术后早期炎性肠梗阻的诊断与治疗

目的 探讨术后早期炎性肠梗阻的特点和诊断，治疗原则。方法 分析近期经治的术后早期炎性肠梗阻23例。结果 23例病人均经胃肠减压，应用生长抑素，肾上腺皮质激素及肠外营养等治疗后痊愈，平均治愈时间13.2天，无一例再手术引起；（3）症状以腹胀为主，腹痛相对较轻；（4）很少发生肠绞窄。（5）最好先试行保守治疗2-4周，多数有效。     

预激综合征合并阵发性快速型心房颤动1例

预激综合征（WPW）合并快速型心房纤颤是一种常见的心律失常,1930年Wolff、Parkinson、White首先报告,在临床工作中一直倍受重视。WPW患者除了合并房室折返性心动过速外,并发心房颤动（Af）也较常见,发生率高达11%和39%。由于快速的心室率可诱发恶性室性心律失常,导致血流动力学紊乱,有猝死的危险。现将我科l例预激综合征合并阵发性快速型心房颤动的心电图资料总结分析,并报道如下。     

肩关节镜术后关节腔内注射皮质类固醇激素安全性的系统评价与Meta分析

文题释义：肩关节镜：随着肩关节镜手术适应证的扩大及手术技术和器械的不断更新发展，在过去20年间肩关节镜手术越来越普遍。肩关节镜手术是临床诊断肩袖撕裂、撞击综合征和不稳定性、SLAP损伤、Bankart损伤等疾病的主要诊断和治疗工具。 皮质类固醇激素：关节内注射皮质类固醇激素是一种有效缓解术后肩部疼痛和僵硬的方法之一，因为其可以减少滑膜炎症，减轻疼痛感并加速术后早期功能恢复。然而人们仍然担心使用皮质类固醇激素是否会增加肩关节镜术后相关并发症，例如术后感染、术后早期肌腱断裂、延缓肌腱愈合等，其安全性及临床疗效尚存争议。 背景：肩关节镜术后关节内注射皮质类固醇激素是一种有效缓解术后肩部疼痛和僵硬的方法之一，但使用皮质类固醇激素是否会增加肩关节镜术后相关并发症仍有争议。 目的：系统评价肩关节镜术后关节腔内注射皮质类固醇激素的安全性及临床疗效。 方法：应用计算机检索PubMed、EMBASE、Cochrane Central Register of Controlled Trials(CENTRAL)数据库中肩关节镜术后关节腔内注射皮质类固醇激素的临床对照试验，检索时间为建库至2019年9月。文献数据提取及质量评价由2位研究者按照纳入和排除标准独立进行，采用Rev man 5.3 版本软件进行效应量的合并与分析。 结果与结论：①共纳入6篇相关文献，包括7 418例患者，其中激素注射组3 920例、对照组3 498例；②Meta分析显示，两组再撕裂率、Constant评分、ASES评分、UCLA评分比较差异均无显著性意义[OR=0.71，95%CI[0.45，1.13]，P=0.15；MD=-0.99，95%CI(-12.44，10.46)，P=0.87；MD=-0.12，95%CI (−1.80，1.56)，P=0.89；MD=−1.46，95%CI(−3.22，0.30)，P=0.10]；激素注射组肩关节镜术后1个月内感染率高于对照组(P < 0.05)，两组肩关节镜术后2-4个月的感染率比较差异无显著性意义(P > 0.05)；③结果表明，肩关节镜术后注射皮质类固醇激素并不会增加术后再撕裂率，但肩关节镜术后1个月内注射类固醇激素会增加术后感染率，因此在肩关节镜术后应用皮质类固醇激素治疗时，临床医师应根据患者实际情况权衡利弊，同时注意避免在术后1个月内注射关节内激素治疗。 ORCID: 0000-0002-5259-5160(范智荣) 中国组织工程研究杂志出版内容重点：人工关节；骨植入物；脊柱；骨折；内固定；数字化骨科；组织工程     

