Atrial fibrillation and recurrent ventricular fibrillation during hypokalemia in Brugada syndrome

A 41-year-old man with Brugada syndrome (BS) and no previous episodes of aborted sudden death or syncope referred to local emergency room for an episode of symptomatic atrial fibrillation. Blood chemistry results showed hypokalemia (2.9 mEq/L). The other parameters were within the normal range. After few minutes, an episode of ventricular fibrillation treated with biphasic DC shock 150 J occurred. In successive 2 hours, the patient experienced recurrent episodes of ventricular tachycardia and fibrillation. Each biphasic DC shock 150 J was effective to restore sinus rhythm. No further episodes occurred after normalization of serum levels of potassium. Before discharge, an implantable cardioverter defibrillator was inserted to prevent sudden cardiac death. Hypokalemia increases the risk of arrhythmic events in BS.     

早期复极综合征在动态心电图检查中的特点

目的：了解动态心电图对早期复极综合征的检出率并分析其特点。方法：回顾四年间2 460例动态心电图,对符合早期复极综合征诊断者进行分析。结果：符合早期复极综合征患者40例,检出率1.62%,均为男性,年龄22～70岁。动态心电图检出比率明显高于常规心电图（1 0 0%∶1 5%,P〈0.0 5）,Ⅰ型明显多于Ⅱ型（8 5%∶1 5%,P〈0.05）。结论：动态心电图对早期复极综合征检出Ⅰ型为主,以青壮年多见。     

Theophylline as an adjunct to control malignant ventricular arrhythmia associated with early repolarization

Early repolarization (ER) has been associated with an increased risk of sudden cardiac arrest. Interestingly, ventricular arrhythmias seem to be triggered by parasympathetic stimulation. In the present case report, we describe complete control of highly frequent malignant ventricular arrhythmias after adding theophylline to ineffective oral hydroquinidine and high‐rate pacing in a patient suffering from malignant ER. We hypothesize that the theophylline‐mediated enhanced beta‐adrenergic stimulation could reduce the transmural myocardial voltage discrepancy by increasing the inward I_Ca,L current.     

Atrial fibrillation associated with hypokalemia due to primary hyperaldosteronism (Conn's syndrome)

Aldosterone is a major regulator of the body potassium stores through its role in potassium excretion by the kidney. However, it is unclear whether aldosterone affects transcellular distribution of potassium in atrial myocytes, and whether hypokalemia associated with primary hyperaldosteronism increases susceptibility to atrial fibrillation (AF). We report a case of a 58-year-old male with Conn's syndrome in whom symptomatic AF was related to hypokalemia.     

健康体检中早期复极综合征的临床意义探讨

目的：了解早期复极综合征（ERS）的发生率与性别、年龄、心率、机体有氧活动量的关系，探讨其临床意义。方法：采用整群抽样原则对10000例年龄在20-60岁的健康体检者的心电图进行分析。结果：共检出ERS338例，发生率3．38％，其中男320例，女18例。随着年龄的增加及心率的增快ERS的发生率逐渐降低。轻度劳动强度者发生率2．31％，中度以上劳动强度者发生率4．18％。结论：ERS多见于青壮年劳动强度较高男性，发病机制多认为与迷走神经张力增加有关，其心电图特点不具有指证心血管病变的临床意义。     

早期复极综合征与左心室纤维肌束关系的初步研究

目的：探讨左心室纤维肌束及其特征与早期复极综合征的关系，方法，选择31例早期复极综合征患者（ERS组），简单随机法选择100例健康人（对照组），检测其左室纤维肌束，并对左室纤维肌束发生率，左室纤维肌束位置及数目的构成比，左室纤维肌束的长度，宽度及左室纤维肌束与室间隔的夹角进行统计学分析，结果：ERS组与对照组相比较，左室纤维肌束的发生率差异无显著性意义（P＞0．05），两组左室纤维肌束的不同数目例数构成比，长度、宽度均差异无显著性意义（P＞0．05），两组之间左室纤维肌束位置的构成比差异有显著性意义（P＜0．001），ERS组起于室间隔中部而止于左室游离壁中段的左室纤维肌束约47％，对照组仅2％；ERS组左室纤维肌束与室间隔的夹角显著高于对照组（P＜0．01），结论：左室纤维肌束的位置及夹角是导致早期复极综合征的独立危险因素，推测其原因主要与左室纤维肌束对起止点的牵拉引起部分内膜下心肌较正常激动顺序提前复极，造成复极不一致有关。     

Contrast‐induced early repolarization pattern and ventricular fibrillation

Malignant arrhythmias during coronary angiography consist a complication of the procedure. Clinicians should be aware that intracoronary infusion of contrast medium can lead to physiological changes that lower the ventricular fibrillation threshold.     

