低血钾为心跳骤停的一个原因:电生理试验及远期随访结果

众所周知,低血钾可引起恶性室性心律失常。一些学者偶然发现心跳骤停复苏者血钾水平较低。本文作者对10例低血钾相关性心跳骤停者进行电生理研究,以期弄清这些病人是否需用抗心律失常药物治疗,及维持血钾水平正常能否预防再发心跳骤停。10例中6例室颤,2例单形性室速,2例多形性室速伴尖端扭转型室速的形态学特征。均由利尿剂诱发低血钾(2.2～3.3mEq/L)。QTc 间期延长,低血钾纠正后缩短。血清钙、镁水平正常。心跳骤停时7例正用地高辛,但地高辛水平治疗范围内。2例正用奎尼丁,另1例用普鲁卡因酰胺治疗室性早搏。心跳骤停前均无晕厥或室速、室颤史。     

长QT综合征的危险分层

长QT综合征(Long QT Syndrome,LQTS)是指具有心电图上QT间期延长,T波异常,易产生室性心律失常、晕厥和猝死的一组综合征。按病因可分为获得性和遗传性两种类型[1]。本文综述对遗传性LQTS患者进行危险分层方面的研究进展。1 LQTS的临床表现 LQTS患者极易发生一种称做尖端扭转型室速(TdP)的室性心律失常(见图1)[2],后者可促进晕厥事件的发生。这种疾病常于青春期发病,典型地表现为剧烈运动与情绪波动后晕厥发作。在大多数情况下,这种心律失常可以自动终止,但TdP也可     

急性心肌梗死早期的恶性室性心律失常与低血钾关系的探讨

目的:探讨急性心肌梗死(AMI)早期发生恶性室性心律失常(室速、室扑、室颤)与低血钾的关系。方法:选择112例AMI患者于发病后24至72小时内测血清钾,根据血钾浓度分为低血钾组(血钾<3.6mmol/L.,44例).及血钾正常组(血钾为3.7-5.5mmol/L,68例),观察、比较两组病人恶性室性心律失常的发生率。结果:低血钾组发生恶性室性心律失常者为38例,占86.3％,血钾正常组发生恶性室性心律失常者为8例.占11.7％,两组间有显著差异(P<0.01)。结论:低血钾是急性心肌梗死早期发生恶性室性心律失常的一个重要危险因素。     

长QT综合征的交感神经链切除术治疗

长QT综合征(LQTS)是一种少见的严重心律失常，系心肌细胞膜离子通道的异常引起，可引起多形性室性心动过速或尖端扭转型室性心动过速(Tdp)，自限性者导致晕厥，不能中止者导致室颤，是年轻人心源性猝死的主要原因之一。     

DCG监护对Brugada综合征的诊断意义

Brugada综合征是一种常染色体显性遗传性疾病，男性多见，有特征性的心电图表现、伴有多形性室速或室颤等恶性心律失常诱发的晕厥、心脏骤停或猝死。患者多有类似表现的家族史，心电图表现为正常的QT间期、右束支传导阻滞、右胸导联ST段特征性抬高(呈下斜型或马鞍型)，发作性的室速、室颤等恶性心律失常，系Brugada 1992年首次报告。回顾分析1992～2002年10年来我院8224例动态心电图(DCG)监护资料，发现3例符合或基本符合Brugada综合征的临床诊断标准，报告于后。     

长QT综合征的诊断及治疗

<正>1定义长QT间期综合征(LQTS)是以心电图上QT间期延长为基础而诊断的,可伴T波及ST段改变,临床上则表现为易发生恶性室性心律失常如尖端扭转型室速(Torsades de Pointes,Tdp)、室颤等,患者可有反复发作的黑矇、晕厥,甚至猝死。2 LQTS的病理生理基础及病因学分类2.1病理生理基础各种LQTS共同的病理生理基础是由于先天性或获得性原因使心肌细胞膜上的离子通道功能异常,如编码钠和钾     

恶性室性心律失常的药物治疗现状

恶性室性心律失常是指伴有严重血流动力学障碍的室速、室颤或具有潜在危险的室性心律失常，易恶化为室颤，均为致命性心律失常。此类心律失常常见于器质性心脏病，如冠心病、心肌梗死、非缺血性心脏病、肥厚性心脏病、致心律失常性右室发育不全、重症心肌炎，少见于无心脏结构异常者，如特发性左室室速、右室流出道室速、LQTS、Brugada综合征、特发性多形性室速、室颤等。     