高血压性脑出血70例术后死亡原因分析

目的总结高血压脑出血（HCH）术后死亡的原因，探讨手术指征，选择合适的手术病例，降低死亡率。方法对70例HCH手术后死亡患者的临床资料进行回顾性分析，找出与死亡相关的主要因素。结果术前脑疝形成使中枢衰竭在1周内死亡者43例，其中双侧瞳孔散大30例，单侧瞳孔散大13例；各种并发症在2-3周内死亡者27例：肺部感染11例，上消化道出血6例，急性肾功能衰竭5例，多脏器功能衰竭3例，心功能衰竭1例，体液代谢紊乱1例。结论脑出血后脑疝形成及术后多脏器并发症是术后死亡的主要原因。脑血肿残腔再出血，恶性脑肿胀，营养衰竭是术后死亡的危险因素。及时手术减少术前脑疝形成，术后严格监测生命体征，稳定血压，早期对并发症预防性治疗及合理的营养支持是降低死亡率的关键。     

急性不完全脑缺血大鼠心房特殊颗粒变化的形态学及形态计量学研究

本实验应用形态计量学的方法研究了心房特殊颗粒的变化与脑缺血的关系。实验用中老年 Wistar大鼠 ,采取双侧颈总动脉夹闭 2 h后去夹再灌流的方法制作急性不完全性脑缺血模型。于再灌后 6h、2 4h、3 d及 7d,处死大鼠 ,在 10 0 s内取出右心耳 ,常规超薄切片及染色 ,电镜观察心房特殊颗粒的变化并进行形态计量学研究。结果显示 :脑缺血再灌后 6h,心房特殊颗粒几乎释放殆尽 ,2 4h及 3 d数量明显减少 ,颗粒变小 ;形态计量研究表明 ,缺血再灌组大鼠心房特殊颗粒的体积密度、面数密度、数密度及颗粒的平均直径 ,除 7d者外 ,其余均比假手术组有不同程度的减小 ( P<0 .0 1,P<0 .0 5 )。本实验结果表明 ,心房特殊颗粒内所含的心房肽参与早期脑缺血缺氧的病理生理过程 ,在遏制脑细胞损伤方面起了积极的作用     

甘露醇在四肢骨折中的应用（附80例报告）

目的观察甘露醇在四肢骨折中的应用的疗效。方法本组共80例骨折病人，在骨折早期及骨折术后早期使用甘露醇进行脱水治疗，观察用药后的疗效。结果术后无一例发生骨筋膜室综合症(OCS)及严重伤口感染，早期未肿胀病例经预防治疗后无一例发生张力性水泡，未见有严重药物毒副作用发生。结论甘露孵可作为四肢骨折的临床辅助用药，该方法具有简单、安全和经济的特点。     

药物洗脱球囊和药物洗脱支架对支架内再狭窄的疗效比较

文题释义： 支架内再狭窄：是指支架内全程和/或支架两端5 mm节段内管腔丢失，导致管腔狭窄程度≥50%；临床定义为冠状动脉支架植入后需要靶病变或靶血管血运重建的症状性再狭窄，临床表现为缺血性胸痛，如心绞痛或急性心肌梗死等。 药物洗脱球囊：通过向冠状动脉血管壁释放抗增殖药物(紫杉醇)，抑制血管内膜增生，适用于小血管疾病、分叉疾病和支架内再狭窄病变、支架内再狭窄，优点在于无异物植入，降低了血栓形成风险，减少了再狭窄的发生，后续抗血小板治疗时间较短。 背景：国内外一系列的研究显示针对药物洗脱支架内再狭窄病变，药物洗脱球囊和药物洗脱支架优于其他介入方式，但是这两种治疗方式都存在着各自的局限。 目的：评价药物洗脱球囊与药物洗脱支架植入治疗药物洗脱支架内再狭窄的疗效。 方法：选择2016年1月至2017年12月内蒙古医科大学第一附属医院收治的药物洗脱支架内再狭窄患者63例，其中32例进行药物洗脱球囊植入治疗，另31例进行药物洗脱支架植入治疗，记录两组患者介入术前、术后即刻冠状动脉情况，随访1 年后冠状动脉造影情况、主要不良心血管事件发生及支架内再狭窄的危险因素分析。研究得到内蒙古医科大学伦理委员会的同意及支持。 结果与结论：①随访1年，两组支架内最小管腔直径、参考血管直径、支架内晚期管腔丢失比较差异均无显著性意义(P均> 0.05)，二次再狭窄概率比较差异无显著性意义(18%，16%，P=0.216)。靶病变血运重建发生率比较差异无显著性意义(6%，6%，P=0.513)，主要不良心脏事件发生率比较差异无显著性意义(9%，10%，P=0.334)；药物洗脱支架组2例发生消化道出血，药物洗脱球囊组未发生消化道出血，两组比较差异有显著性意义(P < 0.01)；②多因素分析发现，吸烟、糖尿病、高同型半胱氨酸血症是支架内再狭窄的危险因素；③结果表明，药物洗脱球囊与药物洗脱支架均是治疗支架内再狭窄的理想方法，临床实践中需综合多因素考虑需采取个体化治疗方案。 ORCID: 0000-0002-6209-874X(谢秀峰) 中国组织工程研究杂志出版内容重点：生物材料；骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性；组织工程     

