预成型电极临时心内膜起搏在院前急救中的应用

目的 探讨心电监护下直接推送预成型电极行临时心内膜起搏在院前急救中的价值.方法 18例严重心动过缓患者均在120救护车上紧急穿刺右颈内静脉或左锁骨下静脉,采用心电监护下直接推送预成型电极行心内膜临时起搏,观察耗时长短、起搏的有效性和并发症.结果 18例患者即刻心内膜起搏均成功,其中穿刺右颈内静脉13例,左锁骨下静脉5例,电极置入深度（36.2±3.0） cm,从穿刺开始到成功起搏耗时（3.5±1.5） min,最长5 min,起搏阈值（1.1±0.4） mV,所有患者均成功持续起搏并安全转运至医院进一步治疗,所有患者均无严重并发症发生.结论 120院前急救中直接推送预成型电极临时心内膜起搏抢救严重的缓慢性心律失常安全有效、操作简便.     

不同剂量瑞舒伐他汀对Ⅲ度房室传导阻滞起搏器术后患者NT-proBNP及心脏重构的影响

目的 探讨不同剂量瑞舒伐他汀对Ⅲ度房室传导阻滞双腔起搏器治疗患者NT-proBNP 及心脏重构的影响.方法 选取2011 年12 月至2012 年8 月于我院心血管内科因Ⅲ度房室传导阻滞(AVB)住院并行双腔起搏器(DDD)治疗的患者60 例,随机分为对照组、可定5 mg 组及可定10 mg 组各20 例.分别测定术前、术后12 个月三组患者NT-proBNP 水平、左房内径(LA)、左室舒张末内径(LVEDD)、左室收缩末内径(LVESD)及左心室射血分数(LVEF).结果 三组患者治疗前NT-proBNP、LA、LVEDD、LVESD、LVEF 差异无统计学意义(P＞0.05).治疗后起搏器组及可定10 mg 组患者血浆NT-proBNP 水平较治疗前下降(P＝0.045,P＜0.01),可定10 mg 组较单纯起搏器组下降更明显,差异有统计学意义(P＝0.013).治疗后三组患者LVEDD 均较术前减小,且随可定用量增加减小更明显.治疗后可定5 mg 组LVESD 较术前减小(P＜0.01),LVEF 明显增高(P＝0.032);治疗后可定10 mg 组LA、LVESD 较术前减小(P 均＜0.01),LVEF 明显增高(P＝0.017).治疗后可定5 mg 组及可定10 mg 组LA 较起搏器组明显减小(P＝0.048,P＝0.043),LVESD 减小,差异有统计学意义(P＝0.037,P＝0.031).治疗后三组患者射血分数增高差异无统计学意义.结论 瑞舒伐他汀在一定程度上可逆转Ⅲ度房室传导阻滞双腔起搏器置入患者心脏重构,改善心功能.     

生理性起搏器治疗缓慢型心律失常的临床观察

目的探讨生理性起搏器在缓慢型心律失常中的临床疗效与安全性。方法共85例患者,起搏器包括双腔起搏器DDD[心房＋心室（起搏心腔）;心房＋心室（感知心腔）;双重（1抑制＋T触发）（感知后反应方式）]60例,双腔起搏器VDD[心室（起搏心腔）;心房＋心室（感知心腔）;双重（1抑制＋T触发）（感知后反应方式）]3例,双腔起搏器VVIR[心房＋心室（起搏心腔）;心房＋心室（感知心腔）十（1抑制）（感知后反应方式）;R频率调整（程控功能）]22例。结果85例患者均手术成功,术中测得心室起搏阈值为（0．42±0．13）V／0．5ms,阻抗（560±130）Ω,R波振幅（9．8±2．2）mV;右心房起搏阈值为（0．89±0．27）V／0．5ms,阻抗（670±180）Ω,P波振幅（2．8±1．2）mV,P波感知灵敏度（0．48±0．3）mV。A—V间期程控在140-160ms,频率适应参数程控为反应时间和恢复时间取中档值,增益取低档值,下限频率程控为60-70次／min,上限频率程控于110-130次／min,感知阈值取中档,频率适应档次取4～5。随访4-50个月,所有患者的生活质量明显提高,无起搏器并发症发生。结论生理性起搏可产生较好的血液动力学效应,改善心功能,提高运动耐量,对有适应证的起搏器患者应首先推荐使用各类生理性起搏器。     