先天性长QT综合征患者尖端扭转型室速发作的分类及机制

尖端扭转型室性心动过速(TdP)是一种QRS波尖端围绕等电位线扭转的多形性室性心动过速(室速),常发生于获得性或先天性长QT综合征(LQTS)患者,并易发生室颤致心源性猝死. 方法该研究分析了24例先天性LQTS患者的111次TdP发作的心电图,通过分析TdP发作之前三个连续的R-R间期(C_0为发作起始早搏的联律间期,C_1为发作前面第一个R-R间期,C_2为发作前面第二个R-R间期)之间的关系,据     

急性冠脉综合征患者发生恶性室性心律失常预后影响

<正>急性冠脉综合征(ACS)患者反复发作恶性室性心律失常,尤其是多形性室性心动过速和室颤是引起心肌梗死患者早期死亡的主要原因,在发病的最初几小时内,心肌严重缺血坏死,心电极不稳定,以室颤最为危险,是心肌梗死患者猝死的重要原因。在急性心肌梗死幸存的人群中,50%以上死于致命的室性心律失常,有关研究指出非ST段抬高心肌梗死患者室性心律失常发生率(2%)低于ST段抬高心肌梗死患者(10%~     

Brugada综合征患者心律失常及临床特点分析

目的通过动态心电图(Holter)检查、置入式心脏复律除颤器(ICD)分析并综合患者临床情况,研究Brugada综合征(Brs)患者心律失常事件发生特征及临床特点。方法对我院近5年诊断的12例Brs住院患者的临床情况进行随访观察;均行Holter检查分析心律失常事件发生特征;根据ICD的随访资料,分析室颤发作的时间特征。结果 Holter显示,其中8例患者室性期前收缩总数为0～80个/d,另外4例以夜间至清晨为主的频发室性期前收缩及短阵室性心动过速(其中1例伴有阵发性心房颤动;1例伴有频发房性期前收缩及房性心动过速,并且夜间心率缓慢29次/min伴交界性逸搏心律)。9例患者置入ICD后随访6～50个月,70次室颤发作中92.8%集中在22:00～07:00。12例患者均有晕厥病史,9例在住院期间发生室速/室颤,2例有猝死家族史,随访期间2例猝死。结论 Brs患者的室速/室颤发作多集中在夜间和凌晨;伴有房性心律失常和缓慢心律失常的Brs患者室速/室颤发生率更高。确诊的Brs患者发生心悸等不适时,应全面了解心律失常发生的情况,并酌情给予相应的治疗。     

Brugada syndrome with ventricular tachycardia and fibrillation related to hypokalemia.

A 60-year-old man with asymptomatic Brugada syndrome and neither a history of syncope nor family history of sudden death was admitted because of bronchial asthma. Serum potassium concentration was 3.8 mmol/L on admission, and decreased to 3.1 mmol/L on the 6th day, probably as a side effect of steroid therapy. The patient was found unconscious on the 7th day, and his serum potassium concentration was 3.4 mmol/L immediately after the episode. On the 8th day, the patient was again found unconscious, and polymorphic ventricular tachycardia and fibrillation (VT/VF) was documented on electrocardiographic (ECG) monitoring. The coved type of ST-segment elevation in leads V(1-3) was observed on the ECG after spontaneous recovery of sinus rhythm, and VT/VF associated with Brugada syndrome was diagnosed. The serum potassium concentration decreased to 2.9 mmol/L immediately after the episode, but QT prolongation was not observed during the clinical course. After the correcting the serum potassium concentration, there was no further recurrence of the malignant ventricular arrhythmia and syncope. An implantable cardioverter defibrillator was inserted to prevent sudden death. Hypokalemia that does not induce QT prolongation may contribute to the occurrence of VT/VF in Brugada syndrome.     

Comparison of event rates and survival in patients with unexplained syncope without documented ventricular tachyarrhythmias versus patients with documented sustained ventricular tachyarrhythmias both treated with implantable cardioverter-defibrillators

