A quantitative analysis of the effect of cycle length on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts

The clinically established proarrhythmic effect of bradycardia and antiarrhythmic effect of lidocaine (10 μM) were reproduced in hypokalaemic (3.0 mM K⁺) Langendorff-perfused murine hearts paced over a range (80–180 ms) of baseline cycle lengths (BCLs). Action potential durations (at 90% repolarization, APD₉₀s), transmural conduction times and ventricular effective refractory periods (VERPs) were then determined from monophasic action potential records obtained during a programmed electrical stimulation procedure in which extrasystolic stimuli were interposed following regular stimuli at successively decreasing coupling intervals. A novel graphical analysis of epicardial and endocardial, local and transmural relationships between APD₉₀, corrected for transmural conduction time where appropriate, and VERP yielded predictions in precise agreement with the arrhythmogenic findings obtained over the entire range of BCLs studied. Thus, in normokalaemic (5.2 mM K⁺) hearts a statistical analysis confirmed that all four relationships were described by straight lines of gradients not significantly (P > 0.05) different from unity that passed through the origin and thus subtended constant critical angles, θ with the abscissa (45.8° ± 0.9°, 46.6° ± 0.5°, 47.6° ± 0.5° and 44.9° ± 0.8°, respectively). Hypokalaemia shifted all points to the left of these reference lines, significantly (P < 0.05) increasing θ at BCLs of 80–120 ms where arrhythmic activity was not observed (∼63°, ∼54°, ∼55° and ∼58°, respectively) and further significantly (P < 0.05) increasing θ at BCLs of 140–180 ms where arrhythmic activity was observed (∼68°, ∼60°, ∼61° and ∼65°, respectively). In contrast, the antiarrhythmic effect of lidocaine treatment was accompanied by a significant (P < 0.05) disruption of this linear relationship and decreases in θ in both normokalaemic (∼40°, ∼33°, ∼39° and ∼41°, respectively) and hypokalaemic (∼40°, ∼44°, ∼50° and ∼48°, respectively) hearts. This extended a previous approach that had correlated alterations in transmural repolarization gradients with arrhythmogenicity in murine models of the congenital long QT syndrome type 3 and hypokalaemia at a single BCL. Thus, the analysis in terms of APD₉₀ and VERP provided a more sensitive indication of the effect of lidocaine than one only considering transmural repolarization gradients and may be particularly applicable in physiological and pharmacological situations in which these parameters diverge.     

2293例老年人动态心电图心律失常特征的分析

目的研究老年人动态心电图的特点。方法回顾性分析我院于2011年12月至2013年11月期间2293例老年心律失常患者动态心电图(Holter)检查和12导同步心电图检查(12-ECG)资料。结果本组动态心电图(Holter)检出心律失常的2293例老年患者中,12导同步心电图检查367例出现心律失常,检出率16.01%。两种检查检出率有非常显著差异,具有统计学意义。结论加强动态心电图在老年患者临床检测中的应用,能够提高对心律失常的检出率。     

稳心颗粒联合胺碘酮急性心肌梗死后心律失常的疗效分析

目的观察稳心颗粒联合胺碘酮急性心肌梗死后心律失常的疗效。方法按照随机数字表法将139例急性心肌梗死后心律失常患者分为观察组（69例）和对照组（70例）,对照组患者在常规治疗基础上给予胺碘酮治疗,观察组在对照组基础上给予患者稳心颗粒治疗。结果观察组总有效率（95．65％）显著高于对照组（80.00％）,P〈0．05;两组不良反应发生率差异无统计学意义,P〉0.05。结论胺碘酮联合稳心颗粒治疗急性心肌梗死后室性心律失常疗效确切,安全可行,值得临床借鉴。     