Impact of chronic kidney disease on mortality in older adults treated with pacemaker implantation

Objective To investigate whether chronic kidney disease could negatively impact survival in older adults needing pacemaker implantation after admission for bradyarrhythmias. Methods This retrospective observational study considered 538 older adults consecutively admitted, who had been followed-up for 31 ± 20 months. Subjects with poor short-term prognosis were excluded. Charlson comorbidity index (CCI) and estimated glomerular filtration rate (eGFR) was calculated, along with the independent relationship between all-cause mortality and clinical data. Hazard Ratio (HR) was calculated by Cox regression analysis. Results Mean age of the population was 85 ± 3.7 years, and causes for implantation were atrioventricular block in 51.9% and other bradyarrhythmias in 48.1% of cases. Mean eGFR was 58.3 ± 24 mL/min per 1.73 m2, and mean CCI was 3.65 ± 2.28. Death for all-causes was recorded in 213 subjects. Deceased patients were older, had lower eGFR, higher comorbidity, higher prevalence of myocardial infarction, congestive heart failure, cerebrovascular disease, dementia and chronic pulmonary disease. Age (HR: 1.081, 95% CI: 1.044–1.119; P < 001), CCI (HR: 1.651, 95% CI: 1.286–2.121, P < 001) and eGFR ≤ 45 mL/min per 1.73 m2 (HR: 1.360, 95% CI: 1.024–1.806; P = 0.033) were predictors of death. Conclusions Renal dysfunction, as well as comorbidity, impacts negatively survival of older adults treated with pacemaker implantation because of bradyarrhythmias.     

参附注射液治疗缓慢性心律失常随机对照临床观察

[目的]探讨参附注射液治疗缓慢性心律失常的临床疗效。[方法]将收治的92例缓慢性心律失常患者随机分为治疗组47例和对照组45例,治疗组采用参附注射液静滴,对照组给予阿托品口服,比较两组患者的疗效和不良反应情况。[结果]参附注射液治疗缓慢性心律失常疗效较阿托品有明显优势,且不良反应较少,症状较轻,两组比较差异均有统计学意义(P<0.05)。[结论]参附注射液治疗缓慢性心律失常临床疗效显著,不良反应少,有助于提高患者的生活质量。     

米力农治疗慢性心力衰竭伴缓慢性心律失常临床疗效及安全性观察

目的观察米力农治疗慢性心力衰竭伴缓慢性心律失常患者的临床疗效及安全性。方法将63例慢性心力衰竭合并缓慢性心律失常的患者随机分为两组,对照组予以常规抗心衰治疗,治疗组在常规治疗基础上加用米力农。观察两组治疗前后临床心功能NYHA分级、B型利钠肽(BNP)水平、左室射血分数(EF)、左室舒张末期内径(LVEDD)、24小时动态心电图指标:平均心室率、室性心律失常、长RR间期。结果两组患者治疗后心功能分级、B型利钠肽(BNP)水平、左室射血分数(EF)均有显著改善,治疗前后差异具有统计学意义(P0.05);治疗组较对照组患者BNP下降水平、LVEF升高幅度更显著,差异具有统计学意义(P0.05);但两组左室舒张末期内径(LVEDD)治疗前后改善不明显,无统计学差异(P0.05)。两组治疗前后平均心率、室性心律失常、长RR间期事件无明显增加,组间及组内差异无统计学意义(P0.05)。结论在常规抗心衰治疗基础上短期使用米力农治疗慢性心力衰竭伴缓慢性心律失常,临床疗效显著且安全可靠。     