Patients with unexplained syncope and inducible ventricular tachyarrhythmias during electrophysiologic testing have an increased cardiac mortality rate. We compared event rates and survival of 178 patients with unexplained syncope and no documented ventricular arrhythmias (syncope group) versus 568 patients with documented sustained ventricular tachycardia (VT or fibrillation (VF) (VT/VF group) treated, as part of a lead (Ventritex TVL) investigation, with similar implantable cardioverter-defibrillators (ICDs) capable of extensive data storage. The 2 groups shared similar clinical characteristics. The mean follow-up was 11 months for the syncope group and 14 months for the VT/VF group. The mean time from device implantation to first appropriate therapy was similar in the 2 groups (109 +/- 140 vs 93 +/- 131 days, p = 0.40). Actuarial probability of appropriate ICD therapy was 49% and 55% at 1 and 2 years, respectively, in syncope group and 49% and 58% in VT/VF group (p = 0.57). Recurrent syncope was associated with ventricular tachyarrhythmias in 85% and 92% of the syncope group and VT/VF group, respectively (p = 0.54). At 2 years, actuarial survival was 91% in the syncope group and 93% in VT/VF group (p = 0.85). We conclude that patients treated with ICD with unexplained syncope and induced VT/VF have an equally high incidence of appropriate ICD therapy and low mortality compared with similar patients with documented VT/VF. These findings, plus the high association between recurrent syncope and ventricular arrhythmias, indicate that VT/VF are likely etiologies in selected patients with unexplained syncope and support ICD therapy in such cases.     

Hypokalemia after theophylline intoxication. The effects of acute vs chronic poisoning

To characterize the frequency and pattern of hypokalemia (serum potassium level less than 3.5 mmol/L) after theophylline poisoning, we prospectively evaluated 88 consecutive patients with theophylline intoxication (serum theophylline concentration greater than or equal to 0.165 mmol/L). This mean admission serum theophylline concentration of this cohort was 0.331 mmol/L, with a range of 0.165 to 0.982 mmol/L. The simultaneous mean serum potassium concentration was 3.36 mmol/L (range, 2.20 to 5.80 mmol/L). Fifty-three patients (60%) were hypokalemic on hospital arrival. When, on the basis of recent ingestion, patients were separated into acute, chronic, or acute-on-chronic categories of theophylline intoxication, significant differences in serum potassium were found: Patients with acute theophylline intoxication had a mean serum potassium concentration of 2.94 mmol/L; 85% were hypokalemic. In contrast, patients with chronic theophylline intoxication had a mean serum potassium concentration of 3.83 mmol/L, with a 32% frequently of hypokalemia. These data demonstrate that hypokalemia is common after theophylline intoxication and has a significantly higher incidence after acute overdose. The difference in the frequency of hypokalemia between patients with acute vs chronic intoxication has unclear origins but may be related to the disparities in clinical course (particularly the appearance of seizures and cardiac arrhythmias) that have been observed after acute vs chronic theophylline intoxication.     

Hydroquinidine therapy in Brugada syndrome

OBJECTIVES: We sought to assess hydroquinidine (HQ) efficacy in selected patients with Brugada syndrome (BrS). BACKGROUND: Management of asymptomatic patients with BrS and inducible arrhythmias remains a key issue. Effectiveness of class Ia antiarrhythmic drugs, which inhibit the potassium transient outward current of the action potential, has been suggested in BrS. METHODS: From a cohort of 106 BrS patients, we studied 35 who received HQ (32 men; mean age 48 +/- 11 years). Patients had asymptomatic BrS and inducible arrhythmia (n = 31) or multiple appropriate shocks from an implantable cardioverter-defibrillator (ICD) (n = 4). Asymptomatic patients with inducible arrhythmia underwent electrophysiologic (EP)-guided therapy. When ventricular tachycardia (VT)/ventricular fibrillation (VF) inducibility was not prevented, or in case of HQ intolerance, an ICD was placed. RESULTS: Hydroquinidine prevented VT/VF inducibility in 76% of asymptomatic patients who underwent EP-guided therapy. Syncope occurred in two of the 21 patients who received long-term (17 +/- 13 months) HQ therapy (1 syncope associated with QT interval prolongation and 1 unexplained syncope associated with probable noncompliance). In asymptomatic patients who received an ICD (n = 10), one appropriate shock occurred during a follow-up period of 13 +/- 8 months. In patients with multiple ICD shocks, HQ prevented VT/VF recurrence in all cases during a mean follow-up of 14 +/- 8 months. CONCLUSIONS: Hydroquinidine therapy prevented VT/VF inducibility in 76% of asymptomatic patients with BrS and inducible arrhythmia, as well as VT/VF recurrence in all BrS patients with multiple ICD shocks. These preliminary data suggest that preventive treatment by HQ may be an alternative strategy to ICD placement in asymptomatic patients with BrS and inducible arrhythmia.     

