Migraine-like headaches associated with nickel allergy requiring removal of atrial septal defect closure device

There is a deficit of literature regarding the association between nickel allergy–induced symptoms and implanted devices. This report describes a case of nickel allergy causing debilitating migraine-like symptoms, failing to resolve with medical therapy, requiring surgical removal of the device and repair of the defect.     

使用自相关和时间序列检测的方法检测心室纤颤信号

心室纤颤信号必须准确而及时地识别,如果不使用除颤器及时进行除颤,病人会迅速死亡。另一方面,如果心室纤颤信号没有发生,而误判为心室纤颤信号,给予电击,则病人的心脏受到不应有的损伤,这也属于严重的医疗事故。因此快速与准确的识别显得十分重要。自70年代以来,世界上许多科学家都在探讨各种方法,以期望使用计算机自动识别心室纤颤信号,但均因达不到实时判别的要求或准确率不够高而不能用于自动除颤器检测的设计方案。本文介绍了一种准确率高而又较简易的快速识别法。这一方法是取一秒心电信号,进行有限长度离散信号的自相关,然后对该自相关函数作零切割,让自相关函数变成一串二进制脉冲串,接着以一秒信号的脉冲串数作为特征参数,设计分类器。经证明,心室纤颤信号(VF信号)(Ventricular Fibrillation)和心动过速信号(VT信号)(Ventricular Tachycar-dia)的特征参数均属于高斯分布。因此可用Wald时间序列检测方法对VF信号和VT信号分类。这个算法可用于计算机进行实时处理和分析,同时此法与取样率无关,适用于各种取样系统,是一个较理想的方法。     

心外膜脂肪组织及其在房颤心肌结构重构和电重构中的作用

心房纤颤（atrial fibrillation, AF）是临床上最常见的心律失常之一,也是心血管疾病发病率和死亡率增加的重要原因。心外膜脂肪（epicardial adipose tissue, EAT）是位于脏层心包和心肌之间的一种特殊脂肪组织,研究表明EAT参与AF的发生与维持,但是具体机制尚未得到完全阐释。EAT来源的脂肪干细胞（adipose-derived stromal cells, ADSCs）分泌的细胞外囊泡(extracellular vesicles, EVs) 近年来受到重视。该文主要从EAT特点、定量检测及其与心肌结构与电重构的关系,特别是EVs对AF发生的影响等方面进行综述,以期进一步认识AF的发病机制,为今后的治疗提供新的思路。     

阵发性心房纤颤患者P波离散度研究

目的 :探讨阵发性心房纤颤患者P波离散度的改变规律及临床价值。方法 :观察 41例非瓣膜性心脏病和2 1例瓣膜性心脏病阵发性心房纤颤患者最宽P波 (Pmax)和P波离散度及与左房大小关系 ,并与 30例正常人对比。结果 :阵发性心房纤颤的左房大小、Pmax、P波离散度、Pmax≥ 110ms、P波离散度≥ 40ms等均显著高于正常对照组(P <0 .0 1) ,非瓣膜性心脏病组年龄大于瓣膜性心脏病组 ,左房大小及Pmax均小于瓣膜性心脏病组 ,差异有非常显著性 (P <0 .0 1)。结论 :Pmax、P波离散度结合左房大小、年龄对预测阵发性心房纤颤的发生有重要意义。     

压力波对豚鼠耳蜗血管纹、毛细胞心钠素免疫活性改变的研究

目的为探讨压力波的致聋机理,对豚鼠耳蜗血管纹(SV)、毛细胞(HC)中心钠素免疫活性(ANP-IR)的改变及与听阈阈移的相关性进行研究。方法采用免疫细胞化学(ABC法)法、图像分析听性脑干反应测听技术(ABR)对压力波暴露后不同时间分组的豚鼠耳蜗SV、HC中ANP-IR产物进行检测。结果压力波暴露后6、12、24h和48h组SV组织中ANP-IR光密度值较对照组均有明显的差异(P<0．05),其中24h组最高;冲击波暴露后6、12、24h组内毛细胞(IHC)中ANP-IR阳性产物的光密度值较对照组明显增高(P<0．05),其中以12h组最高。二者的变化均与听阈阈移有明显的正相关性(r1=0．8175,P＞0．05;r2=0．9185,P＞0．05)。而外毛细胞(OHC)中ANP-IR阳性产物变化不明显。结论压力波暴露后,SV组织中ANP的增高可能是内耳的一种代偿机制;IHC和OHC中ANP-IR的变化可能是冲击波对其损伤机制的不同表现。     

射频消融治疗阵发性室上性心动过速262例分析

经导管射频消融治疗阵发性室上性心动过速（ＰＳＶＴ）２６２例,探讨ＲＦＣＡ治疗ＰＳＶＴ的安全性及疗效。方法：房室结双径路改良采用下位法;左侧旁道采用冠状窦电极粗标,大头电极在心室国标。右侧旁道采用左前斜４５度。大头电极在心房侧三尖瓣环处细标;房扑时标测心房激动顺序,用隐匿必拖法确定折返环部位,在心房内行线性消融方法治疗。结果：２６２例中慢－快型房室结折生心动过速（ＡＶＮＲＴ）７８例。,房室折返性心动     

