Coronary Artery Embolism: Two Case Reports and a Review of the Literature

Coronary embolism (CE) is an uncommon and unique cause of acute myocardial infarction. In this report, we review 216 cases of CE including 2 new cases from our institution. The mean patient age was 52.5 years and 62% of the patients were males. Chest pain was the most common presenting symptom followed by dyspnea, and the most commonly affected vessel was the left anterior descending artery. Leading etiologies of the embolus were atrial fibrillation, septic emboli, and iatrogenic causes. Treatment approaches varied with thrombus aspiration being used in 30% of cases. In-hospital mortality rate was 36% and 13% of the cases were complicated by cerebrovascular accident. CE is a unique pathology that leads to acute myocardial infarction. It portends a high mortality rate and requires a high level of suspicion as symptoms may be misleading. Further research is needed in order to improve recognition and management and to lower associated mortality.     

经肝动脉灌注^131 I-HAblSF（ab’）2治疗肝癌合并门静脉癌栓疗效分析

目的探讨经肝动脉灌注^131 I-HAbl8F（ab’）2治疗肝癌合并门脉癌栓的价值。方法8例合并门脉癌栓的晚期肝癌患者行经肝动脉超选择灌注^131 I-HAbl8F（ab＇）2临床治疗性试验，剂量：0．75mCi／kg。分析症状、卡氏评分、肝功能、AFP及肿瘤CT等影像变化，随访近期疗效。结果7例疼痛患者中，3例症状缓解。3例卡氏评分增加、4例稳定。6例AFP异常患者治疗后3例下降。全组病例用药后肝功能损害均无明显加重。1例无明显症状的弥漫型肝癌患者治疗后病灶减少；余7例中，瘤体增大5例、缩小2例，其中，PR2例，临床有效率28．6％。本组1例1年随访时生存。结论经肝动脉灌注0．75mCi／kg ^131 I-HAbl8F（ab＇）2对合并门脉癌栓的肝癌患者肝功影响小，对门脉分支癌栓患者有较好的疗效。     

肾细胞癌伴静脉癌栓15例临床分析

１９８５～１９９４年治疗肾细胞癌伴静脉癌栓１５例。按癌栓水平分为肾型１０例，肝下型４例，肝上型１例。Ｂ超和ＣＴ检查总确诊率７３％。手术１４例均完整取出癌栓，术后１３例接受５－ＦＵ加ＭＭＣ方案化疗。随访３个月～５年，１例肝下型和２例肾型无瘤存活分别３６、４３、５２个月，余均在术后２年内死亡。认为Ｂ超与ＣＴ互补应用可基本确诊静脉癌栓，除肝上型和已有血管壁浸润者外大部分癌栓可采用松解游离同时渐渐拉出的方式取出，癌栓水平除肝上型外对预后影响不大。     

用纤支镜为支气管哮喘患者作肺灌洗的安全性观察

本文对12例支气管哮喘病人作了22例次支气管肺泡灌洗,其中3例次为重度哮喘发作;8例次为中度发作[1];11例次为缓解期.灌洗方法在一般肺灌洗的基础上经过改良后,12例病人无1例死亡.11例次哮喘发作患者,灌洗后临床症状皆有不同程度改善.11例次缓解期病人,灌洗后皆无不良反应.凡哮喘时间较长者,均能灌洗出较大量脓痰栓.     

Cor pulmonale caused by recurrent pulmonary emboli

A 53-year-old black man developed femoral thrombophlebitis in 1983 following a Harrington nail implantation in his first lumbar vertebral region. There was evidence of pulmonary embolization at that time and recurrently until he developed ventricular fibrillation and died in 1987. The terminal event followed a hypotensive episode during the course of a right ventricular catheterization. Autopsy confirmed the clinical impression that he had multiple recurrent thromboemboli to his lungs. After several years of embolization, the pulmonary arterial circulation was sufficiently occluded to result in pulmonary hypertension. Cor pulmonale was produced, with congestive heart failure leading to a progressively downhill course in the 4 months before his death.     

Pulmonary hypertension due to tumor emboli: A report of three autopsy cases with morphological correlations to radiological findings

Three cases of pulmonary hypertension caused by tumor emboli to the lungs are described. Two of the three cases had a clinical diagnosis of pulmonary thromboembolism until surgical embolectomy, and the other had a diagnosis of primary pulmonary hypertension. Autopsy disclosed chondrosarcoma, choriocarcinoma and gastric cancer as the primary tumors, respectively. Pulmonary vascular obstruction due to tumor embolism leading to pulmonary hypertension is a previously rare clinical entity, and obstructed pulmonary vessels are believed to tend to be small vessels. We compared the autopsy and radiological findings and concluded that pulmonary tumor embolism involved not only the small peripheral arteries but also the segmental and/or lobar arteries.     

