Brugada syndrome and its relevance in the perioperative period

Brugada syndrome is an autosomal dominant genetic disorder associated with an increased risk of sudden cardiac death, as well as ventricular tachyarrhythmias. The defective cardiac sodium channels result in usual electrocardiographic findings of a coved-type ST elevation in precordial leads V1 to V3. The majority of patients have uncomplicated courses with anesthesia, surgery, and invasive procedures. However there is risk of worsening ST elevation and ventricular arrhythmias due to perioperative medications, surgical insult, electrolyte abnormalities, fever, autonomic nervous system tone, as well as other perturbations. Given the increasing numbers of patients with inherited conduction disorders presenting for non-cardiac surgery that are at risk of sudden cardiac death, safe anesthetic management depends upon a detailed knowledge of these conditions.     

Taxol,a Microtubule Stabilizer,Improves Cardiac Functional Recovery during Postischemic Reperfusion in Rat in Vitro

Aims: Microtubule disruption contributes to cellular and organic dysfunction, and is implicated in ischemia/reperfusion (I/R) injury. The purpose of this study was to explore the effects of taxol, a microtubule stabilizer, on cardiac functional recovery during reperfusion. Methods: Left ventricular developed pressure, left ventricular end‐diastolic pressure, maximal time derivatives of pressure and the severity of ventricular arrhythmias were analyzed in isolated rat heart. Microtubule structure was immunohistochemically measured. Apoptosis and necrosis was identified with TUNEL or TTC staining, respectively. Mitochondrial permeability transition pore (mPTP) mRNA expression was examined by real‐time polymerase chain reactions. mPTP opening, reactive oxygen species (ROS), and oxidative enzyme activities were measured with fluorometric or spectrophotometric techniques. Intracellular calcium concentration ([Ca²⁺]_i) and Ca²⁺ transients were examined by Fura‐2‐AM and Fluo‐3‐AM, respectively. Cytosolic cytochrome c, sarcoplasmic reticulum Ca²⁺‐ATPase (SERCA2), ryanodine receptors (RyR), phospholamban (PLB), and PLB phosphorylation were analyzed by Western blot. Effective refractory period (ERP) and afterpotential‐mediated activity were detected using microelectrode. Results: Taxol improved the functional recovery of post‐I/R. Taxol preserved the intact microtubule structure in reperfusion. mPTP mRNA expression was unchanged while the mPTP opening was reduced by taxol, and this effect was accompanied by the decreased ROS level caused by oxidative enzymes activities’ changes. Taxol reduced apoptosis and the level of cytosolic cytochrome c in reperfusion. Taxol also promoted rapid recovery of [Ca²⁺]_i, prevented reduction of the amplitude of Ca²⁺ transients and shortened the decay time of Ca²⁺ transients. The protein expression of SERCA2, RyR, and PLB remained unchanged in reperfusion. Taxol prevented the increase of Phospho‐Thr17‐PLB and Phospho‐Ser16‐PLB in reperfusion. In addition, taxol facilitated rapid recovery of ERP and counter‐acted afterpotential‐mediated activity. Conclusion: Taxol may effectively improve cardiac functional recovery during reperfusion via inhibiting mPTP opening, ameliorating abnormal calcium homeostasis, and reducing the substrates associated with arrhythmias.     

苯那普利对大鼠心肌缺血再灌注心律失常的保护作用

目的　观察苯那普利对大鼠心肌缺血 /再灌注 ( I/ R)心律失常的影响。方法　选用雄性 SD大鼠 3 2只随机等分为二组 :苯那普利组 (苯那普利 10 mg· kg-1 .d-1 )和对照组 (生理盐水 2 ml/ d) ,二周后制作大鼠心肌 I/ R模型 ,观察缺血 10 min再灌注 2 0 min心律失常发生率和持续时间 ,左心室心肌超氧化物歧化酶 ( SOD)、一氧化氮 ( NO)及血压变化。结果　与对照组比苯那普利组大鼠缺血心室颤动 ( VF)发生率、再灌注室性心动过速 ( VT)、VF发生率及死亡率明显降低 ( P<0 .0 1) ;缩短缺血 /再灌注 VT持续时间 ( P<0 .0 1)。苯那普利对血压无明显影响 ( P>0 .0 5 )但可增加左心室心肌 SOD和 NO含量 ( P<0 .0 1)。结论　苯那普利具有抗大鼠 I/ R心律失常作用。     

Triggered activity induced by combined mild hypoxia and acidosis in guinea-pig Purkinje fibers