Transseptal left ventricular endocardial pacing reduces dispersion of ventricular repolarization

Background: Cardiac resynchronization therapy (CRT) may be proarrhythmic in some patients. This may be due to the effect of left ventricular (LV) epicardial pacing on ventricular repolarization. The purpose of this study was to evaluate the effect of endocardial versus epicardial LV biventricular pacing on surface electrocardiogram (ECG) parameters that are known markers of arrhythmogenic repolarization. Methods: ECG markers of repolarization (QT dispersion, QTD; T peak to end, T_peak‐end; T_peak‐end dispersion, T_peak‐endD; QTc) were retrospectively measured before and after CRT in seven patients with transseptal LV endocardial leads (TS group), 28 matched patients with coronary sinus (CS) LV leads (CS group), and eight patients with surgical LV epicardial leads (SUR group). All ECGs were scanned and analyzed using digital callipers. Results: Compared to the CS group, the TS group CRT was associated with a significant postpacing reduction in QTD (?45.2 ± 35.6 vs ?4.3 ± 43.6 ms, P = 0.03) and T_peak‐end (?24.2 ± 22.1 vs 3.4 ± 26.7 ms, P = 0.02). There was a nonsignificant post‐CRT reduction in both T_peak‐endD (?11.3 ± 31.0 vs 2.4 ± 28.9 ms, P = 0.27) and QTc (?50.0 ± 46.4 vs 4.4 ± 70.2 ms, P = 0.06) in the TS versus the CS group. In contrast, there were no differences between the SUR and CS groups in terms of the effect of CRT on these repolarization parameters. Conclusions: CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia. (PACE 2011; 34:1258–1266)     

Current concepts concerning the syndrome of early ventricular repolarization

Electrocardiograms of 1000 patients examined in a polyclinic for various diseases and during prophylactic checkups, were analyzed. The syndrome of early ventricular repolarization (SEVR) was detected in 54 (5.4%) patients. According to the proposed classification scheme of SEVR one could determine its clinical value and the distribution of frequency of its variants and types. The authors put forward present-day ideas as to SEVR assumed genesis with an attempt to verify some of them. Differential-diagnostic pharmacological tests (procainamide, quinidine and propranolol) were recommended for SEVR recognition.     

The clinico-electrocardiographic classification of the early ventricular repolarization syndrome]

Based on an analysis of 4980 ECGs of patients, the authors could distinguish and classify the clinico-electrocardiographic versions of the early ventricular repolarization syndrome (EVRS): permanent, occurring for the first time, suddenly disappearing, intermittent with a gigantic T wave; with a negative T wave, with a short-term T wave inversion, marked by the combination with Wolff-Parkinson-White syndrome, and additional chordae of the left ventricle. The clinico-electrocardiographic classification of the EVRS is of paramount importance for practitioners owing to an assumption that the EVRS is not only a version of the normal ECG but also can be a marker of CHD. The authors view the EVRS as an independent version of the preexcitation syndrome along with Wolff-Parkinson-White and CLK syndromes, with the manifestations of which it may combine.     

Remodeling of ventricular repolarization in a chronic doxorubicin cardiotoxicity rat model

Doxorubicin, one of the most effective anticancer drugs, is characterized by severe cardiotoxic effects, which induce cardiac remodeling and congestive heart failure. The aim of the study was to evaluate remodeling of ventricular repolarization heterogeneity in chronic doxorubicin cardiotoxicity in rats. Doxorubicin cardiotoxicity was produced by six equal intraperitoneal injections of the drug in a cumulative dose of 15 mg/kg in a 2‐week period. Electrophysiological mapping of the ventricular epicardium in situ was performed 6 weeks after the last injection of doxorubicin. Activation–recovery intervals (ARIs) were used for the evaluation of the heterogeneity in repolarization durations. The major findings were as follows: (1) ARIs on the ventricular epicardium of both ventricles were significantly prolonged in the doxorubicin group and (2) this inhomogeneous prolongation of ARIs on the ventricular epicardium resulted in (i) the increase in the dispersion of repolarization across the ventricular epicardium and (ii) the inhomogeneous alterations of the regional ARI gradients on the ventricular epicardium. These changes in repolarization could explain the electrocardiographic alterations, that is, the prolongation of the QT interval and flattening of the T wave.     

Pathology of the cardiovascular system and early ventricular repolarization syndrome

An attempt was made for the first time to determine the prevalence of the early ventricular repolarization syndrome (EVRS) in cardiovascular diseases in order to specify the clinico-electrocardiographic significance of the given electrophysiological phenomenon and its interrelationship with the rate of rhythm and heart conduction disorders. The changes discovered cast doubt on the generally accepted concept of the benign character of the EVRS and orient to the necessity of pharmacological correction in more frequent arrhythmogenic episodes in EVRS carriers suffering from cardiovascular pathology. Some diagnostic methods (electrocardiography, pharmacological tests) have been evaluated and suggested as optimal for diagnosing the EVRS.     