Regional cerebral blood flow after occlusion of the middle cerebral artery

Occlusions of the middle cerebral artery (MCA) are mostly of embolic origin (appr. 80%) and give rise to about one third of all ischemic strokes, most of these being major strokes. MCA occlusions lasting for less than 1/2 h are tolerated without occurrence of permanent tissue damage. Occlusions lasting between 1/2 h to 4-8 h lead to permanent tissue damage and neurological deficits that are proportional to the duration of occlusion. Maximal tissue damage is obtained after 4-8 h occlusion. A cerebral blood flow of 8-23 ml/100 gr/min is sufficient for cellular viability but insufficient for normal tissue function ("ischemic penumbra"). Cellular function is completely abolished in the interval 8-16 ml/100 gr/min and flow at that level is tolerated only for 1-3 h before neuronal death ensues. In the interval 18-23 ml/100 gr/min there is some functional activity although it is reduced. Experimental and clinical evidence suggests that flow in this interval may be tolerated for several days, months or even longer ("chronic ischemic penumbra"). After MCA occlusion the blood flow falls below 8 ml/100 gr/min in most cases and permanent MCA occlusion always leads to relatively large areas of frank infarction. The ischemic infarcts may be surrounded by collaterally perfused areas where the blood flow is pressure-dependent (impaired autoregulation) and quite commonly insufficient for normal neuronal function (below 23 ml/100 gr/min). Such collaterally perfused areas may include a "chronic ischemic penumbra". Emboli causing MCA occlusions commonly disintegrate and/or migrate more peripherally within the first few weeks post stroke. This leads to reperfusion and changes of ischemic infarcts into hyperemic infarcts where flow is severely increased. The vascular reactivity is completely abolished in hyperemic infarcts and the hyperemic state lasts for about two weeks. Probably, anemic infarcts are equivalent to ischemic infarcts while the hemorrhagic variety is equivalent to hyperemic infarcts. The "partial infarct" with selective neuronal necrosis occurs in experimental animals after MCA occlusions of less than four h but not after permanent MCA occlusion. The significance of partial infarction in human stroke is not clarified. The extent of irreversible tissue damage can be reduced only if therapy sets in within 4-8 h after the occlusion. If a "chronic penumbra" exists the extension of reversible tissue damage can be reduced if therapy aimed at increasing the blood flow in the penumbra sets in within weeks or even months after the stroke.(ABSTRACT TRUNCATED AT 400 WORDS)     

肺气/灌注显像与螺旋CT诊断肺栓塞的对比分析

目的比较肺通气／灌注(Lung perfusion／ventilation scintigraphy．Q／V)显像与螺旋CT肺动脉造影(Computerized tomography pulmonary angiography．CTPA)在肺栓塞(Pulmonary embolism，PE)定性及定位诊断对治疗决策的影响、溶栓及抗凝治疗后的疗效观察等方面的临床价值。方法回顾性分析了23例PE患者的肺Q/V显像(35例次)，并与CTPA(31例次)结果进行对比分析。结果肺Q／V与CTPA定性诊断符合率91．3％；定位诊断符合率53．37％；治疗前肺Q/V提示大面积肺栓塞的4例急性PE患者行溶栓治疗．1例CTPA提示大面积肺栓塞的急性PE患者行溶栓治疗：PE患者溶栓治疗后4例复查肺Q/V及2例复查CTPA、抗凝治疗后3例复查肺Q/V及2例复查CTPA结果显示受累肺段的改善情况与溶栓治疗疗效、与患者症状改善相一致。结论肺Q/V与CTPA定性诊断PE有很好的一致性。但定位方面存在差异．CTPA与肺Q/V存在互补关系。但尚无法取代肺Q/V显像。     

III期结直肠癌中NLRC3与预后和肿瘤免疫的关系

目的：探讨核苷酸寡聚化结构域样受体家族半胱天冬酶募集结构域蛋白3(nucleotide binding oligomerization domain-like receptor family caspase recruitment domain containing 3,NLRC3)与III期结直肠癌的预后及肿瘤免疫相关指标 的关系。方法：回顾性收集中南大学湘雅医院2012年至2013年122例经手术根治切除的III期结直肠癌患者的相关资 料。利用免疫组织化学法分析NLRC3与CD8+ T细胞的表达情况,利用患者的术前临床资料计算中性粒细胞/淋巴细 胞比值(neutrophil to lymphocyte ratio,NLR),并检测其微卫星稳定性。采用χ2检验分析NLRC3与临床病理因素之间的 关系,采用COX回归模型分析III期结直肠癌的独立预后因素。结果：在III期结直肠癌中,肿瘤组织CD8+ T细胞浸润 分期(χ2=27.79,P<0.01)、NLR值(χ2=6.35,P<0.05)、淋巴结转移分期(χ2=10.12,P<0.01)以及微卫星稳定性(χ2=6.05, P<0.05)与NLRC3的表达有关。NLRC3(OR=0.066,95% CI：0.020~0.218)、血管癌栓(OR=3.119,95% CI：1.547~6.286) 及NLR(OR=5.103,95% CI：2.465~10.563)对III期结直肠癌的5年总生存期(overall survival,OS)有影响(均P<0.05);另 外,NLRC3(OR=0.144,95% CI：0.055-0.377)、血管癌栓(OR=3.589,95% CI：1.859~6.932)及NLR(OR=2.939,95% CI： 1.509~5.723)对III期结直肠癌的无病生存期(disease free survival,DFS)同样有影响(均P<0.05)。结论：NLRC3,血管癌栓 和NLR是III期结直肠癌的独立预后因素。NLRC3通过抑制系统性炎症、促进局部抗肿瘤免疫而使III期结直肠癌患者 具有良好的预后。