纯氧45 min,1次/d,共治疗5次.分光光度法测量血清中超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛( malondialdehyde,MDA)含量并计算SOD/MDA值.结果 各HBO治疗组SOD活性[(280.00±80.47)U/ml]、SOD/MDA值[(85.57±35.60)U/nmol]与各创伤组[(221.81±43.35) U/ml、(46.38±18.38)U/nmol]比较差异有统计学意义(P＜0.01);MDA含量低于创伤组,但差异无统计学意义.各HBO组SOD活性均高于相应脑创伤组,亚急性期(建模后第5天)开始行HBO治疗组SOD活性[(305.66±68.23) U/ml]、SOD/MDA值[(96.58±31.11)U/nmol]与相应脑创伤组[(209.07±19.65) U/ml、(51.42±8.56) U/nmol]比较差异有统计学意义(P＜0.05).结论 在损伤后特定时间段内给予HBO治疗,可使模型大鼠抗氧化能力短时间内迅速提高.所以适时、适量的HBO治疗不会加重氧化损伤.     

高压氧对脑出血患者高敏C反应蛋白及血糖的影响

目的 探讨高压氧(HBO)治疗对急性脑出血患者高敏C反应蛋白(hs-CRP)及血糖(BG)的影响.方法 脑叶血患者112例(其中HBO治疗组55例,常规治疗组57例)及正常对照组50例,分别观察治疗前及治疗后不同时段血清hs-CRP、BG含量的变化并进行治疗前和治疗后第15、30天进行神经功能缺损评分(NIHSS)及日常生活活动能力评分(ADL).结果 常规治疗组[(15.68±4.96)mg/L,(9.85±4.32)mmol/L]和HBO组[(15.72±5.11)mg/L,(9.81±4.45)mmol/L]入院当日的血清hs-CRP、BG含量均高于正常对照组[(3.76±1.25)mg/L,(4.28±1.12)mmol/L](P＜0.01),但2组间差异无统计学意义;治疗后2组hs-CRP、BG含量均明显下降,HBO组[(4.26±1.72)mg/L,(4.37±1.08)mmol/L]下降较常规治疗组[(5.39 ±2.14)mg/L,(4.79±1.16)mmoL/L]更为显著,差异有统计学意义(P＜0.05),HBO组治疗2个疗程后hs-CRP、BG含量基本恢复正常,与正常对照组相比差异无统计学意义(P＞0.05).治疗后15、30 d,HBO组NIHSS、BI(15 d:9.75±2.12,55.40±11.26;30 d:6.23±1.85,75.03±12.16)较常规治疗组(15 d:11.24±2.17,48.23±10.52;30 d:8.04±1.96,65.18±11.52)均有显著改善(P＜0.01).结论 HBO治疗能有效降低脑出血患者血清hs-CRP及BG含量,改善患者神经功能缺损,提高日常生活活动能力.     

MRI in the assessment of the supportive soft tissues of the cervical spine in acute trauma in children

We carried out a retrospective analysis of imaging and clinical findings in 52 children with a history of cervical spinal trauma. No patient had evidence of a fracture on plain films or CT. All had MRI at 1.5 T because of persistent or delayed symptoms, unexplained findings of injury or instability, or as further assessment of the extent of soft-tissue injury. Clinical follow-up ranged from 6 months to 3.5 years. MRI was evaluated for its influence on therapy and outcome. MRI was positive in 16 (31 %) of 52 patients. Posterior soft-tissue or ligamentous injury was the most common finding in the 10 patients with mild to moderate trauma, while acute disc bulges and longitudinal ligament disruption, each seen in one case, were uncommon. MRI was superior to CT for assessment of the extent of soft-tissue injury and for identification of spinal cord injuries and intracanalicular hemorrhage in the six patients with more severe trauma. MRI specifically influenced the management of all four patients requiring surgery by extending the level of posterior stabilization. No patients with normal MRI or any of the 10 with radiographically stable soft-tissue injury on MRI, developed delayed clinical or radiographic evidence of instability or deformity. Received: 5 August 1997 Accepted: 13 October 1997     