Implantable defibrillator event rates in patients with idiopathic dilated cardiomyopathy, nonsustained ventricular tachycardia on Holter and a left ventricular ejection fraction below 30%

OBJECTIVES: This study investigated the incidence of appropriate implantable cardioverter defibrillator (ICD) interventions for ventricular tachycardia (VT) or ventricular fibrillation (VF) in patients with idiopathic dilated cardiomyopathy (IDC) and nonsustained VT in the presence of a left ventricular ejection fraction below 30%, versus in patients with syncope and patients with a history of VT or VF. BACKGROUND: To date, only limited information is available about the prophylactic use of ICDs in patients with IDC. METHODS: From January 1993 to July 2000, 101 patients with IDC underwent implantation of ICDs with electrogram storage capability at our institution. Patients were placed into one of three groups according to their clinical presentation: asymptomatic or mildly symptomatic nonsustained VT in the presence of a left ventricular ejection fraction < or = 30% (49 patients, prophylactic group), unexplained syncope or near syncope (26 patients, syncope group) and a history of sustained VT or VF (26 patients, VT/VF group). RESULTS: During 36 +/- 22 months follow-up, 18 of 49 patients (37%) in the prophylactic group received appropriate shocks for VT or VF, compared with 8 of 26 patients (31%) in the syncope group and with 9 of 26 patients (35%) of the VT/VF group. Multivariate Cox analysis of baseline clinical variables identified left ventricular ejection fraction, atrial fibrillation and a history of sustained VT or VF as predictors for appropriate ICD interventions during follow-up. CONCLUSIONS: Patients with IDC and prophylactic ICD implantation for nonsustained VT in the presence of a left ventricular ejection fraction < or = 30% had an incidence of appropriate ICD interventions similar to that of patients with a history of syncope or sustained VT or VF. These findings indicate that ICDs may have a role in not only secondary but also primary prevention of sudden death in IDC.     

Role of programmed ventricular stimulation in patients with Brugada syndrome: a meta-analysis of worldwide published data.

AIMS: Brugada syndrome (BS) is an ion channelopathy with the risk of sudden cardiac death. The role of programmed ventricular stimulation (PVS) in risk stratification has been controversially discussed. Therefore, we performed a meta-analysis on the prognostic role of PVS in BS. METHODS AND RESULTS: A Medline search until July 2006 documented 822 entries for BS. Only English publications with > 10 patients and a follow-up period were considered (n = 15). Patients [n = 1217; 974 males (80%)] were divided into three groups: survived sudden cardiac arrest (SCA) [n = 222 (18%)], syncope (Syncope) [n = 275 (23%)], and asymptomatic patients (Asympt) [n = 720 (59%)]. PVS was conducted in 1036 patients (85%). In 548 patients (53%), sustained ventricular tachyarrhythmias (VT) or ventricular fibrillation (VF) was inducible. During follow-up (34 +/- 40 months), VT/VF occurred in 141 patients. SCA bore the highest chance for a VT/VF occurrence during follow-up [odds ratio (OR) 14.4 compared with asymptomatic patients; P < 0.0005]. However, except for one study, the OR for VT/VF during follow-up in relation to VT/VF inducibility was non-significant (OR 1.5; P = ns). CONCLUSION: The main finding is that we were unable to identify a significant role of PVS with regard to arrhythmic events during follow-up in BS, thus questioning the role of PVS for risk stratification in patients with BS. Patients with BS and survived SCA show the highest chance for VT/VF occurrence during follow-up.     

低钾血症对急性心肌梗死患者预后的影响

目的探讨急性心肌梗死(AMI)患者低钾血症的发生情况及其对预后的影响。方法对929例ST段抬高的AMI患者于入院时抽血测定血钾、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、肌钙蛋白I(cTnI),根据血钾水平分为低血钾组(血钾<3.5 mmol/L)和正常血钾组(血钾3.5~5.5 mmol/L),同时观察住院期间严重不良事件(室性心动过速、心室颤动和猝死)的发生情况。结果低钾血症的发生率为13.7%,下壁+后壁AMI的发生率最低(10.4%),明显低于下后壁+右心室、前间壁和广泛前壁心肌梗死;发病至抽血时间≤3 h的低钾血症发生率为17.3%,明显高于发病时间>3 h者;低血钾组的CK、CK-MB和cTnI峰值明显高于正常血钾组;低血钾组总的严重不良事件发生率(23.8%)明显高于正常血钾组(15.8%)。结论低钾血症与AMI患者的梗死时间、部位和面积相关,并严重影响患者的预后。     

Three cases of corticosteroid therapy triggering ventricular fibrillation in J-wave syndromes

We describe three cases of J-wave syndrome in which ventricular fibrillation (VF) was probably induced by corticosteroid therapy. The patients involved were being treated with prednisolone for concomitant bronchial asthma. One of the three patients had only one episode of VF during her long follow-up period (14 years). Two patients had hypokalemia during their VF episodes. Corticosteroids have been shown to induce various types of arrhythmia and to modify cardiac potassium channels. We discuss the possible association between corticosteroid therapy and VF in J-wave syndrome based on the cases we have encountered.     