急性心肌梗塞患者早期尿激酶溶栓治疗甲襞微循环动态研究

目的：动态观察急性心肌梗塞（AMI）病人早期尿激酶（UK）溶栓治疗甲襞微循环变化，并探讨其发生的可能机制，为临床AMI的治疗及再灌注损伤（RI）的预防提供理论依据。方法：运用显微电视录像系统结合加权积分法对21例AMI病人甲襞微循环进行研究。结果：再灌注即刻，血液流态恶化（P＜0．01）；再灌注心律失常发生率与血液流态积分值有关（P＜0．05）。结论；1、AMI早期UK治疗随冠脉再通，甲襞微循环特征性改变为红细胞高度聚集，白微栓大量形成即血流状态的恶化。提示纤溶的同时凝血功能亢进。支持AMI溶栓前后应用ASA、肝素等抗凝治疗。2、微循环异常改变参与AMI及RI发生和发展，临床应加以重视。     

硬膜外镇痛与静脉镇痛对老年下肢关节置换及植入物内固定治疗后早期认知功能的影响

背景：术后认知功能障碍与老年人术后并发症的发生及死亡率密切相关。设定相同麻醉条件下硬膜外镇痛比静脉镇痛对老年患者下肢关节置换及内固定后早期认知功能的影响较小。 目的：比较两种不同的镇痛方法对老年患者下肢骨科手术后早期认知功能的影响。 方法：60例拟行择期下肢手术的老年患者,随机接受椎管内麻醉继以术后静脉镇痛或以硬膜外镇痛。 结果与结论：术后认知功能障碍发生率静脉镇痛组为47%(14/30),硬膜外镇痛组为30% (9/30例),两组间差异非常显著(P < 0.01 )。Logistic回归分析显示受教育年限短和髋关节置换术是发生术后早期认知功能障碍的独立危险因素。结果表明,老年患者在下肢关节置换及内固定后早期有38%的患者发生了认知功能障碍,且硬膜外镇痛较静脉镇痛发生术后认知功能障碍明显降低。受教育年限短和髋关节置换本身是术后早期认知功能障碍的危险因素。     

AF钉治疗胸腰段脊椎爆裂型骨折120例

目的：总结采用AF钉内固定术治疗胸腰段脊椎爆裂型骨折的临床疗效。方法：应用AF钉治疗胸腰段脊椎爆裂型骨折患者120例，全部采用后人路AF钉复位、内固定。结果：术后X线片示椎体高度、椎间隙高度和生理弧度完全恢复，脱位纠正；合并脊髓神经功能障碍者神经功能恢复率达87％；平均随访18个月，有11例断钉，14例伤椎椎体高度丢失10％左右；112例恢复劳动能力。结论：后路AF钉内固定对胸腰段爆裂型骨折的复位、固定和对椎管间接减压更加简便、有效，无需电视监视条件；为防止断钉等并发症发生，应严格限制术后早期负重活动。     