心脏起搏器植入后的规范化随访与程控

目的探讨心脏起搏器植入后如何进行规范化随访与程控及其意义。方法对植入起搏器的缓慢性心律失常患者共1278例进行随访与程控,程控内容包括参数测试、参数优化、降低输出电压、酌情开启自动化功能及其他功能等,总结程控随访的内容及意义。结果规范化随访与程控可发现并处理起搏器功能异常、模仿生理性起搏、节能、简化操作、优化治疗等。结论起搏器植入后应进行规范化随访与程控,使起搏器发挥最佳的治疗效果。     

Kardiale Wirkungen von Adenosin

Zusammenfassung Zusammenfassend läßt sich sagen, daß Adenosin am Vorhof negativ inotrop wirkt (direkter negativ inotroper Effekt). Am Ventrikel wirkt Adenosin nur bei Erhöhung des zellulären cAMP-Gehaltes durch Stimulation der Adenylatcyclase oder Hemmung der Phosphodiesterase negative inotrop (indirekter negative inotroper Effekt). Diese Wirkung ist von einer Abnahme des langsamen Ca²⁺-Einwärtsstromes begleitet. Ob diese Abnahme mit einer Hemmung der Adenylatcyclase erklärt werden kann oder ob Mechanismen, die der cAMP-Bildung nachgeschaltet sind (z.B. Hemmung cAMP-abhängiger Proteinkinasen, Aktivierung von Proteinphosphatasen), eine Rolle spielen, ist bisher umstritten. Der indirekte negativ inotrope Effekt konnte kürzlich auch an isoliertem menschlichen Ventrikelmyokard nachgewiesen werden, so daß Adenosin möglicherweise auch am menschlichen Herzen eine Rolle als physiologischer Feedback-Hemmstoff bei exzessiver Katecholaminstimulation und bei Hypoxie spielen könnte. Diese Hemmung einer Stimulation kardialer -Adrenozeptoren könnte eine antiarrhythmische Wirkung bei katecholamininduzierten Tachyarrhythmien bewirken. Eine defekte adenosinvermittelte Regulation des Herzens könnte schließlich auch eine Bedeutung in der Pathogenese von Herzerkrankungen wie der hypertrophen Kardiomyopathie haben. Hierüber liegen allerdings keine klinischen oder experimentellen Daten vor. Andererseits wirkt Adenosin negativ chronotrop und dromotrop und vermittelt wahrscheinlich bradykarde Herzrhythmusstörungen während myokardialer Hypoxie. Entsprechend seiner negativ dromotropen Wirkung eignet es sich zur Therapie von supraventrikulären Tachykardien mit Beteiligung des AV-Knotens. Seine kurze Wirkdauer läßt es als vorteilhaft gegenüber einer konventionellen Therapie mit Ca²⁺-Antagonisten erscheinen.

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Cardiac effect of adenosine: Mechanism of action, pathophysiological role and clinical implications

Summary Adenosine has a negative inotropic effect in cardiacatrial preparations (direct negative inotropic effect). This effect is probably due to an activation of a potassium outward current which shortens the action potential duration and hence reduces the force of contraction. A pertussis toxin-sensitive N-protein is involved in the signal transduction from the adenosine receptor to atrial potassium channels. Inventricular cardiac preparations adenosine has no negative or even a weak positive inotropic effect, but it reduces the force of contraction in the presence of cAMP-increasing agents such as isoprenaline (indirect negative inotropic effect). This effect is due to an inhibition of the slow Ca²⁺ inward current which has previously been enhanced by an increase in the cellular cAMP content. This indirect negative inotropic effect of adenosine is also present in the human heart. Since increased amounts of adenosine are released during cardiac stimulation via -adrenoceptors, the indirect effect might protect the heart against excessive stimulation by catecholamines. In addition, adenosine has negative chronotropic actions and prolongs AV conduction by an activation of potassium channels or an inhibition of the slow Ca²⁺ inward current (AV node). Cardiac bradyarrhythmias in hypoxia have been attributed to an increased formation and release of adenosine. Furthermore, adenosine has been shown to terminate supraventricular tachycardias involving the AV node. Since it has a very short duration of action it might prove safe and hence advantageous to conventional therapy in the treatment of supraventricular tachycardias.

