阵发性室上性心动过速复极改变的临床意义探讨

为探讨阵发性室上性心动过速时复极改变与临床分型的关系,对28例房室折返性心动过速患者和22例房室结内折返性心动过速患者的心电图、食管调搏以及心内电生理检查进行回顾性分析。结果发现两组患者室上性心动过速时R-R间期差异并无显著意义(332.1±39.4ms对350±38ms,P>0.05),但在QRS波群电交替、ST-T改变方向差异均有显著意义(54％对14％,61％对27％,P<0.05)。并发现ST-T改变的导联与旁道位置有一定关系。提示分析阵发性室上性今动过速时的复极改变可作为鉴别室上性心动过速类型和旁道位置的一种新的辅助诊断方法。     

Long-Term Efficacy of Atenolol for Atrioventricular Reciprocating Tachycardia in Children Less Than 5 Years Old

Atrioventricular reciprocating tachycardia (AVRT) using an accessory pathway is the most common supraventricular tachycardia observed in infancy and childhood. There is a general agreement to treat children older than 5 years who are on a potentially long-term antiarrhythmic agent with radiofrequency catheter ablation. Atenolol, a relatively long-acting and cardioselective -adrenoceptor blocker, has been used to control the various types of supraventricular tachycardia in children and adults. There are few reports on the use of atenolol in children <5 years old with AVRT. This retrospective study reports our experience in 22 children <5 years old (median age, 20 months) who received atenolol monotherapy between 1995 and 2001 for treatment of AVRT. AVRT was confirmed in 17 patients by transvenous or transesophageal electrophysiologic study and in 5 patients by documented preexcitation on electrocardiograms. In nine patients atenolol was the first antiarrhythmic drug given. In 15 of the 22 patients (68%) therapy with atenolol was considered successful. The average effective dose of atenolol in these 15 patients was 1.2 ± 0.3 mg/kg/day. During a median follow-up of 41 months (8–74 months), atenolol had been discontinued in 10 patients and no further attacks of tachycardia occurred except in 1 patient. In no case did the drug have to be withdrawn for adverse effects. In conclusion, this retrospective study shows that atenolol as a monotherapy is efficient and relatively safe in the long-term treatment of AVRT in young children. Atenolol can be recommended as a first-line treatment option for the management of AVRT in infants and young children.     

Zebrafish embryos express an orthologue of HERG and are sensitive toward a range of QT-prolonging drugs inducing severe arrhythmia

A wide range of drugs has been shown to prolong the QT interval of the electrocardiogram by blocking the pore-forming subunit of the rapidly activating delayed rectifier K+ channel, HERG (ether-à-go-go-related gene), sometimes leading to life-threatening arrhythmia. In this paper we describe cloning, sequence, and expression of the zebrafish orthologue of HERG, Zerg. Further, we studied effects of Zerg inhibition in zebrafish embryos caused by drugs or by an antisense approach. Zerg is expressed specifically in both heart chambers of zebrafish embryos, is composed of six transmembrane domains, and shows an especially high degree of amino acid conservation in the S6 and pore domain (99% identity). Several QT-prolonging drugs added to the bathing medium elicited bradycardia and arrhythmia in zebrafish embryos. The arrhythmia induced ranged from an atrioventricular 2:1 block, the ventricle beating half as often as the atrium, to more severe irregular arrhythmia with higher concentrations of the drugs. These effects were highly specific, reproducible, and rapid, e.g., 10 microM astemizole caused a 2:1 heartbeat within a minute after addition of the compound in all the embryos studied. Morpholino antisense oligonucleotides targeting Zerg were injected into zebrafish embryos and elicited similar dose-sensitive and specific arrhythmia as the QT-prolonging drugs, suggesting an evolutionarily conserved role for Erg in regulating heartbeat rate and rhythm. Further, we identified a mutation in the Per-Arnt-Sim domain of the Zerg channel in the breakdance mutant, also characterized by a 2:1 atrioventricular block. In conclusion, the zebrafish could be a tractable model organism for the study of Erg function and modulation but might also have a value in the field of cardiovascular pharmacology, e.g., as an early preclinical model for testing drugs under development for potential QT prolongation.     

