阵发性室上性心动过速(SVT)及房室传导阻滞(AVB)伴胸痛或心肌缺血患者冠状动脉造影结果分析

目的　探讨临床诊断为阵发性室上性心动过速 (SVT)及房室传导阻滞 (AVB)伴胸痛或心肌缺血患者心肌缺血的病因及其临床意义。方法　 5 1例 SVT或 AVB伴不同程度胸痛、胸闷、气短或心肌缺血患者 ,在介入检查或治疗的同时行冠状动脉造影和左心室造影术 ,分析冠状动脉造影结果、术后诊断及疾病转归情况 ,并将其中冠状动脉造影正常者及有病变的部分临床资料对比分析。结果　冠状动脉造影正常者 37例 (占 72 .5 % ) ,其中女性 2 0例 (占正常者 5 4 .1% )。 SVT 14例 (占所有 SVT病人的 77.8% ) ,AVB 2 3例 (占所有 AVB病人的 6 9.7% )。单纯传导系统退行性 AVB或合并房性心律失常 19例 (19/ 33,占 5 7.6 % ) ,其中 4例伴退行性瓣膜病变 ,6例伴冠状动脉粥样硬化 ;AVB伴冠心病者 4例 (4/ 33,占 12 .1% )。SVT病人中 ,冠状动脉造影阳性并确诊为冠心病者仅有 2例 (2 / 18,占 11.1% ) ,而大多数不伴器质性心脏病 (14 / 18,占 77.8% )。大多数 AVB病人在安置起搏器后症状及缺血改善。吸烟、血糖、L DI- C及 L p(a)在冠状动脉造影正常与异常之间差异显著 (P分别 <0 .0 1及 <0 .0 5 )。结论　大多数SVT及 AVB病人缺乏冠心病基础 ,所以有典型心绞痛的 SVT及 AVB病人 ,尤其 4 0岁以上男性 ,才有必要在做介入检查或治疗的     

Electrocardiographic Diagnosis of Atrial Tachycardia: Classification,P‐Wave Morphology,and Differential Diagnosis with Other Supraventricular Tachycardias

Atrial tachycardia is defined as a regular atrial activation from atrial areas with centrifugal spread, caused by enhanced automaticity, triggered activity or microreentry. New ECG classification differentiates between focal and macroreentrant atrial tachycardia. Macroreentrant atrial tachycardias include typical atrial flutter and other well characterized macroreentrant circuits in right and left atrium. Typical atrial flutter has been described as counterclockwise reentry within right atrial and it presents a characteristic ECG “sawtooth” pattern on the inferior leads. The foci responsible for focal atrial tachycardia do not occur randomly throughout the atria but tend to cluster at characteristic anatomical locations. The surface ECG is a very helpful tool in directing mapping to particular areas of interest. Atrial tachycardia should be differentiated from other supraventricular tachycardias. We propose a diagnostic algorithm in order to help the physician to discriminate among those. Holter analysis could offer further details to differentiate between atrial tachycardia and another supraventricular tachycardia. However, if the diagnosis is uncertain, it is possible to utilize vagal maneuvers or adenosine administration. In conclusion, in spite of well–known limits, a good interpretation of ECG is very important and it could help the physician to manage and to treat correctly patients with atrial tachycardia.     

aVR导联ST段抬高对阵发性室上性心动过速的鉴别价值

目的探讨aVR导联ST段抬高及其持续时间对阵发性室上性心动过速（PSVT）的鉴别价值。方法126例行射频消融治疗成功的PSVT患者，其中房室折返性心动过速（AVRT）65例，房室结折返性心动过速（AVNRT）61例。分析其aVR导联ST段抬高幅度及持续时间。结果65例AVRT中aVR导联ST抬高且持续时间≥0．08s有46例，61例AVNRT中有13例，诊断AVRT的敏感性、特异性及阳性预测值分别为70．8％，78．7％，78．0％；46例aVR导联ST段抬高的AVRT中左侧旁道占38例，诊断左侧旁道的敏感性、特异性及阳性预测值分别为79．2％，52．9％，82．6％。结论aVR导联ST段抬高及其持续时间有助于鉴别阵发性室上性心动过速，且其多发生于左侧旁道。     

An approach to therapy of supraventricular tachyarrhythmias: An algorithm versus individualized therapy

Approaches to the treatment of supraventricular arrhythmias, including atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular (AV) reentrant tachycardia, and AV nodal reentrant tachycardia, continue to evolve. Within the past two decades, many new and effective treatments have become available. These include several new antiarrhythmic agents, ablative therapies, pacing and surgical modalities, and cardioversion/defibrillation techniques. This paper provides an algorithm for the treatment of these supraventricular arrhythmias which includes therapy for the acute episode as well as the prevention of subsequent episodes of the tachyarrhythmia.     