Detection of atrial-flutter and atrial-fibrillation waveforms by fetal magnetocardiogram

Two cases of fetal tachycardia are reported: atrial flutter and fibrillation. The waveforms from each case were detected by fetal magnetocardiograms (FMCGs) using a 64-channel superconducting quantum interference device (SQUID) system. Because the magnitude of supraventricular arrhythmia signals is very weak, two subtraction methods were used to detect the fetal MCG waveforms: subtraction of the maternal MCG signal, and subtraction of the fetal QRS complex signal. It was found that atrial-flutter waveforms showed a cyclic pattern and that atrial-fibrillation waveforms showed f-waves with a random atrial rhythm. Fast Fourier transform analysis determined the main frequency of the atrial flutter to be about 7 Hz, and the frequency distribution of atrial fibrillation consisted of small, broad peaks. To visualise the current pattern, current-arrow maps, which simplify the observation of pseudo-current patterns in fetal hearts, of the averaged atrial flutter and fibrillation waveforms were produced. The map of the atrial flutter had a circular pattern, indicating a re-entry circuit, and the map of the atrial fibrillation indicated one wavelet, which was produced by a micro-re-entry circuit. It is thus concluded that an FMCG can detect supraventricular arrhythmia, which can be characterised by re-entry circuits, in fetuses.     

Time-frequency coherence analysis of atrial fibrillation termination during procainamide administration

A time-frequency coherence estimator is developed and applied to study changes in signal characteristics as atrial fibrillation converts to sinus rhythm during administration of procainamide. A coherence spectrogram (CS) using multiple sinusoidal tapers is used in this study to assess phase relations between electrogram recordings at multiple atrial sites of seven patients who received procainamide to terminate atrial fibrillation. CSs are calculated (0 to 60 Hz) with 1 sec time resolution and 6.2 Hz frequency resolution. In agreement with previous studies, CSs generally exhibit low coherence during atrial fibrillation. Conversion to sinus rhythm is concomitant with an increase in coherence and emergence of structured time-frequency topography. Transition from atrial fibrillation to sinus rhythm is associated with a variety of time-frequency dynamics. Both gradual and abrupt increases in coherence coincide with conversion. Results suggest transient electrical organization in the atria during atrial fibrillation not seen in previous low-resolution coherence studies. CSs permit investigation of rhythm organization with unparalleled time and frequency resolution and thus are useful for studying transient changes in cardiac rhythms that may reflect underlying mechanisms.     

The relation between mitral annulus motion and left ventricular ejection fraction in atrial fibrillation.

Mitral annulus motion (MAM) has recently been introduced as an index of left ventricular function. Previous studies have shown a good agreement between MAM (mm) x 5 and ejection fraction in middle-aged and elderly patients. These studies only included patients with sinus rhythm, while patients with atrial fibrillation were excluded. In the present study, MAM was reduced in patients with atrial fibrillation while ejection fraction (EF) did not differ from age-matched control patients with sinus rhythm. The 'conversion factor' (EF/MAM) was 7.2 in the group with atrial fibrillation and 5. 1 in controls with sinus rhythm. This difference must be taken into account when MAM is used to estimate left ventricular function in patients with atrial fibrillation. Patients with atrial fibrillation had lower stroke volume and higher heart rate than patients with sinus rhythm. A decreased systolic long-axis shortening was found (P<0.005) compared to patients with sinus rhythm, but no difference in short-axis diameter shortening.     

Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment.