Differences in complication rates among the centres in the SPACE study

Introduction  Despite the high grade of standardisation of study protocols, there is still room for variability among the centres in specific treatment aspects. We evaluated the treatment risk in stent-protected angioplasty of the carotid versus endarterectomy (SPACE) associated with the specific patient enrolment rates of the centres. Materials and methods  The analysed endpoints were ipsilateral stroke or death [primary outcome event (pOE)] and any stroke or death [secondary outcome event (sOE)] until 30 days after treatment. A binary logistic regression analysis with random effects was performed separately for each treatment arm. The centres were secondarily categorised in three classes: I) ≥25 patients enrolled, II) ten to 24 patients and III) <10 patients and a hierarchic log linear model was fitted to test the three-way interaction of treatment, number of patients per class and outcome. Results  The random effects logistic regression analysis in the carotid artery stenting (CAS) arm proved a significant increase in pOE with decreasing number of patients enrolled (−0.0190 ± 0.0085, p = 0.025, deviance 35.7 with 32 df), whereas no such effect was found in the carotid endartectomy (CEA) arm (−0.010 ± 0.008, p = 0.24, deviance 39.78 with 32 df). In the log linear model, there was a significant interaction between treatment, number of patients per centre and sOE (p = 0.023). The odds ratios for sOE in the enrolment classes (CAS vs. CEA) were 0.98 (95% CI 0.50–1.94, p = 0.95) for class I, 1.13 (95% CI 0.47–2.77, p = 0.77) for class II and 11.56 (95% CI 1.40–253.45, p = 0.01) for class III centres. Conclusion  Despite rigorous standardisation and quality requirements for operator qualification, there seemed to be a decrease in complication rate with increasing patient enrolment numbers in the CAS arm while this signal could not be detected in the CEA arm of SPACE.     

Functional alterations in the coronary circulation as mirrored in the angiogram

The ability of coronary arteriography to disclose the presence of abnormalities in the coronary arteries is undisputed. On the other hand, it is less clear whether the angiographic examination of the coronary circulation permits an assessment of functional abnormalities, which may involve the coronary circulation in toto or regionally. The most commonly practiced grading of angiographically demonstrated coronary artery disease is based on the degree of arterial narrowing and the number of major vessels that are involved. This approach, however, suffers from significant shortcomings, which are mainly related to the limitations in accuracy of measuring such lesions angiographically. Secondary angiographic signs of impaired coronary flow, such as contrast propagations through collateral channels, delayed, stagnant, and reciprocal flow pattern, and the appearance of excessive peripheral myocardial contrast accumulation may gain great importance. In conjunction with the presentation of a number of cases considered to be representative for different situations of chronic and acute myocardial ischemia, the primary and secondary angiographic findings are accounted for in detail and discussed as to the most likely existing pathophysiology. The discussion also includes knowledge based on experiments performed in in vitro or animal models and tries to establish a synthesis between the different angiographic phenomena and the present status of our understanding of the pathophysiology of myocardial injury. It is concluded that such detailed analysis of the angiographic events may yield important information for the most appropriate management of the individual patient.     

Diagnostic errors in the echography of the hip in newborns

Neonatal hip sonography according to Graf employs a standardized image in a frontal section plane ("3-point system") and a good scanner adjustment (the femoral head must be anechoic, like the hyaline cartilage roof triangle). Pathologic conditions can change some of these parameters. The authors examined 6,000 neonatal hips in order to point out the commonest causes of diagnostic error. Two types of error were considered: method errors and interpretation errors. Method errors: they are due to the choice of transducer and frequency, to scanner adjustment and definition of the standard section plane. Their incidence was 2.25% and supported by an uncorrect definition of the standard section plane. Interpretation errors: they come from the wrong localization of some reference points--i.e., lower iliac margin, labrum--, uncorrect evaluation of increased echogenicity of the cartilaginous roof, infant age, application of radiographic criteria and uncorrect measurements of alpha and beta angles. Interpretation errors had 5.5% incidence; they were all due to the uncorrect measurement of alpha (3.18%) and beta (2.33%) angles, especially in pathological hips (68%). To reduce the number of errors, the authors suggest to strictly apply Graf's method, to make a diagnosis based on the morphological changes of the cartilaginous and osseous acetabular roof and, only later on, to measure alpha and beta angles to confirm the diagnosis or in the follow-up.