心律平药动学和药效学观察

应用高效液相色谱法测定１１例阵发性室上性心动过速静脉注射心律平和１５例室性心律失常口服心律平的药浓度时间曲线。静脉注射者药动学符合二室开放模型，主要药动学参数：分布相半衰期（Ｔ（１／２）α）０．０５５±０．０１ｈ，清除半衰期（Ｔ（１／２）β）２．９９±０．５３ｈ，中央分布容积（Ｖｃ）０．０４８±０．０１１Ｌ／ｋｇ，终止室上性心动过速有效血浓度１０３２．６±６２４．１μｇ／ｍｌ。口服者药动学参数Ｔ（１／２）α０．３３±０．２ｈ，Ｔ（１／２）β６．８９±２．７ｈ，ＴＰＫ１．９５±０．４ｈ，ＣＳＴ２４３±１６１μｇ／ｍｌ。１３例口服４５０ｍｇ／ｄ控制室性早搏有效率６９．２％，有效血浓度２９７．７±２６４．６ｎｇ／ｍｌ。提示心律平代谢９３％为强代谢型，应用同等剂量，血浓度差别甚大，有效血浓度个体间差异也不小，因此不能根据剂量估测血浓度高低，也不能根据血浓度预测疗效和促心律失常反应，其治疗应根据临床观察、个体化剂量予以调整。     

Safety of flecainide versus propafenone for the long-term management of symptomatic paroxysmal supraventricular tachyarrhythmias: Report from the Flecainide and Propafenone Italian Study (FAPIS) group

In order to compare the long-term safety of flecainide and propafenone,an open label, randomized, parallel group study was performedin 335 patients with paroxysmal atrial fibrillation (n=200)or paroxysmal supra ventricular tachycardia (n=135), and nohistory of heart disease. Patients were treated with an initialdaily dose of flecainide 100 mg (n=72) or propafenone 450 mg(n=63) for paroxysmal supraventricular tachycardia and flecainide200 mg (n=97) or propafenone 450 mg (n=103) for paroxysmal atrialfibrillation. Dose escalations were permitted after 2 attacks,up to a maximum of flecainide 300 mg or propafenone 900 mg.day^–1. Follow-up duration was 12 months, or when patientsstopped the treatment as a result of inadequate efficacy oradverse experiences. Twelve patients on flecainide reported 16 cardiac adverse experiences,of whom six discontinued the treatment. Seven propafenone patientshad eight cardiac adverse experiences, of whom five discontinuedthe treatment. Serious proarrhythmic events were infrequent:one case of ventricular tachycardia on propafenone; two casesof atrial fibrillation with rapid ventricular response on flecainide,associated in one patient with pulmonary oedema. An intention-to-treat analysis showed that the probability of12 months' safe and effective treatment of paroxysmal supraventriculartachycardia was 93% for flecainide and 86% for propafenone (P=0·24),whereas in paroxysmal atrial fibrillation it was 77% for flecainideand 75% for propafenone (P=0·72). In conclusion, flecainide and propafenone were safe in the long-termtreatment of patients with paroxysmal supraventricular tachyarrhythmiasand without evidence of clinically significant heart disease.     

Adenosine‐Induced Ventricular Arrhythmias in Patients with Supraventricular Tachycardias

Background: Adenosine is widely used for the diagnosis and the termination of supraventricular arrhythmias. There are many case reports and few series about the proarrhythmic potential of adenosine. We sought to evaluate the proarrhythmic potential of adenosine used to terminate the supraventricular arrhythmias. Methods: The records of all patients that received adenosine for the termination of supraventricular tachycardia were reviewed retrospectively and those with a continuous electrocardiographic (ECG) recording during adenosine administration were included to the study. Results: Our search identified 52 supraventricular episodes of 46 patients with a continuous ECG recording during adenosine administration. Following adenosine administration, premature ventricular contraction (PVC) or ventricular tachycardia (VT) developed in 22 (47.8%) patients and in 26 (50%) tachycardia episodes. No patient had a sustained VT. Nonsustained VT developed in eight (17.4%) patients. All VT episodes were polymorphic, short, and self‐terminating. When the basal and demographic properties of patients with PVC or VT and those without PVT or VT were compared, there was no significant difference. Conclusions: Adenosine is a quite safe and effective drug for the termination of narrow QRS complex tachycardia but it often induces nonsustained VT or PVC that are clinically insignificant in the absence of other accompanying heart disease.     

Mechanism of repolarization change during initiation of supraventricular tachycardia

INTRODUCTION: Previous literature has documented the association between narrow QRS supraventricular tachycardia (SVT) and pronounced ST-T segment change. The aim of this study was to evaluate repolarization changes during SVT initiation and demonstrate the possible mechanism. METHODS AND RESULTS: Fifty-one consecutive patients (20 men and 31 women; mean age 46.1 +/- 16.4 years) with narrow QRS SVT (32 patients with AV nodal reentrant tachycardia and 19 patients with AV reentrant tachycardia) were included. We retrospectively analyzed the intracardiac recordings and ST-T segment changes on 12-lead surface ECGs during SVT initiation. Twenty-six (51%) patients developed ST segment repolarization changes during SVT initiation. Patients with shorter baseline sinus cycle length, shorter tachycardia cycle length, elevated systolic blood pressure before tachycardia induction, and greater reduction of systolic blood pressure had a higher incidence of repolarization changes. However, multivariate analysis showed that reduction of systolic blood pressure after SVT induction was the only independent predictor of repolarization changes. Furthermore, the maximal degree of ST segment depression during SVT correlated with the reduction of systolic blood pressure (r = 0.75, P < 0.001). CONCLUSION: Repolarization changes during SVT initiation were caused mainly by concurrent hemodynamic change after SVT initiation with abrupt cycle length shortening.