The effects of prolonged exposure to combined mild hypoxia (Po2 230 +/- 20 mmHg) and acidosis (pH: 6.8 +/- 0.05) were studied in guinea-pig left ventricular myocardium superfused in vitro. Only Purkinje fibers were impaled by microelectrodes. Triggered activity developed in depolarized Purkinje fibers after 48 +/- 9 min of exposure to hypoxic and acid conditions and was initiated either by short periods of rapid electrical driving or by the background slow Purkinje automaticity. Triggered activity occurred when a delayed afterdepolarization attained its threshold potential and terminated after a subthreshold afterdepolarization. Interaction between triggered activity and slow background automaticity was observed until 90 to 180 min of exposure to hypoxic and acid conditions. These effects were reversed by replacement in standard conditions (Po2 510 +/- 20 mmHg; pH 7.35 +/- 0.05). Norepinephrine (1 X 10(-6)M) significantly accelerated the rate of discharge of triggered foci and led to a stable sustained triggered activity. Increasing extracellular Ca2+ concentration aggravated the effects of combined mild hypoxia and acidosis and led to the occurrence of early afterdepolarizations initiating triggered activity. In addition abnormal automaticity developed in quiescent fibers without any triggering action potential. Lidocaine and verapamil suppressed the triggered activity following a subthreshold afterdepolarization. Their effects were reversed on wash-out. It is concluded that prolonged exposure to combined mild hypoxia and acidosis induces triggered activity by a basic mechanism common to other situations leading to a calcium overload and showing such behaviour.     

急性心肌梗塞时静脉输注硫酸镁对室性心律失常的影响

32名急性心肌梗塞患者(镁盐组)住院头三天每日静脉输注硫酸镁2.0g。结果表明:镁盐组和对照组心律失常发生率分别为22%(7/32)和63%(19/30)(P<0.01)。说明急性心肌梗塞早期补镁可能有助于减少心律失常发生。     

体表记录心室晚电位对冠心病室性心律失常临床意义

本文应用体表记录心室晚电位的方法,对220人(正常人78名);急性心肌梗塞92例;陈旧心肌梗塞50例;心绞痛10例进行了检测。正常人无一例晚电位阳性,而陈旧心肌梗塞合并室性心动过速(室速)者晚电位阳性率高达66.7%。心肌梗塞部位、室壁瘤及左室射血分数与晚电位缺乏相关性。体表记录心室晚电位对于冠心病室性心律失常的检测不失为一种有价值的非创伤性手段。     

Antiarrhythmic and electrophysiological effects of alpha adrenoceptor blockade during myocardial ischaemia and reperfusion in isolated guinea-pig heart

An isolated buffer perfused guinea-pig heart preparation has been used to study the antiarrhythmic and cellular electrophysiological effects of alpha adrenoceptor blockade during myocardial ischaemia and reperfusion. Phentolamine 5 X 10(-6) M and indoramin 2 X 10(-6) M significantly reduced the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) during ischaemia and reperfusion. Both drugs prolonged action potential duration (APD) and refractory period and reduced Vmax during normal perfusion and these effects were maintained during ischaemia. Reperfusion led to prompt recovery in all hearts but with initial transient shortening of APD. Phentolamine and indoramin abolished shortening of the APD whether added prior to ischaemia or immediately prior to reperfusion, and attenuated the reduction in refractory period, due to higher values at the end of ischaemia. Myocardial catecholamine depletion also significantly reduced ventricular tachycardia and ventricular fibrillation during ischaemia and reperfusion. Catecholamine depletion had similar effects on APD, refractory period and conduction, but phentolamine produced no additional effects when added to catecholamine depleted hearts suggesting that the effects observed here are mediated via adrenergic rather than direct myocardial effects.     

《中华心律失常学杂志》载文被引的分析研究

目的从文献引证的角度了解《中华心律失常学杂志》的学术水平和期刊质量。方法依据中国生物医学期刊引文数据库（CMCI），采用文献计量学方法对1997至2004年《中华心律失常学杂志》载文被CMCI来源期刊引用的情况进行统计学分析及评价。结果1997至2004年该刊载文被引用1863次，单篇论文平均被引次数为3．29次；被引作者群的地域分布33个省、自治区和直辖市（包括国外），北京居首位；有337种期刊引用该刊。结论该刊创刊时间不长，但论文学术质量不断提高，是我国心血管病学研究领域重要的信息源之一．是我国医学领域的主要期刊。     

Syncope in hypertrophic cardiomyopathy: mechanisms and consequences for treatment.

Hypertrophic cardiomyopathy (HCM) is an inherited disease with marked phenotypic variability that includes the extent of hypertrophy, the presence and severity of symptoms, and the natural history of the disease. Symptoms of impaired consciousness (syncope and pre-syncope) occur in approximately 15-25% of patients with hypertrophic cardiomyopathy (HCM). In young patients a history of recurrent syncope is associated with an increased risk of sudden death. Detailed investigations identify a probable mechanism in a minority of these, usually paroxysmal atrial fibrillation or ventricular tachycardia. In the majority, however, no likely mechanism is found despite extensive investigation. Although this may be the case, it is still of vital importance to exclude potentially treatable causes of syncope.