乌药水提取物抗心律失常作用的研究

目的研究乌药水提取物的抗心律失常作用。方法采用常规抗心律失常方法,将三氯甲烷诱发小鼠室颤试验和氯化钙诱发大鼠室颤试验分为生理盐水组、维拉帕米组、10．0mg／kg乌药水提取物组和30．0mg／kg乌药水提取物组：将肾上腺素诱发家兔心律失常试验分为给药前后组;蟾蜍离体坐骨神经动作电位试验分为任氏液组、1．0％盐酸普鲁卡因溶液组、0．5g/ml和1．0/md乌药水提取物组。结果乌药水提取物对三氯甲烷诱发的小鼠室颤具有明显的治疗作用（P〈0．05）,对氯化钙诱发的大鼠室颤具有明显的预防效果（P〈0．05）,能明显对抗肾上腺素诱发的家兔心律失常（P〈0．01）,可明显降低蟾蜍离体坐骨神经动作电位振幅（P〈O．05）。结论乌药水提取物具有明显的抗试验性心律失常作用,能对抗由三氯甲烷、氯化钙、肾上腺素等诱发的心律失常,其抗心律失常作用可能与其抑制Na＋内流及与阻断β一肾上腺素受体有关。     

亚临床甲状腺功能减退症对非ST段抬高型心肌梗死患者心律失常事件的影响

目的探索亚临床甲状腺功能减退症(SH)对非ST段抬高型心肌梗死(NSTEMI)患者发生心律失常事件的影响。方法收集2016年1月至2018年8月就诊于河北省人民医院的NSTEMI患者。据患者甲状腺激素(TH)水平分组:甲状腺功能正常组(EU):促甲状腺素(TSH)、总甲状腺素(TT4)水平在正常范围内,n=237;SH组:TSH>4.2 mIU/L,TT4在正常范围内,n=28。比较两组患者基线资料、院内心律失常事件、院内终点事件发生情况。结果与EU组相比,SH组住院期间硝酸酯类药物使用(P=0.012)、天冬氨酸转移酶(P=0.022)、肌酸激酶(P=0.004)、红细胞计数(P=0.030)均较低,且左室收缩末期内径较小(P=0.020)。经多因素Logistic回归分析,SH组发生窦性心动过缓(OR=9.564,95%CI:1.634~55.989,P=0.012)、心房扑动(OR=7.824,95%CI:1.652~37.055,P=0.010)、房室交界区期前收缩(OR=4.940,95%CI:1.468~16.625,P=0.010)等心律失常事件风险仍较高。结论与EU组相比,SH组患者出现窦性心动过缓、心房扑动等心律失常风险增高。提前识别SH并监测NSTEMI患者的甲状腺功能有助于提前识别心律失常发作高危患者,从而使更多的患者获益。     

小儿先天性心脏病直视手术后心律失常的影响因素及处理

目的　探讨先天性心脏病直视手术后心律失常的影响因素及预防、处理措施。方法　对 2 87例心脏直视手术患儿术后心律失常的发生因素进行分析。结果　 6 7例患儿术后出现心律失常 79例次 ,发生率为 2 3.3%。包括各类早搏、室上性心动过速、心房颤动、 度或 度房室传导阻滞。复杂心血管畸形术后心律失常发生率较高。低年龄、心功能差、体外循环和阻断主动脉时间长、术后低血钾和低心排出量是术后心律失常的影响因素 ,P<0 .0 1。结论　心脏直视手术后心律失常的发生与手术复杂程度、患者年龄、心功能、术中体外循环和阻断主动脉时间、术后低血钾和低心排出量有密切关系。术前设法改善心功能 ,术中尽量缩短体外循环和阻断主动脉时间 ,术后及时纠正低血钾和低心排出量 ,是预防术后心律失常发生的重要措施。     