Adenosine for the management of patients with tachycardias--a new protocol

We developed a new protocol for diagnosis and treatment of patientswith sustained tachycardias (heart rate > 150 beats. min^–1).The patients first underwent vagal manoeuvres; if those remainedunsuccessful, i.v. adenosine in increasing doses of 6, 12, and18 mg was administered until sinus rhythm (SR) or transientatrioventricular (AV) block, unmasking the underlying rhythm,was recorded. In the latter and in the non-responding casesother antiarrhythmics were applied. Ninety-three episodes of tachycardia in 46 patients were treatedaccording to this protocol. Six episodes (6%) were terminatedby carotid massage, 64 of the remaining 87 episodes (74%) respondedto adenosine with return to SR. Conversion to SR occurred moreoften in episodes with narrow- than in wide-complex tachycardia(81 vs 59%, P<005). To achieve SR, the mean adenosine dosewas lower in narrow- than in wide-complex tachycardia (13±8vs 21 ± 10 mg; P<0.01). The duration of asystole afteradenosine did not differ between these two groups, whereas theduration of arrhythmia after adenosine differed significantly(8.5 ± 5.8 vs 18.6 ± 22.9 s; P<0.05). Sideeffects of adenosine such as flush, dyspnoea, and chest paindid not seem to be dose dependent and occurred in about 20%. According to our protocol, in more than 75% SR was achievedin patients with sustained tachycardias after vagal manoeuvresand adenosine.     

Some observations on the mechanism of pressure related atrial fibrillation

In order to investigate the effect of atrial pressure on thepropensity of the atria to fibrillate and the mechanism of thisassociation, the right atrial pressure was changed acutely bytransfusion-bleeding in 12 anaesthetized open-chest dogs. Undervarious atrial pressures the conduction time was measured betweentwo pairs of hook electrodes positioned on the two atrial appendagesrespectively. The effective refractory period was measured bycontinuous pacing of the right atrium at a 250 ms cycle lengthat double threshold intensity and interpolating a progressivelyearlier stimulus after each eighth paced beat. The propensityof fibrillation was studied by rapid (450 min^–1) pacingof the atria at double threshold intensity for 10 s at differentatrial pressures. At a high (14 mmHg) atrial pressure the conductiontime (45.7 ± 14.2 ms) was significantly (P<0.01) longer,the effective refractory period (157.9 ± 15.2 ms) significantly(P<0.01) longer and the atrial fibrillation (11/19 or 57.9%)significantly (X² = 9.95, P<0.001) more common than at alow ( 10 mmHg) pressure (35.2 ± 11.6, 146.2 ±12.4, 3/24 or 12.5%, respectively). Analysis of variance showedthat the probability of atrial fibrillation was significantlyaffected by the atrial pressure but not by either the conductiontime or the effective refractory period The findings suggestthat an increase in right atrial pressure by acute volume overloadprolongs the inter-atrial conduction time and right atrial refractorinessand increases the propensity of the atria tofibrillate by rapidatrial stimulation. The effect of atrial pressure on fibrillationdoes not seem to be mediated by the prolonged atrial refractorinessor conduction time.     

Pharmacokinetic-pharmacodynamic (PK-PD) modeling for a new antihypertensive agent (neutral metalloendopeptidase inhibitor SCH 42354) in patients with mild to moderate hypertension

SCH 42354, a neutral metalloendopeptidase (NEP) inhibitor, is the pharmacologically active form of the prodrug SCH 42495. It exerts antihypertensive effects by potentiating atrial natriuretic peptide (ANP) activity through inhibition of its hydrolysis by NEP. The objective of this study was to characterize the pharmacokinetics (PK) and pharmacodynamics (PD) of SCH 42354 in hypertensive males. SCH 42495 12.5 to 400 mg was administered orally to hypertensive men twice daily in a double-blind, placebo controlled multiple-dose parallel group design. Plasma SCH 42354 concentration and diastolic blood pressure (DBP) data were used to develop a PK-PD model using two approaches. In the first (non-integrated) approach, the link model was used to predict effect-site concentrations, and was applied to data obtained at the 300 and 400 mg BID doses only; data at the other (lower) doses were not amenable to modeling because of high variability. Effect-site concentration and DBP data were then fit to a sigmoid E_max PD model. For the 300 mg BID dose, PD parameters were: maximum effect (E_max), 8.1mmHg; no-drug effect (Eo), 3.6 mmHg; concentration corresponding to 50% of maximum response (EC₅₀), 0.87 g·ml^–1; and gamma, 3.9. In the second (time-integrated) approach, plasma SCH 42354 concentration and effect data obtained over the entire dose range were integrated with respect to time. Average plasma concentration and DBP data were then fit to a simple E_max PD model. PD parameters obtained over the dose range were: E_max, 10.3 mmHg; Eo, 2.0 mmHg; and EC₅₀, 0.7 g·ml^–1. These were similar to the estimates obtained from the first approach, demonstrating that the integrated (average) data allow PK-PD modeling over the (entire) dose range. The analysis showed that, at steady-state, a 400 mg BID dose of SCH 42495 produced an approximate 10 mmHg decrease in DBP in hypertensive males; the average plasma SCH 42354 concentration attained at this dose was approximately 1.8 g·ml^–1.