Stability of ventricular repolarization in conscious dogs with chronic atrioventricular dissociation and his-bundle pacing

Following AVN ablation, eight dogs were surgically instrumented for chronic (continuous) HIS-bundle pacing. For data collection, implanted pacemakers were transiently programmed to pace in stepwise ascending ramps at rates from 50 to 200 beats/min in 30-beat/min steps. Each rate was held for 60 seconds. At each rate, ECG signals were collected from conscious dogs for measurements of QT intervals during the last 10 seconds of each paced rate to construct a QT-HR ramp. This QT-HR ramp was repeated twice on each day of study 10 minutes apart. Dogs were randomly assigned to two groups and studied weekly for a minimum of 6 weeks. Group 1 dogs had pacemakers programmed to a rate of 80 beats/min for the duration of the study. Group 2 dogs were paced at 80 beats/min for weeks 1-3, then increased to 140 beats/min for weeks 4-6. The difference between paired QT-HR ramps within 1 day was <3 ms. QT-HR ramps were statistically indistinguishable over the 6-week study for group 1 dogs. Group 2 dogs experienced a slight flattening in the slope of the QT-HR ramps from week 3 to week 6 due to a reduction in QT interval at low HRs (50 and 80 beats/min) only. This conscious HIS-pacing model in dogs is a sensitive, stable, and reproducible method to define ventricular repolarization characteristics over a range of programmable HRs and experimental conditions.     

不同ST段形态早复极人群心率变异性、心率减速力及心室复极离散度的研究

目的探讨不同ST段形态早复极人群心率变异性（HRV）、心率减速力（DC）及心室复极离散度。方法研究对象早复极个体100例,分为ST段水平上升或下斜型下降50例和ST段上升或上斜型上升50例。正常对照组50例。三组患者均行24 h动态心电图检测,分析HRV、DC、心室复极离散度等指标。结果 ST段水平上升或下斜型下降组患者心率变异性明显降低,心率减速力下降,心室复极离散度增加。结论 ST段水平上升或下斜型下降的早复极个体发生恶性心律失常风险大,心率变异性、心率减速力及心室复极离散度等可以作为相关评价指标。     

K+channels and control of ventricular repolarization in the heart

Summary— K+ channels form a large family, in which voltage-operated and ligand-operated channels can be distinguished. Under physiological conditions, four K+ currents contribute to the repolarization process and their role is discussed: i) the transient outward current (i_1o) is responsible for the rapid initial repolarization process from the crest of the action potential to the plateau level; ii) the delayed K+ current (i_K) is involved in the overall repolarization process during the plateau; iii) the inward rectifier (i_K1) is responsible for the final rapid repolarization and the maintenance of the resting potential; iv) a ligand-operated channel activated by acetylcholine and adenosine participates in the repolarization process and the maintenance of the resting potential in nodal, atrial and Purkinje cells. In the context of antiarrhythmic interventions, block of outward K+ current and prolongation of refractoriness is currently considered as an alternative to block of the Na+ current and reduction of conduction velocity. Although some of these drugs show use-dependent block, the frequency-dependent changes in current and action potential duration are not ideal.     

Mechanisms of hypokalemia‐induced ventricular arrhythmogenicity

Hypokalemia is a common biochemical finding in cardiac patients and may represent a side effect of diuretic therapy or result from endogenous activation of renin–angiotensin system and high adrenergic tone. Hypokalemia is independent risk factor contributing to reduced survival of cardiac patients and increased incidence of arrhythmic death. Animal studies demonstrate that hypokalemia‐induced arrhythmogenicity is attributed to prolonged ventricular repolarization, slowed conduction, and abnormal pacemaker activity. The prolongation of ventricular repolarization in hypokalemic setting is caused by inhibition of outward potassium currents and often associated with increased propensity for early afterdepolarizations. Slowed conduction is attributed to membrane hyperpolarization and increased excitation threshold. Abnormal pacemaker activity is attributed to increased slope of diastolic depolarization in Purkinje fibers, as well as delayed afterdepolarizations caused by Ca²⁺ overload secondary to inhibition of Na⁺–K⁺ pump and stimulation of the reverse mode of the Na⁺–Ca²⁺ exchange. Hypokalemia effect on repolarization is not uniform at distinct ventricular sites thereby contributing to amplified spatial repolarization gradients which promote unidirectional conduction block. In hypokalemic heart preparations, the prolongation of action potential may be associated with shortening of effective refractory period, thus increasing the propensity for ventricular re‐excitation over late phase of repolarization. Shortened refractoriness and slowed conduction contribute to reduced excitation wavelength thereby facilitating re‐entry. The interplay of triggering factors (early and delayed afterdepolarizations, oscillatory prepotentials in Purkinje fibers) and a favorable electrophysiological substrate (unidirectional conduction block, reduced excitation wavelength, increased critical interval for ventricular re‐excitation) may account for the mechanism of life‐threatening tachyarrhythmias in hypokalemic patients.