Responsiveness to rapid atrial pacing of the specialized atrioventricular conduction system in children

Summary Responsiveness to rapid atrial pacing of the specialized atrioventricular (A-V) conduction system was studied in 25 patients aged 2 months to 18 years. Atrial pacing via a catheter placed at the right atrial superior vena cava junction was initiated at rates slightly greater than the sinus rate and gradually increased to rates as high as 600 stimuli per minute. His bundle electrograms were obtained in most patients. When the atrial pacing rate (x-axis) was plotted against the corresponding ventricular rate (y-axis), the curve was M-shaped. The initial ascending limb occurred during 1:1 A-V conduction with rates as high as 270 stimuli per minute. The first descending limb resulted from Wenckebach type A-V block occurring at rates of 160 to 300 stimuli per minute. The second ascending limb corresponded to periods of 2:1 A-V block observed at rates of 200 to 536 stimuli per minute, and the final descending limb was related to higher degrees of block at both the pacing site and the A-V node. The second descending limb was seen with pacing rates of 296 to 600 stimuli per minute. The rates required to produce Wenckebach type A-V block in this group of children were higher than those reported in adults. One patient with spontaneous first-degree A-V block developed 2:1 A-V block at a pacing rate of only 150 stimuli per minute.This technique for studying the response to rapid atrial pacing of the specialized A-V conduction system characterises its functional capacity. The technique can be applied rapidly and safely in selected patients.     

Permanent third-degree atrioventricular block as clinical presentation of an intracardiac bronchogenic cyst.

Bronchogenic cysts are the most common primary cysts in the mediastinum. However, intracardiac bronchogenic cysts are uncommon. The present case represents a unique situation, in which an intracardiac bronchogenic cyst at the region of the atrioventricular node presented as permanent complete atrioventricular block (AVB) and was associated with the presence of an ostium secundum atrial septal defect.     

Atrioventricular nodal reverse facilitation in connexin40-deficient mice

BACKGROUND: Facilitation is an important physiologic property of the atrioventricular (AV) node. Previous studies demonstrated abnormal AV conduction in connexin (Cx)40-deficient mice. OBJECTIVES: We hypothesize that Cx40-deficient mice display altered patterns of AV nodal facilitation compared with wild-type mice. METHODS: Sixteen 36-week-old mice (eight Cx40(-/-) mice and eight Cx40(+/+) controls) underwent in vivo closed chest electrophysiologic study. A 2Fr octapolar catheter was advanced into the right ventricle to record a His-bundle electrogram. A special facilitation stimulation protocol was performed in each mouse to evaluate facilitation. Following atrial drive pacing (S1S1) at 150 ms, a facilitating beat S2 was delivered prior to the test beat S3. S3H3 was measured for varying S1S2 values at fixed H2S3 intervals. RESULTS: Progressive shortening of S1S2 (from 150 ms to 130, 110, and 90 ms) resulted in gradual prolongation of S2H2. The prolongation was more pronounced in Cx40(-/-) mice for each S1S2 compared with wild-type mice (P <.001). In each wild-type mouse, for a given H2S3 interval, this gradual increase in S2H2 produced progressive shortening of S3H3, so-called AV nodal facilitation phenomenon. However, in each Cx40(-/-) mouse, facilitation was seen only at S1S2 of 130 ms (P <.001 vs S1S2 of 150 ms). Evidence of reverse facilitation was documented at S1S2 of 110 and 90 ms. CONCLUSION: Facilitation is observed in wild-type mice. With similar S1S2 intervals in Cx40-deficient mice, facilitation is seen only at longer S1S2 intervals, whereas reverse facilitation is seen at shorter S1S2 intervals, suggesting that Cx40 is involved in the generation of AV nodal facilitation.     

The diagnostic process and perioperative and anesthetic management of an undiagnosed congenital cyanotic cardiac defect in an adult for trauma surgery

A 39-year-old patient awaiting emergency surgery due to a crush foot injury, with an undiagnosed cyanotic cardiac lesion that was diagnosed later as a complete atrioventricular canal defect, is presented. Complete atrioventricular canal defects usually present in the first few months of life and can be fatal if not treated in the first few years. Adult patients with congenital cardiac malformations seem to be at increased risk for noncardiac surgery. The diagnostic process, perioperative management, and anesthetic implications are discussed.     

Diagnostic trilemma: Isorhythmic AV dissociation mimicking intermittent preexcitation and acute inferior myocardial infarction

In this case report, we present a patient with intermittent isorhythmic atrioventricular dissociation mimicking two different electrocardiographic entities: ventricular preexcitation pattern and recurrent acute inferior myocardial infarction.