BACKGROUND: Atrial fibrillation cannot always be converted to sinus rhythm by transthoracic electrical cardioversion. We examined the effect of ibutilide, a class III antiarrhythmic agent, on the energy requirement for atrial defibrillation and assessed the value of this agent in facilitating cardioversion in patients with atrial fibrillation that is resistant to conventional transthoracic cardioversion. METHODS: One hundred patients who had had atrial fibrillation for a mean (+/-SD) of 117+/-201 days were randomly assigned to undergo transthoracic cardioversion with or without pretreatment with 1 mg of ibutilide. We designed a step-up protocol in which shocks at 50, 100, 200, 300, and 360 J were used for transthoracic cardioversion. If transthoracic cardioversion was unsuccessful in a patient who had not received ibutilide pretreatment, ibutilide was administered and transthoracic cardioversion attempted again. RESULTS: Conversion to sinus rhythm occurred in 36 of 50 patients who had not received ibutilide (72 percent) and in all 50 patients who had received ibutilide (100 percent, P<0.001). In all 14 patients in whom transthoracic cardioversion alone failed, sinus rhythm was restored when cardioversion was attempted again after the administration of ibutilide. Pretreatment with ibutilide was associated with a reduction in the mean energy required for defibrillation (166+/-80 J, as compared with 228+/-93 J without pretreatment; P<0.001). Sustained polymorphic ventricular tachycardia occurred in 2 of the 64 patients who received ibutilide (3 percent), both of whom had an ejection fraction of 0.20 or less. The rates of freedom from atrial fibrillation after six months of follow-up were similar in the two randomized groups. CONCLUSIONS: The efficacy of transthoracic cardioversion for converting atrial fibrillation to sinus rhythm was enhanced by pretreatment with ibutilide. However, use of this drug should be avoided in patients with very low ejection fractions.     

Amiodarone in atrial fibrillation

Twenty-seven patients with atrial fibrillation without any concomitant conduction abnormality have been treated with oral amiodarone in a daily maintenance dose of 200 mg. The drug has been used for three purposes: 1) to block atrioventricular conduction, thereby decreasing the ventricular rate during atrial fibrillation (9 patients), 2) as prophylaxis against paroxysmal atrial fibrillation (8 patients), 3) as prophylaxis against recurrence of atrial fibrillation after DC conversion to sinus rhythm (13 patients). All patients were considered refractory to other antiarrhythmic drugs in these respects. In the second group, 4 of the 8 patients reported complete cessation of attacks and the others a marked reduction of the attack rate. In the third group, 10 of the 13 patients have maintained sinus rhythm for a longer period on treatment with amiodarone than with other drugs, resulting more than a triple prolongation of the time in sinus rhythm. In 3 patients the drug has been discontinued because of side-effects. In conclusion, amiodarone affords protection from episodes of paroxysmal atrial fibrillation, as well as from recurrence of atrial fibrillation after DC conversion to sinus rhythm. If the drug is ineffective in either of these respects, it may still be useful as a means of moderating the ventricular response in atrial fibrillation.     

Can we improve outcomes in AF patients by early therapy?

Atrial fibrillation affects at least 1% of the population and causes marked society-wide morbidity and mortality. Current management of atrial fibrillation including antithrombotic therapy and management of concomitant conditions in all patients, rate control therapy in most patients, and rhythm control therapy in patients with severe atrial fibrillation-related symptoms can alleviate atrial fibrillation-related symptoms but can neither effectively prevent recurrent atrial fibrillation nor suppress atrial fibrillation-related complications. Hence, there is a need for better therapy of atrial fibrillation.     

Pathophysiological mechanisms of atrial fibrillation: a translational appraisal

Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological alterations promoting AF have been studied extensively in animal models. Atrial tachycardia or AF itself shortens atrial refractoriness and causes loss of atrial contractility. Aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. These changes in electrical, contractile, and structural properties of the atria have been called "atrial remodeling." The resulting electrophysiological substrate is characterized by shortening of atrial refractoriness and reentrant wavelength or by local conduction heterogeneities caused by disruption of electrical interconnections between muscle bundles. Under these conditions, ectopic activity originating from the pulmonary veins or other sites is more likely to occur and to trigger longer episodes of AF. Many of these alterations also occur in patients with or at risk for AF, although the direct demonstration of these mechanisms is sometimes challenging. The diversity of etiological factors and electrophysiological mechanisms promoting AF in humans hampers the development of more effective therapy of AF. This review aims to give a translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process. We pay attention to translation of pathophysiological insights gained from in vitro experiments and animal models to patients. Also, suggestions for future research objectives and therapeutical implications are discussed.     