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Abkürzungen s Sekunde - mN Millinewton - mV Millivolt - cAMP cyclisches Adenosin-3,5-monophosphat - cGMP cyclisches Guanosin-3,5-monophosphat - PIA (-)-N⁶-Phenylisopropyladenosin - NECA 5-N-Äthylcarboxamidadenosin     

起搏器心房自动阈值管理功能的临床研究

目的:通过对植入起搏器患者的随访,了解心房自动阈值管理功能的可靠性和安全性。方法:选择植入Medtronic Enpulse双腔起搏器的患者43例,于植入起搏器后的1、3、6个月分别程控随访,用人工测定法和自动测定法测定起搏器的心房输出阈值、感知和导线阻抗。结果:植入起搏器1、3、6个月后,随访时人工测定和自动测定的心房输出阈值分别为(0.60±0.26)V与(0.60±0.23)V、(0.55±0.19)V与(0.56±0.18)V、(0.58±0.20)V与(0.59±0.21)V,差异无统计学意义;且心房感知度和导线阻抗的人工测定与自动测定间无差异。在心房自动起搏阈值测定过程中未诱发任何心律失常。结论:起搏器的心房自动阈值管理功能的临床应用是可靠和安全的。     

Beta-blocker use and risk of symptomatic bradyarrhythmias: a hospital-based case-control study

Objective To investigate the risk factors of symptomatic bradyarrhythmias in relation to β-blockers use. Methods A hospital-based case-control study [228 patients: 108 with symptomatic bradyarrhythmias (cases) and 120 controls] was conducted in Sultanah Aminah Hospital, Malaysia between January 2011 and January 2014. Results The mean age was 61.1 ± 13.3 years with a majority of men (68.9%). Cases were likely than control to be older, hypertensive, lower body mass index and concomitant use of rate-controlling drugs (such as digoxin, verapamil, diltiazem, ivabradine or amiodarone). Significantly higher level of serum potassium, urea, creatinine and lower level of estimated glomerular filtration rate (eGFR) were observed among cases as compared to controls. On univariate analysis among patients on β-blockers, older age (crude OR: 1.07; 95% CI: 1.03–1.11, P = 0.000), hypertension (crude OR: 5.6; 95% CI: 1.51–20.72, P = 0.010), lower sodium (crude OR: 0.04; 95% CI: 0.81–0.99, P = 0.036), higher potassium (crude OR: 2.36; 95% CI: 1.31–4.26, P = 0.004) and higher urea (crude OR: 1.23; 95% CI: 1.11–1.38, P = 0.000) were associated with increased risk of symptomatic bradyarrhythmias; eGFR was inversely and significantly associated with symptomatic bradyarrhythmias in both ‘β-blockers’ (crude OR: 0.97; 95% CI: 0.96–0.98, P = 0.000) and ‘non-β-blockers’ (crude OR: 0.99; 95% CI: 0.97–0.99, P = 0.023) arms. However, eGFR was not significantly associated with symptomatic bradyarrhythmias in the final model of both ‘β-blockers’ (adjusted OR: 0.98; 95% CI: 0.96–0.98, P = 0.103) and ‘non-β-blockers’ (adjusted OR: 0.99; 95% CI: 0.97–1.01, P = 0.328) arms. Importantly, older age was a significant predictor of symptomatic bradyarrhythmias in the ‘β-blockers’ as compared to the ‘non-β-blockers’ arms (adjusted OR: 1.09; 95% CI: 1.03–1.15, P = 0.003 vs. adjusted OR: 1.03; 95% CI: 0.98–1.09, P = 0.232, respectively). Conclusion Older age was a significant predictor of symptomatic bradyarrhythmias in patients on β-blockers than those without β-blockers.