Prognosis after cardiac arrest due to ventricular tachycardia or ventricular fibrillation associated with acute myocardial infarction (the MILIS Study). Multicenter Investigation of the Limitation of Infarct Size

Previous studies have reached conflicting conclusions about whether cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF) in acute myocardial infarction (AMI) is of long-term prognostic significance. The mortality rate in 849 patients with confirmed AMI was analyzed. The mortality rate during the initial hospitalization was higher for patients in whom VT/VF occurred (27% vs 7%, p less than 0.001). The in-hospital mortality rate for patients with primary VT/VF, that is, VT/VF occurring in the absence of hypotension or heart failure, was similar to that of patients who did not have VT/VF (8% vs 7%, difference not significant), whereas the rate for patients with secondary VT/VF was significantly greater than that for patients with no VT/VF (51% vs 7%, p less than 0.001). The timing of occurrence of VT/VF also influenced mortality: Patients in whom VT/VF occurred more than 72 hours after admission had a higher in-hospital mortality rate than did patients in whom it occurred within 72 hours (57% vs 20%, p less than 0.05). All cases of primary VT/VF occurred within the first 72 hours of admission. The long-term mortality rate for hospital survivors was not significantly different for patients who had had VT/VF during acute infarction compared with those who had not (19% vs 21%) (mean follow-up 32 months). Thus, cardiac arrest due to ventricular tachyarrhythmia was associated with a higher in-hospital mortality rate but was not a prognostic factor among hospital survivors. Patients resuscitated from primary VT/VF, which characteristically occurs early after AMI, do not have an adverse prognosis.     

Mechanisms determining sudden death. A cooperative study of 69 cases recorded using the Holter method

A cooperative study involving 23 centres enabled review of 69 cases of sudden death occurring less than one hour after onset of symptoms recorded by the Holter method and not related to recent, clinically documented myocardial infarction or to class IV cardiac failure. The 15 cases of asystole (22 p. cent) were observed in elderly patients (73.3 +/- 2.7 years) whose known ischaemic heart disease (12/15) was confirmed in 10 cases as the direct cause by the preceding acute ST changes. In 2 cases, death resulted from AV block presumed to be iatrogenic. The 13 episodes of torsades de point (19 p. cent) occurred mainly in younger women (58.8 +/- 6 years) without apparent cardiac disease (8 cases) and were provoked by a Group IA antiarrhythmic drug (7 cases) or by hypokalemia (3 cases). Apart from 1 case of congenital long QT syndrome, slowing of the sinus rhythm was observed (78.3 +/- 2.6 to 60.2 +/- 2.7 bpm, p less than 0.001) in the 3 hours preceding these episodes, and ventricular bigeminy with a long coupling interval was recorded in the lasts seconds before the torsades. The 41 (59 p. cent) cases of ventricular fibrillation (VF) were observed in men aged 64.9 +/- 2 years with coronary artery disease (39/41). However signs of acute ischaemia were only found in 5 cases. The VF was primary in 8 cases and secondary to ventricular tachycardia (VT in 33 cases). An acceleration of the cardiac rhythm (83.3 +/- 3.4 to 90 +/- 4.1 bpm, p less than 0.01) was recorded in the hour preceding VF and other arrhythmias were common: atrial tachycardia (4 cases), atrial extrasystoles (4 cases), a new type of ventricular extrasystoles (VES). The VF and VT were preceded by a long cycle in 17 cases. The first complex was different from previous VES in 10 cases and identical to the previous VES in 16 cases; in 4 cases this feature could not be identified and in 11 cases there were no premonitory VES. The coupling interval of the initial VES was shorter than that of the most premature preceding VES (368 +/- 13 ms vs 442 +/- 19 ms, p less than 0.001), especially in primary VF (335 +/- 9 ms, N = 8) compared to polymorphic VT (360 +/- 12 ms, N = 11) or monomorphic VT (384 +/- 18 ms N = 22).(ABSTRACT TRUNCATED AT 250 WORDS)