IKs blockade reduces dispersion of repolarization in heart failure

BACKGROUND: The slow and rapid (I(Kr)) components of I(K) are major determinants of ventricular repolarization. Unlike I(Kr), which is homogeneously expressed across the transmural wall, I(Ks) expression is reduced in midmyocardial cells and presumably contributes significantly to transmural dispersion of repolarization. Increased dispersion of repolarization during pharmacologic blockade of I(Kr) is proarrhythmic, primarily due to relatively selective prolongation of midmyocardial cell action potential duration (APD). The mechanisms underlying proarrhythmia in heart disease associated with impaired repolarization, such as heart failure, are unknown. We hypothesize that, in contrast to I(Kr) blockade, I(Ks) blockade will have little effect on midmyocardial cells and hence decrease dispersion of repolarization in heart failure. OBJECTIVES: The purpose of this study was to determine the effect of blockade of the slow component of the delayed rectifier current (I(Ks)) on arrhythmogenic dispersion of repolarization and proarrhythmia in heart failure. METHODS: Optical action potentials were simultaneously recorded from 256 sites spanning the transmural wall of the arterially perfused canine wedge preparation. Hearts from dogs with heart failure induced by rapid pacing (n = 6) were compared with normals (n = 6). RESULTS: Baseline dispersion of repolarization, as measured from the range of transmural APD during stimulation at a cycle length of 2,000 ms, was significantly higher in heart failure (75 +/- 24 ms) compared with controls (39 +/- 21 ms, P < .04). I(Ks) blockade with 30 microM chromanol decreased dispersion of repolarization by 40% (P < .02) in heart failure, reducing it to values found in normals. Decreased dispersion of repolarization was due to a larger, relatively selective, drug-induced APD prolongation of epicardial (23%) compared with midmyocardial cells (9%, P < .02). VT could not be induced in failing hearts under conditions of I(Ks) blockade, and no proarrhythmia was observed. CONCLUSION: I(Ks) blockade significantly reduced heart failure-induced dispersion of repolarization to values seen in nonfailing hearts. By prolonging repolarization without increasing dispersion of repolarization, I(Ks) blockade may have antiarrhythmic effects without creating proarrhythmia.     

乙酰胆碱诱发冠状动脉痉挛时的心电图改变及其与血管内皮功能关系

目的探讨血管内皮细胞功能紊乱与乙酰胆碱试验诱发冠状动脉痉挛时心电图ST段变化与缓慢型心律失常的关系。方法选择以静息性胸痛为主要临床表现、接受乙酰胆碱激发试验的患者为研究对象,根据是否发生冠状动脉痉挛分为阳性组和阴性组,冠状动脉痉挛发作时心电图变化分为ST段抬高和非ST段抬高组以及缓慢型心律失常和无缓慢型心律失常组,测定其血浆一氧化氮和内皮素1浓度,比较各组一氧化氮和内皮素1水平以及痉挛血管的分布。结果ST段抬高组一氧化氮水平显著低于阴性组,而内皮素1显著高于阴性组(P<0.01),非ST段抬高组一氧化氮水平亦显著低于阴性组,但高于ST段抬高组(P<0.05),而内皮素1显著高于阴性组但低于ST段抬高组(P<0.05);缓慢型心律失常组和无缓慢型心律失常组的血浆一氧化氮和内皮素1水平以及痉挛血管的分布差异无统计学意义(P>0.05)。结论乙酰胆碱试验诱发的冠状动脉痉挛以及ST段变化与血管内皮细胞功能紊乱有关,乙酰胆碱试验中的缓慢型心律失常与血管内皮细胞功能或痉挛血管的分布无关。     

Sarcoidosis presenting with tachy- and brady-arrhythmias.

We describe a case report of a 49-year-old man admitted to a cardiology unit with a series of arrhythmias with no initially obvious aetiology. Further assessment and the use of cardiac magnetic resonance imaging and histology allowed a diagnosis of cardiac sarcoidosis to be made. Cardiac sarcoidosis is a major cause of death in patients with systemic sarcoidosis. Cardiac magnetic resonance imaging is an additional diagnostic tool for this condition without ionizing radiation exposure.