Dedifferentiation of atrial cardiomyocytes in cardiac valve disease: unrelated to atrial fibrillation

BACKGROUND: Valvular heart disease has become an important public health concern. The increased wall stress and underlying disease entity associated with mitral valve disease provide unfavorable circumstances for atrial cardiomyocytes. The expression of the alpha-smooth muscle actin isoform is considered characteristic of cardiomyocyte dedifferentiation (embryonic cardiomyocyte), and cardiomyocyte dedifferentiation may indicate an adaptive state, enabling cardiomyocytes to survive despite unfavorable circumstances. METHODS: This study comprised 20 adult patients with symptomatic severe mitral valve disease and moderate to severe tricuspid valve disease and without coronary artery disease undergoing valve operations for congestive heart failure. Ten patients had persistent atrial fibrillation and 10 patients had never been in atrial fibrillation by history and electrocardiograms before surgery. Atrial tissues of the right atrial appendage were obtained during surgery. RESULTS: Immunohistochemical study demonstrated that alpha-smooth muscle actin protein expression was not altered by atrial fibrillation, and alpha-smooth muscle actin protein expression in atrial tissues was higher in patients with sinus rhythm than in those with atrial fibrillation (the percentage of cells that were alpha-smooth muscle actin-positive was 51.5+/-34.9% for right atria from patients in sinus rhythm vs. 16.2+/-15.0% for right atria from patients with atrial fibrillation) (P<.03). Semiquantitation of alpha-smooth muscle actin by immunoblotting of extracts from atrial tissues showed similar findings as in the immunohistochemical observations: that is, atrial fibrillation did not influence the expression of alpha-smooth muscle actin protein. Interstitial fibrosis represented 43.2+/-13.9% of the right atrial tissue in the sinus group, whereas interstitial fibrosis comprised 49.8+/-8.2% of the right atrial tissue in the atrial fibrillation group (P=.320). CONCLUSIONS: Dedifferentiation of atrial cardiomyocytes occurs in patients with cardiac valve disease, even without atrial fibrillation.     

Schlafbezogene Atmungsstörungen und kardiale Arrhythmien

Sleep-disordered breathing is a highly prevalent and clinically relevant co-morbidity in patients with heart rhythm disorders. An increased incidence of atrial fibrillation as well as a premature reoccurrence of atrial fibrillation following electrical cardioversion or catheter ablation has previously been demonstrated. Patients with chronic heart failure seem to face an increased risk for malignant arrhythmic events. Furthermore, in patients with obstructive sleep apnea sudden cardiac death occurs more frequently during sleeping hours. Preliminary data suggest beneficial effects on arrhythmia occurrence in patients with obstructive sleep apnea (OSA) undergoing continuous positive airway pressure. However, as in patients with Cheyne-Stokes respiration, randomized, controlled trial results for ventilation therapy are still lacking.     

Analysis of arrhythmias based on atrial wall motion. Usefulness and feasibility of recording left and right atrial systole by echocardiography

The usefulness and feasibility of recording atrial wall motion by M-mode echocardiography guided by two-dimensional examination was evaluated in three groups of consecutive patients: 7 with undefined tachyarrhythmias, 25 in sinus rhythm, and 20 with atrial flutter or fibrillation. Atrial systole was recorded in the left and right atrium in 58 and 98% of the patients, respectively (p less than 0.05). Six of the patients with undefined tachyarrhythmias exhibited electrocardiographic atrioventricular dissociation revealed by preceding echocardiography in all. The precise timing of left and right atrial systole could be recorded in patients in sinus rhythm; right atrial contraction preceded left atrial systole by 42 +/- 31 msec (mean +/- SD). Among patients with atrial flutter or fibrillation, one case of dissimilar atrial rhythms was revealed by echocardiography. Thus, recording of atrial wall motion is feasible in the majority of patients and provides information which is otherwise available only by esophagus ECG or by invasive means.